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	<entry>
		<id>https://www.wikidoc.org/index.php?title=Coronary_artery_aneurysm&amp;diff=761993</id>
		<title>Coronary artery aneurysm</title>
		<link rel="alternate" type="text/html" href="https://www.wikidoc.org/index.php?title=Coronary_artery_aneurysm&amp;diff=761993"/>
		<updated>2012-09-29T02:35:19Z</updated>

		<summary type="html">&lt;p&gt;Varun Kumar: /* Epidemiology and Demographics */&lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;{{Infobox_Disease |&lt;br /&gt;
  Name           = {{PAGENAME}} |&lt;br /&gt;
  Image          = |&lt;br /&gt;
  Caption        = |&lt;br /&gt;
  DiseasesDB     = |&lt;br /&gt;
  ICD10          = {{ICD10|I|25|4|i|20}} |&lt;br /&gt;
  ICD9           = {{ICD9|414.11}} |&lt;br /&gt;
  ICDO           = |&lt;br /&gt;
  OMIM           = |&lt;br /&gt;
  MedlinePlus    = |&lt;br /&gt;
  eMedicineSubj  = |&lt;br /&gt;
  eMedicineTopic = |&lt;br /&gt;
  MeshID         = D003323 |&lt;br /&gt;
}}&lt;br /&gt;
{{SI}}&lt;br /&gt;
&lt;br /&gt;
{{CMG}}&lt;br /&gt;
  &lt;br /&gt;
&#039;&#039;&#039;Associate Editor-In-Chief:&#039;&#039;&#039;  {{CZ}}; {{VK}}&lt;br /&gt;
&lt;br /&gt;
==Overview==&lt;br /&gt;
&#039;&#039;&#039;Coronary artery aneurysm&#039;&#039;&#039; (CAA) is an abnormal dilatation of a [[coronary artery]] segment over 1.5 times the diameter of normal adjacent segment.&amp;lt;ref name=&amp;quot;pmid4897732&amp;quot;&amp;gt;{{cite journal| author=Jarcho S| title=Bougon on coronary aneurysm (1812). | journal=Am J Cardiol | year= 1969 | volume= 24 | issue= 4 | pages= 551-3 | pmid=4897732 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;amp;tool=sumsearch.org/cite&amp;amp;retmode=ref&amp;amp;cmd=prlinks&amp;amp;id=4897732  }} &amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Epidemiology and Demographics==&lt;br /&gt;
&lt;br /&gt;
The incidence of CAA ranges widely between 0.3-5.3% within angiographic series with a mean incidence of 1.65%.&amp;lt;ref name=&amp;quot;pmid4052280&amp;quot;&amp;gt;{{cite journal| author=Hartnell GG, Parnell BM, Pridie RB| title=Coronary artery ectasia. Its prevalence and clinical significance in 4993 patients. | journal=Br Heart J | year= 1985 | volume= 54 | issue= 4 | pages= 392-5 | pmid=4052280 | doi= | pmc=PMC481917 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;amp;tool=sumsearch.org/cite&amp;amp;retmode=ref&amp;amp;cmd=prlinks&amp;amp;id=4052280  }} &amp;lt;/ref&amp;gt; A highest incidence of 10-12% was reported in a study from India. Perhaps reflecting a specific genetic and/or environmental predisposition.&amp;lt;ref name=&amp;quot;pmid2086442&amp;quot;&amp;gt;{{cite journal| author=Sharma SN, Kaul U, Sharma S, Wasir HS, Manchanda SC, Bahl VK et al.| title=Coronary arteriographic profile in young and old Indian patients with ischaemic heart disease: a comparative study. | journal=Indian Heart J | year= 1990 | volume= 42 | issue= 5 | pages= 365-9 | pmid=2086442 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;amp;tool=sumsearch.org/cite&amp;amp;retmode=ref&amp;amp;cmd=prlinks&amp;amp;id=2086442  }} &amp;lt;/ref&amp;gt; &lt;br /&gt;
&lt;br /&gt;
CAA most commonly occurs in [[right coronary artery]] accounting for 40-87% followed by [[left anterior descending artery]] and [[left circumflex artery]].&amp;lt;ref name=&amp;quot;pmid16230889&amp;quot;&amp;gt;{{cite journal| author=Villines TC, Avedissian LS, Elgin EE| title=Diffuse nonatherosclerotic coronary aneurysms: an unusual cause of sudden death in a young male and a literature review. | journal=Cardiol Rev | year= 2005 | volume= 13 | issue= 6 | pages= 309-11 | pmid=16230889 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;amp;tool=sumsearch.org/cite&amp;amp;retmode=ref&amp;amp;cmd=prlinks&amp;amp;id=16230889  }} &amp;lt;/ref&amp;gt;&amp;lt;ref name=&amp;quot;pmid6847792&amp;quot;&amp;gt;{{cite journal| author=Swaye PS, Fisher LD, Litwin P, Vignola PA, Judkins MP, Kemp HG et al.| title=Aneurysmal coronary artery disease. | journal=Circulation | year= 1983 | volume= 67 | issue= 1 | pages= 134-8 | pmid=6847792 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;amp;tool=sumsearch.org/cite&amp;amp;retmode=ref&amp;amp;cmd=prlinks&amp;amp;id=6847792  }} &amp;lt;/ref&amp;gt;. CAA of left main artery or triple-vessel CAA are rare&amp;lt;ref name=&amp;quot;pmid16230889&amp;quot;&amp;gt;{{cite journal| author=Villines TC, Avedissian LS, Elgin EE| title=Diffuse nonatherosclerotic coronary aneurysms: an unusual cause of sudden death in a young male and a literature review. | journal=Cardiol Rev | year= 2005 | volume= 13 | issue= 6 | pages= 309-11 | pmid=16230889 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;amp;tool=sumsearch.org/cite&amp;amp;retmode=ref&amp;amp;cmd=prlinks&amp;amp;id=16230889  }} &amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Diagnosis==&lt;br /&gt;
&lt;br /&gt;
It is often found coincidentally on [[coronary angiography]].&amp;lt;ref name=&amp;quot;pmid17063947&amp;quot;&amp;gt;{{cite journal |author=Pahlavan PS, Niroomand F |title=Coronary artery aneurysm: a review |journal=Clin Cardiol |volume=29 |issue=10 |pages=439–43 |year=2006 |month=October |pmid=17063947 |doi= |url=}}&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Causes==&lt;br /&gt;
&lt;br /&gt;
Causes include [[atherosclerosis]],&amp;lt;ref name=&amp;quot;pmid18466032&amp;quot;&amp;gt;{{cite journal |author=Nichols L, Lagana S, Parwani A |title=Coronary artery aneurysm: a review and hypothesis regarding etiology |journal=Arch. Pathol. Lab. Med. |volume=132 |issue=5 |pages=823–8 |year=2008 |month=May |pmid=18466032 |doi= |url=http://journals.allenpress.com/jrnlserv/?request=get-abstract&amp;amp;issn=0003-9985&amp;amp;volume=132&amp;amp;page=823}}&amp;lt;/ref&amp;gt; [[Kawasaki disease]]&amp;lt;ref name=&amp;quot;pmid17456996&amp;quot;&amp;gt;{{cite journal |author=Fukazawa R, Ikegam E, Watanabe M, &#039;&#039;et al&#039;&#039; |title=Coronary artery aneurysm induced by Kawasaki disease in children show features typical senescence |journal=Circ. J. |volume=71 |issue=5 |pages=709–15 |year=2007 |month=May |pmid=17456996 |doi= |url=http://joi.jlc.jst.go.jp/JST.JSTAGE/circj/71.709?from=PubMed}}&amp;lt;/ref&amp;gt; and [[coronary catheterization]] as well as vasculitides and collagen vascular diseases. &lt;br /&gt;
&lt;br /&gt;
==Prognosis==&lt;br /&gt;
&lt;br /&gt;
It has a good prognosis.&amp;lt;ref name=&amp;quot;pmid17063947&amp;quot;&amp;gt;{{cite journal |author=Pahlavan PS, Niroomand F |title=Coronary artery aneurysm: a review |journal=Clin Cardiol |volume=29 |issue=10 |pages=439–43 |year=2006 |month=October |pmid=17063947 |doi= |url=}}&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Definition==&lt;br /&gt;
&lt;br /&gt;
A localized arterial widening (dilatation) that usually manifests itself as a bulge. Its presence may lead to weakening of the wall and eventual rupture.&lt;br /&gt;
&lt;br /&gt;
===Grade 0===&lt;br /&gt;
&lt;br /&gt;
None – no [[ectasia]] present.&lt;br /&gt;
&lt;br /&gt;
===Grade 1===&lt;br /&gt;
&lt;br /&gt;
[[Ectasia]] – visual assessment of [[ectasia]] &amp;gt;1 &amp;amp; &amp;lt; 1.5 times the normal artery diameter located anywhere in the culprit artery.&lt;br /&gt;
&lt;br /&gt;
===Grade 2===&lt;br /&gt;
&lt;br /&gt;
Aneurysm – visual assessment of an [[aneurysm]] &amp;gt; 1.5 times the normal artery diameter located anywhere in the culprit artery.&lt;br /&gt;
&lt;br /&gt;
*NOTE: An [[aneurysm]] can be further classified as either [[saccular]] (wider than it is long) or [[fusiform]] (elongated).&lt;br /&gt;
&lt;br /&gt;
==References==&lt;br /&gt;
{{reflist|2}}&lt;br /&gt;
&lt;br /&gt;
{{Circulatory system pathology}}&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[[Category:Cardiology]]&lt;br /&gt;
[[Category:Angiographic Definitions]]&lt;br /&gt;
&lt;br /&gt;
{{WikiDoc Help Menu}}&lt;br /&gt;
{{WikiDoc Sources}}&lt;/div&gt;</summary>
		<author><name>Varun Kumar</name></author>
	</entry>
	<entry>
		<id>https://www.wikidoc.org/index.php?title=Coronary_artery_aneurysm&amp;diff=761987</id>
		<title>Coronary artery aneurysm</title>
		<link rel="alternate" type="text/html" href="https://www.wikidoc.org/index.php?title=Coronary_artery_aneurysm&amp;diff=761987"/>
		<updated>2012-09-29T01:37:03Z</updated>

		<summary type="html">&lt;p&gt;Varun Kumar: &lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;{{Infobox_Disease |&lt;br /&gt;
  Name           = {{PAGENAME}} |&lt;br /&gt;
  Image          = |&lt;br /&gt;
  Caption        = |&lt;br /&gt;
  DiseasesDB     = |&lt;br /&gt;
  ICD10          = {{ICD10|I|25|4|i|20}} |&lt;br /&gt;
  ICD9           = {{ICD9|414.11}} |&lt;br /&gt;
  ICDO           = |&lt;br /&gt;
  OMIM           = |&lt;br /&gt;
  MedlinePlus    = |&lt;br /&gt;
  eMedicineSubj  = |&lt;br /&gt;
  eMedicineTopic = |&lt;br /&gt;
  MeshID         = D003323 |&lt;br /&gt;
}}&lt;br /&gt;
{{SI}}&lt;br /&gt;
&lt;br /&gt;
{{CMG}}&lt;br /&gt;
  &lt;br /&gt;
&#039;&#039;&#039;Associate Editor-In-Chief:&#039;&#039;&#039;  {{CZ}}; {{VK}}&lt;br /&gt;
&lt;br /&gt;
==Overview==&lt;br /&gt;
&#039;&#039;&#039;Coronary artery aneurysm&#039;&#039;&#039; (CAA) is an abnormal dilatation of a [[coronary artery]] segment over 1.5 times the diameter of normal adjacent segment.&amp;lt;ref name=&amp;quot;pmid4897732&amp;quot;&amp;gt;{{cite journal| author=Jarcho S| title=Bougon on coronary aneurysm (1812). | journal=Am J Cardiol | year= 1969 | volume= 24 | issue= 4 | pages= 551-3 | pmid=4897732 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;amp;tool=sumsearch.org/cite&amp;amp;retmode=ref&amp;amp;cmd=prlinks&amp;amp;id=4897732  }} &amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Epidemiology and Demographics==&lt;br /&gt;
&lt;br /&gt;
The incidence of CAA ranges widely between 0.3-5.3% within angiographic series with a mean incidence of 1.65%.&amp;lt;ref name=&amp;quot;pmid4052280&amp;quot;&amp;gt;{{cite journal| author=Hartnell GG, Parnell BM, Pridie RB| title=Coronary artery ectasia. Its prevalence and clinical significance in 4993 patients. | journal=Br Heart J | year= 1985 | volume= 54 | issue= 4 | pages= 392-5 | pmid=4052280 | doi= | pmc=PMC481917 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;amp;tool=sumsearch.org/cite&amp;amp;retmode=ref&amp;amp;cmd=prlinks&amp;amp;id=4052280  }} &amp;lt;/ref&amp;gt;&lt;br /&gt;
CAA most commonly occurs in [[right coronary artery]] accounting for 40-87% followed by [[left anterior descending artery]] and [[left circumflex artery]].&amp;lt;ref name=&amp;quot;pmid16230889&amp;quot;&amp;gt;{{cite journal| author=Villines TC, Avedissian LS, Elgin EE| title=Diffuse nonatherosclerotic coronary aneurysms: an unusual cause of sudden death in a young male and a literature review. | journal=Cardiol Rev | year= 2005 | volume= 13 | issue= 6 | pages= 309-11 | pmid=16230889 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;amp;tool=sumsearch.org/cite&amp;amp;retmode=ref&amp;amp;cmd=prlinks&amp;amp;id=16230889  }} &amp;lt;/ref&amp;gt;&amp;lt;ref name=&amp;quot;pmid6847792&amp;quot;&amp;gt;{{cite journal| author=Swaye PS, Fisher LD, Litwin P, Vignola PA, Judkins MP, Kemp HG et al.| title=Aneurysmal coronary artery disease. | journal=Circulation | year= 1983 | volume= 67 | issue= 1 | pages= 134-8 | pmid=6847792 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;amp;tool=sumsearch.org/cite&amp;amp;retmode=ref&amp;amp;cmd=prlinks&amp;amp;id=6847792  }} &amp;lt;/ref&amp;gt;&lt;br /&gt;
==Diagnosis==&lt;br /&gt;
&lt;br /&gt;
It is often found coincidentally on [[coronary angiography]].&amp;lt;ref name=&amp;quot;pmid17063947&amp;quot;&amp;gt;{{cite journal |author=Pahlavan PS, Niroomand F |title=Coronary artery aneurysm: a review |journal=Clin Cardiol |volume=29 |issue=10 |pages=439–43 |year=2006 |month=October |pmid=17063947 |doi= |url=}}&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Causes==&lt;br /&gt;
&lt;br /&gt;
Causes include [[atherosclerosis]],&amp;lt;ref name=&amp;quot;pmid18466032&amp;quot;&amp;gt;{{cite journal |author=Nichols L, Lagana S, Parwani A |title=Coronary artery aneurysm: a review and hypothesis regarding etiology |journal=Arch. Pathol. Lab. Med. |volume=132 |issue=5 |pages=823–8 |year=2008 |month=May |pmid=18466032 |doi= |url=http://journals.allenpress.com/jrnlserv/?request=get-abstract&amp;amp;issn=0003-9985&amp;amp;volume=132&amp;amp;page=823}}&amp;lt;/ref&amp;gt; [[Kawasaki disease]]&amp;lt;ref name=&amp;quot;pmid17456996&amp;quot;&amp;gt;{{cite journal |author=Fukazawa R, Ikegam E, Watanabe M, &#039;&#039;et al&#039;&#039; |title=Coronary artery aneurysm induced by Kawasaki disease in children show features typical senescence |journal=Circ. J. |volume=71 |issue=5 |pages=709–15 |year=2007 |month=May |pmid=17456996 |doi= |url=http://joi.jlc.jst.go.jp/JST.JSTAGE/circj/71.709?from=PubMed}}&amp;lt;/ref&amp;gt; and [[coronary catheterization]] as well as vasculitides and collagen vascular diseases. &lt;br /&gt;
&lt;br /&gt;
==Prognosis==&lt;br /&gt;
&lt;br /&gt;
It has a good prognosis.&amp;lt;ref name=&amp;quot;pmid17063947&amp;quot;&amp;gt;{{cite journal |author=Pahlavan PS, Niroomand F |title=Coronary artery aneurysm: a review |journal=Clin Cardiol |volume=29 |issue=10 |pages=439–43 |year=2006 |month=October |pmid=17063947 |doi= |url=}}&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Definition==&lt;br /&gt;
&lt;br /&gt;
A localized arterial widening (dilatation) that usually manifests itself as a bulge. Its presence may lead to weakening of the wall and eventual rupture.&lt;br /&gt;
&lt;br /&gt;
===Grade 0===&lt;br /&gt;
&lt;br /&gt;
None – no [[ectasia]] present.&lt;br /&gt;
&lt;br /&gt;
===Grade 1===&lt;br /&gt;
&lt;br /&gt;
[[Ectasia]] – visual assessment of [[ectasia]] &amp;gt;1 &amp;amp; &amp;lt; 1.5 times the normal artery diameter located anywhere in the culprit artery.&lt;br /&gt;
&lt;br /&gt;
===Grade 2===&lt;br /&gt;
&lt;br /&gt;
Aneurysm – visual assessment of an [[aneurysm]] &amp;gt; 1.5 times the normal artery diameter located anywhere in the culprit artery.&lt;br /&gt;
&lt;br /&gt;
*NOTE: An [[aneurysm]] can be further classified as either [[saccular]] (wider than it is long) or [[fusiform]] (elongated).&lt;br /&gt;
&lt;br /&gt;
==References==&lt;br /&gt;
{{reflist|2}}&lt;br /&gt;
&lt;br /&gt;
{{Circulatory system pathology}}&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[[Category:Cardiology]]&lt;br /&gt;
[[Category:Angiographic Definitions]]&lt;br /&gt;
&lt;br /&gt;
{{WikiDoc Help Menu}}&lt;br /&gt;
{{WikiDoc Sources}}&lt;/div&gt;</summary>
		<author><name>Varun Kumar</name></author>
	</entry>
	<entry>
		<id>https://www.wikidoc.org/index.php?title=Coronary_artery_aneurysm&amp;diff=761986</id>
		<title>Coronary artery aneurysm</title>
		<link rel="alternate" type="text/html" href="https://www.wikidoc.org/index.php?title=Coronary_artery_aneurysm&amp;diff=761986"/>
		<updated>2012-09-29T01:36:31Z</updated>

		<summary type="html">&lt;p&gt;Varun Kumar: &lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;{{Infobox_Disease |&lt;br /&gt;
  Name           = {{PAGENAME}} |&lt;br /&gt;
  Image          = |&lt;br /&gt;
  Caption        = |&lt;br /&gt;
  DiseasesDB     = |&lt;br /&gt;
  ICD10          = {{ICD10|I|25|4|i|20}} |&lt;br /&gt;
  ICD9           = {{ICD9|414.11}} |&lt;br /&gt;
  ICDO           = |&lt;br /&gt;
  OMIM           = |&lt;br /&gt;
  MedlinePlus    = |&lt;br /&gt;
  eMedicineSubj  = |&lt;br /&gt;
  eMedicineTopic = |&lt;br /&gt;
  MeshID         = D003323 |&lt;br /&gt;
}}&lt;br /&gt;
{{SI}}&lt;br /&gt;
&lt;br /&gt;
{{CMG}}&lt;br /&gt;
  &lt;br /&gt;
&#039;&#039;&#039;Associate Editor-In-Chief:&#039;&#039;&#039;  {{CZ}}; {{VK}}&lt;br /&gt;
&lt;br /&gt;
==Overview==&lt;br /&gt;
&#039;&#039;&#039;Coronary artery aneurysm&#039;&#039;&#039; (CAA) is an abnormal dilatation of a [[coronary artery]] segment over 1.5 times the diameter of normal adjacent segment.&amp;lt;ref name=&amp;quot;pmid4897732&amp;quot;&amp;gt;{{cite journal| author=Jarcho S| title=Bougon on coronary aneurysm (1812). | journal=Am J Cardiol | year= 1969 | volume= 24 | issue= 4 | pages= 551-3 | pmid=4897732 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;amp;tool=sumsearch.org/cite&amp;amp;retmode=ref&amp;amp;cmd=prlinks&amp;amp;id=4897732  }} &amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Epidemiology and Demographics&lt;br /&gt;
==&lt;br /&gt;
The incidence of CAA ranges widely between 0.3-5.3% within angiographic series with a mean incidence of 1.65%.&amp;lt;ref name=&amp;quot;pmid4052280&amp;quot;&amp;gt;{{cite journal| author=Hartnell GG, Parnell BM, Pridie RB| title=Coronary artery ectasia. Its prevalence and clinical significance in 4993 patients. | journal=Br Heart J | year= 1985 | volume= 54 | issue= 4 | pages= 392-5 | pmid=4052280 | doi= | pmc=PMC481917 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;amp;tool=sumsearch.org/cite&amp;amp;retmode=ref&amp;amp;cmd=prlinks&amp;amp;id=4052280  }} &amp;lt;/ref&amp;gt;&lt;br /&gt;
CAA most commonly occurs in [[right coronary artery]] accounting for 40-87% followed by [[left anterior descending artery]] and [[left circumflex artery]].&amp;lt;ref name=&amp;quot;pmid16230889&amp;quot;&amp;gt;{{cite journal| author=Villines TC, Avedissian LS, Elgin EE| title=Diffuse nonatherosclerotic coronary aneurysms: an unusual cause of sudden death in a young male and a literature review. | journal=Cardiol Rev | year= 2005 | volume= 13 | issue= 6 | pages= 309-11 | pmid=16230889 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;amp;tool=sumsearch.org/cite&amp;amp;retmode=ref&amp;amp;cmd=prlinks&amp;amp;id=16230889  }} &amp;lt;/ref&amp;gt;&amp;lt;ref name=&amp;quot;pmid6847792&amp;quot;&amp;gt;{{cite journal| author=Swaye PS, Fisher LD, Litwin P, Vignola PA, Judkins MP, Kemp HG et al.| title=Aneurysmal coronary artery disease. | journal=Circulation | year= 1983 | volume= 67 | issue= 1 | pages= 134-8 | pmid=6847792 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;amp;tool=sumsearch.org/cite&amp;amp;retmode=ref&amp;amp;cmd=prlinks&amp;amp;id=6847792  }} &amp;lt;/ref&amp;gt;&lt;br /&gt;
==Diagnosis==&lt;br /&gt;
&lt;br /&gt;
It is often found coincidentally on [[coronary angiography]].&amp;lt;ref name=&amp;quot;pmid17063947&amp;quot;&amp;gt;{{cite journal |author=Pahlavan PS, Niroomand F |title=Coronary artery aneurysm: a review |journal=Clin Cardiol |volume=29 |issue=10 |pages=439–43 |year=2006 |month=October |pmid=17063947 |doi= |url=}}&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Causes==&lt;br /&gt;
&lt;br /&gt;
Causes include [[atherosclerosis]],&amp;lt;ref name=&amp;quot;pmid18466032&amp;quot;&amp;gt;{{cite journal |author=Nichols L, Lagana S, Parwani A |title=Coronary artery aneurysm: a review and hypothesis regarding etiology |journal=Arch. Pathol. Lab. Med. |volume=132 |issue=5 |pages=823–8 |year=2008 |month=May |pmid=18466032 |doi= |url=http://journals.allenpress.com/jrnlserv/?request=get-abstract&amp;amp;issn=0003-9985&amp;amp;volume=132&amp;amp;page=823}}&amp;lt;/ref&amp;gt; [[Kawasaki disease]]&amp;lt;ref name=&amp;quot;pmid17456996&amp;quot;&amp;gt;{{cite journal |author=Fukazawa R, Ikegam E, Watanabe M, &#039;&#039;et al&#039;&#039; |title=Coronary artery aneurysm induced by Kawasaki disease in children show features typical senescence |journal=Circ. J. |volume=71 |issue=5 |pages=709–15 |year=2007 |month=May |pmid=17456996 |doi= |url=http://joi.jlc.jst.go.jp/JST.JSTAGE/circj/71.709?from=PubMed}}&amp;lt;/ref&amp;gt; and [[coronary catheterization]] as well as vasculitides and collagen vascular diseases. &lt;br /&gt;
&lt;br /&gt;
==Prognosis==&lt;br /&gt;
&lt;br /&gt;
It has a good prognosis.&amp;lt;ref name=&amp;quot;pmid17063947&amp;quot;&amp;gt;{{cite journal |author=Pahlavan PS, Niroomand F |title=Coronary artery aneurysm: a review |journal=Clin Cardiol |volume=29 |issue=10 |pages=439–43 |year=2006 |month=October |pmid=17063947 |doi= |url=}}&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Definition==&lt;br /&gt;
&lt;br /&gt;
A localized arterial widening (dilatation) that usually manifests itself as a bulge. Its presence may lead to weakening of the wall and eventual rupture.&lt;br /&gt;
&lt;br /&gt;
===Grade 0===&lt;br /&gt;
&lt;br /&gt;
None – no [[ectasia]] present.&lt;br /&gt;
&lt;br /&gt;
===Grade 1===&lt;br /&gt;
&lt;br /&gt;
[[Ectasia]] – visual assessment of [[ectasia]] &amp;gt;1 &amp;amp; &amp;lt; 1.5 times the normal artery diameter located anywhere in the culprit artery.&lt;br /&gt;
&lt;br /&gt;
===Grade 2===&lt;br /&gt;
&lt;br /&gt;
Aneurysm – visual assessment of an [[aneurysm]] &amp;gt; 1.5 times the normal artery diameter located anywhere in the culprit artery.&lt;br /&gt;
&lt;br /&gt;
*NOTE: An [[aneurysm]] can be further classified as either [[saccular]] (wider than it is long) or [[fusiform]] (elongated).&lt;br /&gt;
&lt;br /&gt;
==References==&lt;br /&gt;
{{reflist|2}}&lt;br /&gt;
&lt;br /&gt;
{{Circulatory system pathology}}&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[[Category:Cardiology]]&lt;br /&gt;
[[Category:Angiographic Definitions]]&lt;br /&gt;
&lt;br /&gt;
{{WikiDoc Help Menu}}&lt;br /&gt;
{{WikiDoc Sources}}&lt;/div&gt;</summary>
		<author><name>Varun Kumar</name></author>
	</entry>
	<entry>
		<id>https://www.wikidoc.org/index.php?title=Mitral_valve_replacement&amp;diff=663958</id>
		<title>Mitral valve replacement</title>
		<link rel="alternate" type="text/html" href="https://www.wikidoc.org/index.php?title=Mitral_valve_replacement&amp;diff=663958"/>
		<updated>2012-08-03T21:22:25Z</updated>

		<summary type="html">&lt;p&gt;Varun Kumar: /* AHA Guidelines for Antithrombotic Therapy in Patients with Mitral Valve Replacement{{cite journal| author=Bonow RO, Carabello BA, Chatterjee K, de Leon AC, Faxon DP, Freed MD et al.| title=2008 Focused update incorporated into the ACC/AHA 2006 ...&lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;{{SI}}&lt;br /&gt;
{{CMG}}&lt;br /&gt;
&lt;br /&gt;
==Overview==&lt;br /&gt;
&#039;&#039;&#039;Mitral valve replacement&#039;&#039;&#039; is a cardiac surgery procedure in which a patient’s mitral valve is replaced by a different valve. Mitral valve replacement is typically performed robotically or manually, when the valve becomes too tight (mitral valve stenosis) for blood to flow into the left ventricle, or too loose (mitral valve regurgitation) in which case blood can leak into the left atrium and back up into the lung (The Society 1). Some individuals have a combination of mitral valve stenosis and mitral valve regurgitation or simply one or the other.&lt;br /&gt;
&lt;br /&gt;
A mitral valve replacement/repair is performed to treat severe cases of mitral valve prolapse, heart valve stenosis, or other valvular diseases (BCM Para 1). Since a mitral valve replacement is an open heart surgical procedure, it requires placing the patient on cardiopulmonary bypass to stop blood flow through the heart when it is opened up (The Society 1).  &lt;br /&gt;
&lt;br /&gt;
A mitral valve replacement is necessary when the valve doesn’t open or close completely. When the valve narrows or is stenotic the valve doesn’t let blood flow easily into the heart causing the blood to &amp;quot;back up&amp;quot; and pressure to build up in the lungs (The Society 2). This is dangerous because when the leaflets in the valve don’t meet correctly, blood may leak backwards into the lungs each time the heart pumps. If blood leaks backwards, the heart has to pump harder in order to push the same amount of blood forward. This is known as volume overload. The heart may compensate for this overload for many months or even years but eventually the heart begins to fail and patients show symptoms of shortness of breath or fatigue (The Society 2).&lt;br /&gt;
&lt;br /&gt;
==Causes==&lt;br /&gt;
Mitral valve problems are mainly cause from simple wear and tear that causes part of the valve mechanism to fail.  Rheumatic fever may also damage the mitral valve causing stenosis or regurgitation, and occasionally the mitral valve is damaged by infection or bacterial endocarditis. Coronary artery disease is also what may cause the mitral valve to leak (The Society 2).&lt;br /&gt;
&lt;br /&gt;
==Symptoms==&lt;br /&gt;
Some symptoms of patients that need mitral valve repair or replacement include: sensations of feeling the heart beat, chest pain, hard to breathe especially after activity, fatigue, coughing, and shortness of breath while lying flat. These symptoms may develop slowly or the patient my not have any symptoms at all (Gandelman 1).&lt;br /&gt;
&lt;br /&gt;
==Options==&lt;br /&gt;
Some surgeons will first recommend repairing the valve instead of replacement, but if the patient is not a good candidate then they must replace the valve (Maryland Para 1).  &lt;br /&gt;
&lt;br /&gt;
Many mitral valves can be repaired, especially if the leak is due to wear and tear. When the valve is too damaged to repair, the valve must be replaced with an artificial valve (Sundt 2).  There are some advantages to repairing a mitral valve versus replacing it. Some of these advantages are; a lower mortality at the time of operation (1-2% for repair versus 6-8% for replacement), a significantly lower risk of stroke, and a lower rate of infection, improved long-term survival with mitral valve repair. Patients who receive a valve repair stay on the same survival curve as the normal population.  A survival curve tends to be a graph of downward steps with the x-axis as time in months and the y-axis as percent still alive (Motulsky Ch 6). After mitral valve repair, blood thinners are not required, in contrast to the life-long requirement for blood thinners after mechanical mitral valve replacement (University 1).&lt;br /&gt;
&lt;br /&gt;
==Non-Surgical Options==&lt;br /&gt;
Most patients can endure surgery without complications; however there are some whose heart functions is too weak to withstand surgery. Some non surgical approaches to treat heart valve disease without surgery are divided into three categories: Clinical Practice treatment (this is used in every day clinical practice), Investigational treatment (current clinical studies that are underway), Early Development treatment (early stages of investigation) (Heart Para 3).&lt;br /&gt;
&lt;br /&gt;
==Types of Valves==&lt;br /&gt;
There are two primary types of artificial mitral valves -- a metal or mechanical valve and a tissue valve or biological valve (Maryland Para 2). The mechanical valves are made entirely from metal and pyrolytic carbon and last a lifetime (Sundt 2). With this valve, patients are required to take blood-thinning medications to prevent clotting. The tissue valve is made from animal tissues (Sundt 2). The tissue valve doesn’t require a patient to take blood thinners, but it only last 10 to 15 years (Maryland Para 2).&lt;br /&gt;
The choice of which type to use should be made by you and your doctors taking the following into consideration: your age, medical condition, preferences with medication, lifestyle (Sundt 3). &lt;br /&gt;
&lt;br /&gt;
==Details of the procedure==&lt;br /&gt;
A mitral valve replacement procedure is performed under general anesthesia, which will keep you asleep during the whole surgery (BCM Para 1).  The preferred method is to first make an incision under the left breast rather than through the breastbone in the front of the chest, to get to the heart. After the heart is exposed, blood must be rerouted to a heart-lung machine (cardiopulmonary bypass) (BCM 1). An incision is made in the left atrium to expose the mitral valve.  The valve is then replaced with either a biological valve or mechanical valve.  The heart is then closed with sutures (BCM 1).  The patient is then taken off the cardiopulmonary bypass and blood is allowed to flow into the coronary arteries.  If the heart does not beat on its own, an electric shock is used to start it. Then the chest is closed up (BCM 1).&lt;br /&gt;
&lt;br /&gt;
Below is a video of mitral valve &#039;&#039;&#039;replacement with mechanical valve&#039;&#039;&#039;.&lt;br /&gt;
{{#ev:youtube|e8tb0evVGVA}}&lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;Minimally invasive&#039;&#039;&#039; mitral valve replacement.&lt;br /&gt;
{{#ev:youtube|YRo20Fenpyg}}&lt;br /&gt;
&lt;br /&gt;
==Risks==&lt;br /&gt;
With mitral valve replacement surgery, there are risks such as bleeding, infection, or a complicated reaction to anesthesia (BCM 2). Each risk is determined best with each patients own cardiologist and cardiothoracic surgeon.  They will better know each individuals medical history and conditions. Risks depend on a patient’s age, general condition, specific medical conditions, and heart function (Sundt 3).&lt;br /&gt;
&lt;br /&gt;
==Postoperative Complications/ Risks==&lt;br /&gt;
A common postoperative complication with mitral valve surgery in a study involving 99 patients who had surgery for mitral regurgitation from January 1990 to June 1996 is atrial fibrillation.  This occurred in 32% of patients.  A common pulmonary complication is congestion necessitating prolonged use of oxygen.  Other patients required prolonged ventilation of longer than 24 hours for conditions like pulmonary edema, ARDS, and pulmonary thromboemboli (Hurley 1).  Nine patients had renal failure with six of them dying within 30 days after their operation.  Five patients had permanent strokes, and nine patients were readmitted to the hospital within 30 days of their discharge (Hurley 1).&lt;br /&gt;
&lt;br /&gt;
==Effectiveness==&lt;br /&gt;
In a clinical study done of 99 patients who had mitral valve surgery for regurgitation from January 1990 to June 1996, long-term and short-term outcomes were evaluated. These evaluations included; mortality rate, clinical complications, readmissions, valve deterioration, reoperation, and health perception.  Overall mortality was 18%, which included 11 operative deaths and 7 late deaths. Overall 5-year survival rate was 79% (Hurley 1).&lt;br /&gt;
&lt;br /&gt;
==Condition after mitral valve replacement==&lt;br /&gt;
After the surgery the patient is taken to a post-operative intensive care unit for monitoring. A respirator may be required for the first few hours or days after surgery. After a day, the patient should be able to sit up in bed. After two days, the patient may be taken out of the intensive care unit.  Patients are usually discharged after about seven to ten days (BCM 1).  If the mitral valve replacement is successful, patients can expect to return to their regular condition or even better.  Patients who have biological valve are prescribed blood thinners (Anticoagulation) with Coumadin for 6 weeks to 3 months postoperative, while patients with mechanical valves are prescribed blood thinners for the rest of their lives.  These blood thinners are taken to prevent blood clots that can move to other parts of your body and cause serious medical problems, such as a heart attack. Blood thinners will not dissolve a blood clot but they prevent other clots from forming or prevent clots from becoming larger. Blood thinners will not dissolve (Heart Disease 1). Once the patient’s wounds are healed they should have few, if any restrictions from daily activities (Sundt 1).  Patients are advised to walk or to do other physical activities gradually to regain strength.  Patients who have physically demanding jobs will have to wait a little longer than those who don’t.  Patients are also restricted from driving a car for six weeks after the surgery (Mitral 2).  Once a person has a mitral valve procedure, they are required to have prophylactic antibiotics as a preventative measure against infection whenever they have dental work done (Sundt 4).  &lt;br /&gt;
Depending on the method of surgery, some scarring will occur.  If the breastbone is divided, the patient will have a long scar along the breast bone.  If the heart is accessed from under the left breast their will be a smaller scar in the spot (Mitral 2).&lt;br /&gt;
&lt;br /&gt;
==AHA Guidelines for Antithrombotic Therapy in Patients with Mitral Valve Replacement&amp;lt;ref name=&amp;quot;pmid18820172&amp;quot;&amp;gt;{{cite journal| author=Bonow RO, Carabello BA, Chatterjee K, de Leon AC, Faxon DP, Freed MD et al.| title=2008 Focused update incorporated into the ACC/AHA 2006 guidelines for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 1998 Guidelines for the Management of Patients With Valvular Heart Disease): endorsed by the Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons. | journal=Circulation | year= 2008 | volume= 118 | issue= 15 | pages= e523-661 | pmid=18820172 | doi=10.1161/CIRCULATIONAHA.108.190748 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;amp;tool=sumsearch.org/cite&amp;amp;retmode=ref&amp;amp;cmd=prlinks&amp;amp;id=18820172  }} &amp;lt;/ref&amp;gt;==&lt;br /&gt;
{{cquote|&lt;br /&gt;
===[[ACC AHA guidelines classification scheme#Classification of Recommendations|Class I]]===&lt;br /&gt;
&#039;&#039;&#039;1.&#039;&#039;&#039; After mitral valve(MV) replacement with any mechanical valve, [[warfarin]] is indicated to achieve an [[INR]] of 2.5 to 3.5. &#039;&#039;([[ACC AHA guidelines classification scheme#Level of Evidence|Level of Evidence: C]])&#039;&#039;&lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;2.&#039;&#039;&#039; After aortic valve replacement (AVR) or MV replacement with a bioprosthesis and no risk factors,* aspirin is indicated at 75 to 100 mg per day. &#039;&#039;([[ACC AHA guidelines classification scheme#Level of Evidence|Level of Evidence: C]])&#039;&#039;&lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;3.&#039;&#039;&#039; After MV replacement with a bioprosthesis and risk factors,&#039;&#039;&#039;*&#039;&#039;&#039; warfarin is indicated to achieve an INR of 2.0 to 3.0. &#039;&#039;([[ACC AHA guidelines classification scheme#Level of Evidence|Level of Evidence: C]])&#039;&#039;&lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;4.&#039;&#039;&#039; For those patients who are unable to take warfarin after MV replacement or AVR, [[aspirin]] is indicated in a dose of 75 to 325 mg per day. &#039;&#039;([[ACC AHA guidelines classification scheme#Level of Evidence|Level of Evidence: B]])&#039;&#039;&lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;5.&#039;&#039;&#039; The addition of aspirin 75 to 100 mg once daily to therapeutic warfarin is recommended for all patients with mechanical heart valves and those patients with biological valves who have risk factors.&#039;&#039;&#039;*&#039;&#039;&#039; &#039;&#039;([[ACC AHA guidelines classification scheme#Level of Evidence|Level of Evidence: B]])&#039;&#039;&lt;br /&gt;
&lt;br /&gt;
===[[ACC AHA guidelines classification scheme#Classification of Recommendations|Class IIa]]===&lt;br /&gt;
&#039;&#039;&#039;1.&#039;&#039;&#039; During the first 3 months after AVR or MV replacement with a bioprosthesis, in patients with no risk factors,&#039;&#039;&#039;*&#039;&#039;&#039; it is reasonable to give warfarin to achieve an INR of 2.0 to 3.0. &#039;&#039;([[ACC AHA guidelines classification scheme#Level of Evidence|Level of Evidence: C]])&#039;&#039;&lt;br /&gt;
&lt;br /&gt;
===[[ACC AHA guidelines classification scheme#Classification of Recommendations|Class IIb]]===&lt;br /&gt;
&#039;&#039;&#039;1.&#039;&#039;&#039; In high-risk patients with prosthetic heart valves in whom aspirin cannot be used, it may be reasonable to give clopidogrel (75 mg per day) or warfarin to achieve an INR of 3.5 to 4.5. &#039;&#039;([[ACC AHA guidelines classification scheme#Level of Evidence|Level of Evidence: C]])&#039;&#039;}}&lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;*&#039;&#039;&#039;Risk factors include [[atrial fibrillation]], previous [[thromboembolism]], LV dysfunction, and hypercoagulable condition.&lt;br /&gt;
&lt;br /&gt;
==Related chapters==&lt;br /&gt;
* [[Mitral regurgitation]]&lt;br /&gt;
* [[Artificial heart valve]]&lt;br /&gt;
* [[Mitral stenosis]]&lt;br /&gt;
* [[Heart-lung machine]]&lt;br /&gt;
&lt;br /&gt;
==References==&lt;br /&gt;
{{reflist|2}}&lt;br /&gt;
*[http://www.debakeydepartmentofsurgery.org/home/content.cfm?proc_name=mitral+valve+repair+replacement&amp;amp;content_id=274 BCM: The Michael E DeBaker Department of Surgery. Mitral Valve Repair/ Replacement. n.d. 29 Apr. 2007] &lt;br /&gt;
*[http://www.ecu.edu/dhs/news/newsstory.cfm?ID=16 &amp;quot;FDA approves second clinical trial for robotic heart surgery.&amp;quot; Health Sciences News. 9 Nov. 2000. ECU Division of Health Sciences. 2 May 2007]&lt;br /&gt;
*[http://www.nlm.nih.gov/medlineplus/ency/article/000180.htm Gandelman, Glenn. &amp;quot;Medical encyclopedia.&amp;quot; Medline Plus. n.d. 3 May 2007]&lt;br /&gt;
*[http://www.webmd.com/heart-disease/warfarin-other-blood-thinners?page=1 &amp;quot;Heart Disease: Warfarin and Other Blood Thinners.&amp;quot; WebMD. The Cleveland Clinic. 10 May 2007 ]&lt;br /&gt;
*[http://www.clevelandclinic.org/heartcenter/pub/guide/percutaneous/percutaneousValve.htm#investigational#investigational Heart and Vascular Institute. &#039;&#039;Heart Valve Disease - Percutaneous Interventions: Non-surgical approaches.&#039;&#039; 2007. 7 May 2007 ]&lt;br /&gt;
*[http://www.umm.edu/heart/mitral_repla.html &amp;quot;Mitral Valve Replacement.&amp;quot; University of Maryland Medical Center: 1-2. 26 Apr. 2007  ]&lt;br /&gt;
*[http://www.graphpad.com/www/book/survive.htm Motulsky, Harvey. &#039;&#039;Intuitive Biostatistics&#039;&#039;. Oxford University Press Inc, 1995. 2 May 2007 ]&lt;br /&gt;
&lt;br /&gt;
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[[uk:Протезування мітрального клапану]]&lt;/div&gt;</summary>
		<author><name>Varun Kumar</name></author>
	</entry>
	<entry>
		<id>https://www.wikidoc.org/index.php?title=Mitral_valve_replacement&amp;diff=663578</id>
		<title>Mitral valve replacement</title>
		<link rel="alternate" type="text/html" href="https://www.wikidoc.org/index.php?title=Mitral_valve_replacement&amp;diff=663578"/>
		<updated>2012-08-03T15:49:16Z</updated>

		<summary type="html">&lt;p&gt;Varun Kumar: /* AHA Guidelines for Antithrombotic Therapy in Patients with Mitral Valve Replacement{{cite journal| author=Bonow RO, Carabello BA, Chatterjee K, de Leon AC, Faxon DP, Freed MD et al.| title=2008 Focused update incorporated into the ACC/AHA 2006 ...&lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;{{SI}}&lt;br /&gt;
{{CMG}}&lt;br /&gt;
&lt;br /&gt;
==Overview==&lt;br /&gt;
&#039;&#039;&#039;Mitral valve replacement&#039;&#039;&#039; is a cardiac surgery procedure in which a patient’s mitral valve is replaced by a different valve. Mitral valve replacement is typically performed robotically or manually, when the valve becomes too tight (mitral valve stenosis) for blood to flow into the left ventricle, or too loose (mitral valve regurgitation) in which case blood can leak into the left atrium and back up into the lung (The Society 1). Some individuals have a combination of mitral valve stenosis and mitral valve regurgitation or simply one or the other.&lt;br /&gt;
&lt;br /&gt;
A mitral valve replacement/repair is performed to treat severe cases of mitral valve prolapse, heart valve stenosis, or other valvular diseases (BCM Para 1). Since a mitral valve replacement is an open heart surgical procedure, it requires placing the patient on cardiopulmonary bypass to stop blood flow through the heart when it is opened up (The Society 1).  &lt;br /&gt;
&lt;br /&gt;
A mitral valve replacement is necessary when the valve doesn’t open or close completely. When the valve narrows or is stenotic the valve doesn’t let blood flow easily into the heart causing the blood to &amp;quot;back up&amp;quot; and pressure to build up in the lungs (The Society 2). This is dangerous because when the leaflets in the valve don’t meet correctly, blood may leak backwards into the lungs each time the heart pumps. If blood leaks backwards, the heart has to pump harder in order to push the same amount of blood forward. This is known as volume overload. The heart may compensate for this overload for many months or even years but eventually the heart begins to fail and patients show symptoms of shortness of breath or fatigue (The Society 2).&lt;br /&gt;
&lt;br /&gt;
==Causes==&lt;br /&gt;
Mitral valve problems are mainly cause from simple wear and tear that causes part of the valve mechanism to fail.  Rheumatic fever may also damage the mitral valve causing stenosis or regurgitation, and occasionally the mitral valve is damaged by infection or bacterial endocarditis. Coronary artery disease is also what may cause the mitral valve to leak (The Society 2).&lt;br /&gt;
&lt;br /&gt;
==Symptoms==&lt;br /&gt;
Some symptoms of patients that need mitral valve repair or replacement include: sensations of feeling the heart beat, chest pain, hard to breathe especially after activity, fatigue, coughing, and shortness of breath while lying flat. These symptoms may develop slowly or the patient my not have any symptoms at all (Gandelman 1).&lt;br /&gt;
&lt;br /&gt;
==Options==&lt;br /&gt;
Some surgeons will first recommend repairing the valve instead of replacement, but if the patient is not a good candidate then they must replace the valve (Maryland Para 1).  &lt;br /&gt;
&lt;br /&gt;
Many mitral valves can be repaired, especially if the leak is due to wear and tear. When the valve is too damaged to repair, the valve must be replaced with an artificial valve (Sundt 2).  There are some advantages to repairing a mitral valve versus replacing it. Some of these advantages are; a lower mortality at the time of operation (1-2% for repair versus 6-8% for replacement), a significantly lower risk of stroke, and a lower rate of infection, improved long-term survival with mitral valve repair. Patients who receive a valve repair stay on the same survival curve as the normal population.  A survival curve tends to be a graph of downward steps with the x-axis as time in months and the y-axis as percent still alive (Motulsky Ch 6). After mitral valve repair, blood thinners are not required, in contrast to the life-long requirement for blood thinners after mechanical mitral valve replacement (University 1).&lt;br /&gt;
&lt;br /&gt;
==Non-Surgical Options==&lt;br /&gt;
Most patients can endure surgery without complications; however there are some whose heart functions is too weak to withstand surgery. Some non surgical approaches to treat heart valve disease without surgery are divided into three categories: Clinical Practice treatment (this is used in every day clinical practice), Investigational treatment (current clinical studies that are underway), Early Development treatment (early stages of investigation) (Heart Para 3).&lt;br /&gt;
&lt;br /&gt;
==Types of Valves==&lt;br /&gt;
There are two primary types of artificial mitral valves -- a metal or mechanical valve and a tissue valve or biological valve (Maryland Para 2). The mechanical valves are made entirely from metal and pyrolytic carbon and last a lifetime (Sundt 2). With this valve, patients are required to take blood-thinning medications to prevent clotting. The tissue valve is made from animal tissues (Sundt 2). The tissue valve doesn’t require a patient to take blood thinners, but it only last 10 to 15 years (Maryland Para 2).&lt;br /&gt;
The choice of which type to use should be made by you and your doctors taking the following into consideration: your age, medical condition, preferences with medication, lifestyle (Sundt 3). &lt;br /&gt;
&lt;br /&gt;
==Details of the procedure==&lt;br /&gt;
A mitral valve replacement procedure is performed under general anesthesia, which will keep you asleep during the whole surgery (BCM Para 1).  The preferred method is to first make an incision under the left breast rather than through the breastbone in the front of the chest, to get to the heart. After the heart is exposed, blood must be rerouted to a heart-lung machine (cardiopulmonary bypass) (BCM 1). An incision is made in the left atrium to expose the mitral valve.  The valve is then replaced with either a biological valve or mechanical valve.  The heart is then closed with sutures (BCM 1).  The patient is then taken off the cardiopulmonary bypass and blood is allowed to flow into the coronary arteries.  If the heart does not beat on its own, an electric shock is used to start it. Then the chest is closed up (BCM 1).&lt;br /&gt;
&lt;br /&gt;
Below is a video of mitral valve &#039;&#039;&#039;replacement with mechanical valve&#039;&#039;&#039;.&lt;br /&gt;
{{#ev:youtube|e8tb0evVGVA}}&lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;Minimally invasive&#039;&#039;&#039; mitral valve replacement.&lt;br /&gt;
{{#ev:youtube|YRo20Fenpyg}}&lt;br /&gt;
&lt;br /&gt;
==Risks==&lt;br /&gt;
With mitral valve replacement surgery, there are risks such as bleeding, infection, or a complicated reaction to anesthesia (BCM 2). Each risk is determined best with each patients own cardiologist and cardiothoracic surgeon.  They will better know each individuals medical history and conditions. Risks depend on a patient’s age, general condition, specific medical conditions, and heart function (Sundt 3).&lt;br /&gt;
&lt;br /&gt;
==Postoperative Complications/ Risks==&lt;br /&gt;
A common postoperative complication with mitral valve surgery in a study involving 99 patients who had surgery for mitral regurgitation from January 1990 to June 1996 is atrial fibrillation.  This occurred in 32% of patients.  A common pulmonary complication is congestion necessitating prolonged use of oxygen.  Other patients required prolonged ventilation of longer than 24 hours for conditions like pulmonary edema, ARDS, and pulmonary thromboemboli (Hurley 1).  Nine patients had renal failure with six of them dying within 30 days after their operation.  Five patients had permanent strokes, and nine patients were readmitted to the hospital within 30 days of their discharge (Hurley 1).&lt;br /&gt;
&lt;br /&gt;
==Effectiveness==&lt;br /&gt;
In a clinical study done of 99 patients who had mitral valve surgery for regurgitation from January 1990 to June 1996, long-term and short-term outcomes were evaluated. These evaluations included; mortality rate, clinical complications, readmissions, valve deterioration, reoperation, and health perception.  Overall mortality was 18%, which included 11 operative deaths and 7 late deaths. Overall 5-year survival rate was 79% (Hurley 1).&lt;br /&gt;
&lt;br /&gt;
==Condition after mitral valve replacement==&lt;br /&gt;
After the surgery the patient is taken to a post-operative intensive care unit for monitoring. A respirator may be required for the first few hours or days after surgery. After a day, the patient should be able to sit up in bed. After two days, the patient may be taken out of the intensive care unit.  Patients are usually discharged after about seven to ten days (BCM 1).  If the mitral valve replacement is successful, patients can expect to return to their regular condition or even better.  Patients who have biological valve are prescribed blood thinners (Anticoagulation) with Coumadin for 6 weeks to 3 months postoperative, while patients with mechanical valves are prescribed blood thinners for the rest of their lives.  These blood thinners are taken to prevent blood clots that can move to other parts of your body and cause serious medical problems, such as a heart attack. Blood thinners will not dissolve a blood clot but they prevent other clots from forming or prevent clots from becoming larger. Blood thinners will not dissolve (Heart Disease 1). Once the patient’s wounds are healed they should have few, if any restrictions from daily activities (Sundt 1).  Patients are advised to walk or to do other physical activities gradually to regain strength.  Patients who have physically demanding jobs will have to wait a little longer than those who don’t.  Patients are also restricted from driving a car for six weeks after the surgery (Mitral 2).  Once a person has a mitral valve procedure, they are required to have prophylactic antibiotics as a preventative measure against infection whenever they have dental work done (Sundt 4).  &lt;br /&gt;
Depending on the method of surgery, some scarring will occur.  If the breastbone is divided, the patient will have a long scar along the breast bone.  If the heart is accessed from under the left breast their will be a smaller scar in the spot (Mitral 2).&lt;br /&gt;
&lt;br /&gt;
==AHA Guidelines for Antithrombotic Therapy in Patients with Mitral Valve Replacement&amp;lt;ref name=&amp;quot;pmid18820172&amp;quot;&amp;gt;{{cite journal| author=Bonow RO, Carabello BA, Chatterjee K, de Leon AC, Faxon DP, Freed MD et al.| title=2008 Focused update incorporated into the ACC/AHA 2006 guidelines for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 1998 Guidelines for the Management of Patients With Valvular Heart Disease): endorsed by the Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons. | journal=Circulation | year= 2008 | volume= 118 | issue= 15 | pages= e523-661 | pmid=18820172 | doi=10.1161/CIRCULATIONAHA.108.190748 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;amp;tool=sumsearch.org/cite&amp;amp;retmode=ref&amp;amp;cmd=prlinks&amp;amp;id=18820172  }} &amp;lt;/ref&amp;gt;==&lt;br /&gt;
{{cquote|&lt;br /&gt;
===[[ACC AHA guidelines classification scheme#Classification of Recommendations|Class I]]===&lt;br /&gt;
&#039;&#039;&#039;1.&#039;&#039;&#039; After mitral valve(MV) replacement with any mechanical valve, [[warfarin]] is indicated to achieve an [[INR]] of 2.5 to 3.5. &#039;&#039;([[ACC AHA guidelines classification scheme#Level of Evidence|Level of Evidence: C]])&#039;&#039;&lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;2.&#039;&#039;&#039; After aortic valve replacement (AVR) or MV replacement with a bioprosthesis and no risk factors,* aspirin is indicated at 75 to 100 mg per day. &#039;&#039;([[ACC AHA guidelines classification scheme#Level of Evidence|Level of Evidence: C]])&#039;&#039;&lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;3.&#039;&#039;&#039; After MV replacement with a bioprosthesis and risk factors,* warfarin is indicated to achieve an INR of 2.0 to 3.0. &#039;&#039;([[ACC AHA guidelines classification scheme#Level of Evidence|Level of Evidence: C]])&#039;&#039;&lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;4.&#039;&#039;&#039; For those patients who are unable to take warfarin after MV replacement or AVR, [[aspirin]] is indicated in a dose of 75 to 325 mg per day. &#039;&#039;([[ACC AHA guidelines classification scheme#Level of Evidence|Level of Evidence: B]])&#039;&#039;&lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;5.&#039;&#039;&#039; The addition of aspirin 75 to 100 mg once daily to therapeutic warfarin is recommended for all patients with mechanical heart valves and those patients with biological valves who have risk factors.* &#039;&#039;([[ACC AHA guidelines classification scheme#Level of Evidence|Level of Evidence: B]])&#039;&#039;&lt;br /&gt;
&lt;br /&gt;
===[[ACC AHA guidelines classification scheme#Classification of Recommendations|Class IIa]]===&lt;br /&gt;
&#039;&#039;&#039;1.&#039;&#039;&#039; During the first 3 months after AVR or MV replacement with a bioprosthesis, in patients with no risk factors,* it is reasonable to give warfarin to achieve an INR of 2.0 to 3.0. &#039;&#039;([[ACC AHA guidelines classification scheme#Level of Evidence|Level of Evidence: C]])&#039;&#039;&lt;br /&gt;
&lt;br /&gt;
===[[ACC AHA guidelines classification scheme#Classification of Recommendations|Class IIb]]===&lt;br /&gt;
&#039;&#039;&#039;1.&#039;&#039;&#039; In high-risk patients with prosthetic heart valves in whom aspirin cannot be used, it may be reasonable to give clopidogrel (75 mg per day) or warfarin to achieve an INR of 3.5 to 4.5. &#039;&#039;([[ACC AHA guidelines classification scheme#Level of Evidence|Level of Evidence: C]])&#039;&#039;}}&lt;br /&gt;
&lt;br /&gt;
==Related chapters==&lt;br /&gt;
* [[Mitral regurgitation]]&lt;br /&gt;
* [[Artificial heart valve]]&lt;br /&gt;
* [[Mitral stenosis]]&lt;br /&gt;
* [[Heart-lung machine]]&lt;br /&gt;
&lt;br /&gt;
==References==&lt;br /&gt;
{{reflist|2}}&lt;br /&gt;
*[http://www.debakeydepartmentofsurgery.org/home/content.cfm?proc_name=mitral+valve+repair+replacement&amp;amp;content_id=274 BCM: The Michael E DeBaker Department of Surgery. Mitral Valve Repair/ Replacement. n.d. 29 Apr. 2007] &lt;br /&gt;
*[http://www.ecu.edu/dhs/news/newsstory.cfm?ID=16 &amp;quot;FDA approves second clinical trial for robotic heart surgery.&amp;quot; Health Sciences News. 9 Nov. 2000. ECU Division of Health Sciences. 2 May 2007]&lt;br /&gt;
*[http://www.nlm.nih.gov/medlineplus/ency/article/000180.htm Gandelman, Glenn. &amp;quot;Medical encyclopedia.&amp;quot; Medline Plus. n.d. 3 May 2007]&lt;br /&gt;
*[http://www.webmd.com/heart-disease/warfarin-other-blood-thinners?page=1 &amp;quot;Heart Disease: Warfarin and Other Blood Thinners.&amp;quot; WebMD. The Cleveland Clinic. 10 May 2007 ]&lt;br /&gt;
*[http://www.clevelandclinic.org/heartcenter/pub/guide/percutaneous/percutaneousValve.htm#investigational#investigational Heart and Vascular Institute. &#039;&#039;Heart Valve Disease - Percutaneous Interventions: Non-surgical approaches.&#039;&#039; 2007. 7 May 2007 ]&lt;br /&gt;
*[http://www.umm.edu/heart/mitral_repla.html &amp;quot;Mitral Valve Replacement.&amp;quot; University of Maryland Medical Center: 1-2. 26 Apr. 2007  ]&lt;br /&gt;
*[http://www.graphpad.com/www/book/survive.htm Motulsky, Harvey. &#039;&#039;Intuitive Biostatistics&#039;&#039;. Oxford University Press Inc, 1995. 2 May 2007 ]&lt;br /&gt;
&lt;br /&gt;
{{cardiac surgery}}&lt;br /&gt;
{{SIB}}&lt;br /&gt;
&lt;br /&gt;
[[Category:Cardiology]]&lt;br /&gt;
[[Category:Valvular heart disease]]&lt;br /&gt;
{{WikiDoc Help Menu}}&lt;br /&gt;
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[[uk:Протезування мітрального клапану]]&lt;/div&gt;</summary>
		<author><name>Varun Kumar</name></author>
	</entry>
	<entry>
		<id>https://www.wikidoc.org/index.php?title=Mitral_valve_replacement&amp;diff=663562</id>
		<title>Mitral valve replacement</title>
		<link rel="alternate" type="text/html" href="https://www.wikidoc.org/index.php?title=Mitral_valve_replacement&amp;diff=663562"/>
		<updated>2012-08-03T15:39:30Z</updated>

		<summary type="html">&lt;p&gt;Varun Kumar: /* Condition after mitral valve replacement */&lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;{{SI}}&lt;br /&gt;
{{CMG}}&lt;br /&gt;
&lt;br /&gt;
==Overview==&lt;br /&gt;
&#039;&#039;&#039;Mitral valve replacement&#039;&#039;&#039; is a cardiac surgery procedure in which a patient’s mitral valve is replaced by a different valve. Mitral valve replacement is typically performed robotically or manually, when the valve becomes too tight (mitral valve stenosis) for blood to flow into the left ventricle, or too loose (mitral valve regurgitation) in which case blood can leak into the left atrium and back up into the lung (The Society 1). Some individuals have a combination of mitral valve stenosis and mitral valve regurgitation or simply one or the other.&lt;br /&gt;
&lt;br /&gt;
A mitral valve replacement/repair is performed to treat severe cases of mitral valve prolapse, heart valve stenosis, or other valvular diseases (BCM Para 1). Since a mitral valve replacement is an open heart surgical procedure, it requires placing the patient on cardiopulmonary bypass to stop blood flow through the heart when it is opened up (The Society 1).  &lt;br /&gt;
&lt;br /&gt;
A mitral valve replacement is necessary when the valve doesn’t open or close completely. When the valve narrows or is stenotic the valve doesn’t let blood flow easily into the heart causing the blood to &amp;quot;back up&amp;quot; and pressure to build up in the lungs (The Society 2). This is dangerous because when the leaflets in the valve don’t meet correctly, blood may leak backwards into the lungs each time the heart pumps. If blood leaks backwards, the heart has to pump harder in order to push the same amount of blood forward. This is known as volume overload. The heart may compensate for this overload for many months or even years but eventually the heart begins to fail and patients show symptoms of shortness of breath or fatigue (The Society 2).&lt;br /&gt;
&lt;br /&gt;
==Causes==&lt;br /&gt;
Mitral valve problems are mainly cause from simple wear and tear that causes part of the valve mechanism to fail.  Rheumatic fever may also damage the mitral valve causing stenosis or regurgitation, and occasionally the mitral valve is damaged by infection or bacterial endocarditis. Coronary artery disease is also what may cause the mitral valve to leak (The Society 2).&lt;br /&gt;
&lt;br /&gt;
==Symptoms==&lt;br /&gt;
Some symptoms of patients that need mitral valve repair or replacement include: sensations of feeling the heart beat, chest pain, hard to breathe especially after activity, fatigue, coughing, and shortness of breath while lying flat. These symptoms may develop slowly or the patient my not have any symptoms at all (Gandelman 1).&lt;br /&gt;
&lt;br /&gt;
==Options==&lt;br /&gt;
Some surgeons will first recommend repairing the valve instead of replacement, but if the patient is not a good candidate then they must replace the valve (Maryland Para 1).  &lt;br /&gt;
&lt;br /&gt;
Many mitral valves can be repaired, especially if the leak is due to wear and tear. When the valve is too damaged to repair, the valve must be replaced with an artificial valve (Sundt 2).  There are some advantages to repairing a mitral valve versus replacing it. Some of these advantages are; a lower mortality at the time of operation (1-2% for repair versus 6-8% for replacement), a significantly lower risk of stroke, and a lower rate of infection, improved long-term survival with mitral valve repair. Patients who receive a valve repair stay on the same survival curve as the normal population.  A survival curve tends to be a graph of downward steps with the x-axis as time in months and the y-axis as percent still alive (Motulsky Ch 6). After mitral valve repair, blood thinners are not required, in contrast to the life-long requirement for blood thinners after mechanical mitral valve replacement (University 1).&lt;br /&gt;
&lt;br /&gt;
==Non-Surgical Options==&lt;br /&gt;
Most patients can endure surgery without complications; however there are some whose heart functions is too weak to withstand surgery. Some non surgical approaches to treat heart valve disease without surgery are divided into three categories: Clinical Practice treatment (this is used in every day clinical practice), Investigational treatment (current clinical studies that are underway), Early Development treatment (early stages of investigation) (Heart Para 3).&lt;br /&gt;
&lt;br /&gt;
==Types of Valves==&lt;br /&gt;
There are two primary types of artificial mitral valves -- a metal or mechanical valve and a tissue valve or biological valve (Maryland Para 2). The mechanical valves are made entirely from metal and pyrolytic carbon and last a lifetime (Sundt 2). With this valve, patients are required to take blood-thinning medications to prevent clotting. The tissue valve is made from animal tissues (Sundt 2). The tissue valve doesn’t require a patient to take blood thinners, but it only last 10 to 15 years (Maryland Para 2).&lt;br /&gt;
The choice of which type to use should be made by you and your doctors taking the following into consideration: your age, medical condition, preferences with medication, lifestyle (Sundt 3). &lt;br /&gt;
&lt;br /&gt;
==Details of the procedure==&lt;br /&gt;
A mitral valve replacement procedure is performed under general anesthesia, which will keep you asleep during the whole surgery (BCM Para 1).  The preferred method is to first make an incision under the left breast rather than through the breastbone in the front of the chest, to get to the heart. After the heart is exposed, blood must be rerouted to a heart-lung machine (cardiopulmonary bypass) (BCM 1). An incision is made in the left atrium to expose the mitral valve.  The valve is then replaced with either a biological valve or mechanical valve.  The heart is then closed with sutures (BCM 1).  The patient is then taken off the cardiopulmonary bypass and blood is allowed to flow into the coronary arteries.  If the heart does not beat on its own, an electric shock is used to start it. Then the chest is closed up (BCM 1).&lt;br /&gt;
&lt;br /&gt;
Below is a video of mitral valve &#039;&#039;&#039;replacement with mechanical valve&#039;&#039;&#039;.&lt;br /&gt;
{{#ev:youtube|e8tb0evVGVA}}&lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;Minimally invasive&#039;&#039;&#039; mitral valve replacement.&lt;br /&gt;
{{#ev:youtube|YRo20Fenpyg}}&lt;br /&gt;
&lt;br /&gt;
==Risks==&lt;br /&gt;
With mitral valve replacement surgery, there are risks such as bleeding, infection, or a complicated reaction to anesthesia (BCM 2). Each risk is determined best with each patients own cardiologist and cardiothoracic surgeon.  They will better know each individuals medical history and conditions. Risks depend on a patient’s age, general condition, specific medical conditions, and heart function (Sundt 3).&lt;br /&gt;
&lt;br /&gt;
==Postoperative Complications/ Risks==&lt;br /&gt;
A common postoperative complication with mitral valve surgery in a study involving 99 patients who had surgery for mitral regurgitation from January 1990 to June 1996 is atrial fibrillation.  This occurred in 32% of patients.  A common pulmonary complication is congestion necessitating prolonged use of oxygen.  Other patients required prolonged ventilation of longer than 24 hours for conditions like pulmonary edema, ARDS, and pulmonary thromboemboli (Hurley 1).  Nine patients had renal failure with six of them dying within 30 days after their operation.  Five patients had permanent strokes, and nine patients were readmitted to the hospital within 30 days of their discharge (Hurley 1).&lt;br /&gt;
&lt;br /&gt;
==Effectiveness==&lt;br /&gt;
In a clinical study done of 99 patients who had mitral valve surgery for regurgitation from January 1990 to June 1996, long-term and short-term outcomes were evaluated. These evaluations included; mortality rate, clinical complications, readmissions, valve deterioration, reoperation, and health perception.  Overall mortality was 18%, which included 11 operative deaths and 7 late deaths. Overall 5-year survival rate was 79% (Hurley 1).&lt;br /&gt;
&lt;br /&gt;
==Condition after mitral valve replacement==&lt;br /&gt;
After the surgery the patient is taken to a post-operative intensive care unit for monitoring. A respirator may be required for the first few hours or days after surgery. After a day, the patient should be able to sit up in bed. After two days, the patient may be taken out of the intensive care unit.  Patients are usually discharged after about seven to ten days (BCM 1).  If the mitral valve replacement is successful, patients can expect to return to their regular condition or even better.  Patients who have biological valve are prescribed blood thinners (Anticoagulation) with Coumadin for 6 weeks to 3 months postoperative, while patients with mechanical valves are prescribed blood thinners for the rest of their lives.  These blood thinners are taken to prevent blood clots that can move to other parts of your body and cause serious medical problems, such as a heart attack. Blood thinners will not dissolve a blood clot but they prevent other clots from forming or prevent clots from becoming larger. Blood thinners will not dissolve (Heart Disease 1). Once the patient’s wounds are healed they should have few, if any restrictions from daily activities (Sundt 1).  Patients are advised to walk or to do other physical activities gradually to regain strength.  Patients who have physically demanding jobs will have to wait a little longer than those who don’t.  Patients are also restricted from driving a car for six weeks after the surgery (Mitral 2).  Once a person has a mitral valve procedure, they are required to have prophylactic antibiotics as a preventative measure against infection whenever they have dental work done (Sundt 4).  &lt;br /&gt;
Depending on the method of surgery, some scarring will occur.  If the breastbone is divided, the patient will have a long scar along the breast bone.  If the heart is accessed from under the left breast their will be a smaller scar in the spot (Mitral 2).&lt;br /&gt;
&lt;br /&gt;
==AHA Guidelines for Antithrombotic Therapy in Patients with Mitral Valve Replacement&amp;lt;ref name=&amp;quot;pmid18820172&amp;quot;&amp;gt;{{cite journal| author=Bonow RO, Carabello BA, Chatterjee K, de Leon AC, Faxon DP, Freed MD et al.| title=2008 Focused update incorporated into the ACC/AHA 2006 guidelines for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 1998 Guidelines for the Management of Patients With Valvular Heart Disease): endorsed by the Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons. | journal=Circulation | year= 2008 | volume= 118 | issue= 15 | pages= e523-661 | pmid=18820172 | doi=10.1161/CIRCULATIONAHA.108.190748 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;amp;tool=sumsearch.org/cite&amp;amp;retmode=ref&amp;amp;cmd=prlinks&amp;amp;id=18820172  }} &amp;lt;/ref&amp;gt;==&lt;br /&gt;
{{cquote|&lt;br /&gt;
===Class I===&lt;br /&gt;
&#039;&#039;&#039;1.&#039;&#039;&#039; After mitral valve(MV) replacement with any mechanical valve, [[warfarin]] is indicated to achieve an [[INR]] of 2.5 to 3.5. (Level of Evidence: C) &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;2.&#039;&#039;&#039; After aortic valve replacement (AVR) or MV replacement with a bioprosthesis and no risk factors,* aspirin is indicated at 75 to 100 mg per day. (Level of Evidence: C)&lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;3.&#039;&#039;&#039; After MV replacement with a bioprosthesis and risk factors,* warfarin is indicated to achieve an INR of 2.0 to 3.0. (Level of Evidence: C)&lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;4.&#039;&#039;&#039; For those patients who are unable to take warfarin after MV replacement or AVR, [[aspirin]] is indicated in a dose of 75 to 325 mg per day. (Level of Evidence: B) &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;5.&#039;&#039;&#039; The addition of aspirin 75 to 100 mg once daily to therapeutic warfarin is recommended for all patients with mechanical heart valves and those patients with biological valves who have risk factors.* (Level of Evidence: B)&lt;br /&gt;
&lt;br /&gt;
===Class IIa===&lt;br /&gt;
&#039;&#039;&#039;1.&#039;&#039;&#039; During the first 3 months after AVR or MV replacement with a bioprosthesis, in patients with no risk factors,* it is reasonable to give warfarin to achieve an INR of 2.0 to 3.0. (Level of Evidence: C)&lt;br /&gt;
&lt;br /&gt;
===Class IIb===&lt;br /&gt;
&#039;&#039;&#039;1.&#039;&#039;&#039; In high-risk patients with prosthetic heart valves in whom aspirin cannot be used, it may be reasonable to give clopidogrel (75 mg per day) or warfarin to achieve an INR of 3.5 to 4.5. (Level of Evidence: C)}}&lt;br /&gt;
&lt;br /&gt;
==Related chapters==&lt;br /&gt;
* [[Mitral regurgitation]]&lt;br /&gt;
* [[Artificial heart valve]]&lt;br /&gt;
* [[Mitral stenosis]]&lt;br /&gt;
* [[Heart-lung machine]]&lt;br /&gt;
&lt;br /&gt;
==References==&lt;br /&gt;
{{reflist|2}}&lt;br /&gt;
*[http://www.debakeydepartmentofsurgery.org/home/content.cfm?proc_name=mitral+valve+repair+replacement&amp;amp;content_id=274 BCM: The Michael E DeBaker Department of Surgery. Mitral Valve Repair/ Replacement. n.d. 29 Apr. 2007] &lt;br /&gt;
*[http://www.ecu.edu/dhs/news/newsstory.cfm?ID=16 &amp;quot;FDA approves second clinical trial for robotic heart surgery.&amp;quot; Health Sciences News. 9 Nov. 2000. ECU Division of Health Sciences. 2 May 2007]&lt;br /&gt;
*[http://www.nlm.nih.gov/medlineplus/ency/article/000180.htm Gandelman, Glenn. &amp;quot;Medical encyclopedia.&amp;quot; Medline Plus. n.d. 3 May 2007]&lt;br /&gt;
*[http://www.webmd.com/heart-disease/warfarin-other-blood-thinners?page=1 &amp;quot;Heart Disease: Warfarin and Other Blood Thinners.&amp;quot; WebMD. The Cleveland Clinic. 10 May 2007 ]&lt;br /&gt;
*[http://www.clevelandclinic.org/heartcenter/pub/guide/percutaneous/percutaneousValve.htm#investigational#investigational Heart and Vascular Institute. &#039;&#039;Heart Valve Disease - Percutaneous Interventions: Non-surgical approaches.&#039;&#039; 2007. 7 May 2007 ]&lt;br /&gt;
*[http://www.umm.edu/heart/mitral_repla.html &amp;quot;Mitral Valve Replacement.&amp;quot; University of Maryland Medical Center: 1-2. 26 Apr. 2007  ]&lt;br /&gt;
*[http://www.graphpad.com/www/book/survive.htm Motulsky, Harvey. &#039;&#039;Intuitive Biostatistics&#039;&#039;. Oxford University Press Inc, 1995. 2 May 2007 ]&lt;br /&gt;
&lt;br /&gt;
{{cardiac surgery}}&lt;br /&gt;
{{SIB}}&lt;br /&gt;
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[[Category:Valvular heart disease]]&lt;br /&gt;
{{WikiDoc Help Menu}}&lt;br /&gt;
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[[uk:Протезування мітрального клапану]]&lt;/div&gt;</summary>
		<author><name>Varun Kumar</name></author>
	</entry>
	<entry>
		<id>https://www.wikidoc.org/index.php?title=Resistant_hypertension&amp;diff=662668</id>
		<title>Resistant hypertension</title>
		<link rel="alternate" type="text/html" href="https://www.wikidoc.org/index.php?title=Resistant_hypertension&amp;diff=662668"/>
		<updated>2012-08-02T15:29:53Z</updated>

		<summary type="html">&lt;p&gt;Varun Kumar: Created page with &amp;quot;{{CMG}}; {{AOEIC}} {{VK}}  ==Overview== Persistance of hypertension despite use of multiple antihypertensive medications is termed resistant hypertension. This is usually due ...&amp;quot;&lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;{{CMG}}; {{AOEIC}} {{VK}}&lt;br /&gt;
&lt;br /&gt;
==Overview==&lt;br /&gt;
Persistance of hypertension despite use of multiple antihypertensive medications is termed resistant hypertension. This is usually due to secondary etiology. AHA Scientific Statement 2008 defines resistant hypertension as the blood pressure which remains above the goal of 140/90 mm Hg despite concurrent use of 3 antihypertensive medications of different classes at optimal doses.&amp;lt;ref name=&amp;quot;pmid18391085&amp;quot;&amp;gt;{{cite journal| author=Calhoun DA, Jones D, Textor S, Goff DC, Murphy TP, Toto RD et al.| title=Resistant hypertension: diagnosis, evaluation, and treatment. A scientific statement from the American Heart Association Professional Education Committee of the Council for High Blood Pressure Research. | journal=Hypertension | year= 2008 | volume= 51 | issue= 6 | pages= 1403-19 | pmid=18391085 | doi=10.1161/HYPERTENSIONAHA.108.189141 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;amp;tool=sumsearch.org/cite&amp;amp;retmode=ref&amp;amp;cmd=prlinks&amp;amp;id=18391085  }} &amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==References==&lt;br /&gt;
{{reflist|2}}&lt;br /&gt;
&lt;br /&gt;
{{WH}}&lt;br /&gt;
{{WS}}&lt;br /&gt;
&lt;br /&gt;
[[Category:Cardiology]]&lt;br /&gt;
[[Category:Disease]]&lt;/div&gt;</summary>
		<author><name>Varun Kumar</name></author>
	</entry>
	<entry>
		<id>https://www.wikidoc.org/index.php?title=Orbital_cellulitis&amp;diff=657295</id>
		<title>Orbital cellulitis</title>
		<link rel="alternate" type="text/html" href="https://www.wikidoc.org/index.php?title=Orbital_cellulitis&amp;diff=657295"/>
		<updated>2012-07-26T02:46:46Z</updated>

		<summary type="html">&lt;p&gt;Varun Kumar: &lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;{{SI}}&lt;br /&gt;
__NOTOC__&lt;br /&gt;
{{Editor Help}}&lt;br /&gt;
&lt;br /&gt;
== Overview ==&lt;br /&gt;
&#039;&#039;&#039;Orbital cellulitis&#039;&#039;&#039; is a serious infection of the orbital tissues which can lead to restriction of eye movements, loss of vision and even loss of life.&lt;br /&gt;
&lt;br /&gt;
== Diagnosis == &lt;br /&gt;
Orbital cellulitis should be differentiated from preseptal cellulitis which is confined to structures anterior to orbital septum. Where as, orbital cellulitis involves structures posterior to orbital septum which includes fat and ocular muscles.&lt;br /&gt;
&lt;br /&gt;
===History and Symptoms===&lt;br /&gt;
Patients present with sudden onset of fever, [[proptosis]], restricted eye movement, and swelling and redness of the eye lids. It is usually caused by a previous sinusitis. &lt;br /&gt;
&lt;br /&gt;
=== Physical Examination ===&lt;br /&gt;
==== Eyes ====&lt;br /&gt;
[[Image:Orbital_Cellulitis.jpg|thumb|150px|left|Orbital Cellulitis&amp;lt;ref&amp;gt;http://picasaweb.google.com/mcmumbi/USMLEIIImages&amp;lt;/ref&amp;gt;]]&lt;br /&gt;
&amp;lt;BR&amp;gt;&lt;br /&gt;
==== MRI and CT ====&lt;br /&gt;
[[Image:pre- and post-septal Orbital Cellulitis.jpg|thumb|150px|left|Pre- and post-septal Orbital Cellulitis&amp;lt;ref&amp;gt;http://picasaweb.google.com/mcmumbi/USMLEIIImages&amp;lt;/ref&amp;gt;]]&lt;br /&gt;
&lt;br /&gt;
== Treatment ==&lt;br /&gt;
Because of concern for spread of infection, patients must be admitted to the hospital to receive intravenous antibiotics. The feared complications include [[cavernous sinus thrombosis]] and [[meningitis]]. Abscess formation is another complication and may require surgical drainage. &lt;br /&gt;
&lt;br /&gt;
Orbital cellulitis is considered an ophthalmological emergency. &lt;br /&gt;
&lt;br /&gt;
==See also==&lt;br /&gt;
* [[Periorbital cellulitis]]&lt;br /&gt;
&lt;br /&gt;
==External links==&lt;br /&gt;
* [http://eyelearn.med.utoronto.ca/Lectures05-06/RedEye/05Orbit.htm University of Toronto]&lt;br /&gt;
* [http://www.nlm.nih.gov/medlineplus/ency/article/001012.htm MedlinePlus].&lt;br /&gt;
&lt;br /&gt;
==References==&lt;br /&gt;
* {{cite journal |author=Howe L, Jones N |title=Guidelines for the management of periorbital cellulitis/abscess |journal=Clin Otolaryngol Allied Sci |volume=29 |issue=6 |pages=725-8 |year=2004 |pmid=15533168}}&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
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[[Category:Infectious disease]]&lt;br /&gt;
[[Category:Bacterial diseases]]&lt;br /&gt;
[[Category:Disease stubs]]&lt;br /&gt;
[[Category:Ophthalmology]]&lt;br /&gt;
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		<author><name>Varun Kumar</name></author>
	</entry>
	<entry>
		<id>https://www.wikidoc.org/index.php?title=Status_epilepticus&amp;diff=656887</id>
		<title>Status epilepticus</title>
		<link rel="alternate" type="text/html" href="https://www.wikidoc.org/index.php?title=Status_epilepticus&amp;diff=656887"/>
		<updated>2012-07-25T00:23:06Z</updated>

		<summary type="html">&lt;p&gt;Varun Kumar: /* Benzodiazepines */&lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;&#039;&#039;&#039;For patient information, click [[Epilepsy (patient information)|here]]&#039;&#039;&#039;&lt;br /&gt;
{{Infobox_Disease |&lt;br /&gt;
  Name           = {{PAGENAME}} |&lt;br /&gt;
  Image          = |&lt;br /&gt;
  Caption        = |&lt;br /&gt;
  DiseasesDB     = |&lt;br /&gt;
  ICD10          = {{ICD10|G|41||g|40}} |&lt;br /&gt;
  ICD9           = {{ICD9|345.3}} |&lt;br /&gt;
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  OMIM           = |&lt;br /&gt;
  MedlinePlus    = |&lt;br /&gt;
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  MeshID         = D013226 |&lt;br /&gt;
}}&lt;br /&gt;
{{SI}}&lt;br /&gt;
{{CMG}}&lt;br /&gt;
&lt;br /&gt;
==Overview==&lt;br /&gt;
&#039;&#039;&#039;Status epilepticus&#039;&#039;&#039; (SE) refers to a life threatening condition in which the [[brain]] is in a state of persistent [[seizure]].  Definitions vary, but traditionally it is defined as one continuous seizure or recurrent seizures without regaining consciousness between seizures for greater than 30 minutes. Many doctors, however, believe that 5 minutes is sufficient to damage neurons and that seizures are unlikely to self-terminate by that time.&lt;br /&gt;
&lt;br /&gt;
In known epileptics, this condition is associated with poor [[compliance (medicine)|compliance]] (adherence to medication regimen), [[alcohol]] withdrawal, and [[metabolism|metabolic]] disturbances.  As a primary presentation it normally indicates a [[tumour]] or [[abscess]].&lt;br /&gt;
&lt;br /&gt;
It can also be induced by [[nerve agent]]s such as [[soman]].&amp;lt;ref name=&amp;quot;soman&amp;quot;&amp;gt;{{cite journal | first = John H. | last = McDonough | coauthors = A. Benjamin, Joseph D. McMonagle, Thomas Rowland, Shih Tsung-Ming | month = February | year = 2004 | title = Effects of fosphenytoin on nerve agent-induced status epilepticus | journal = Drug and Chemical Toxicology | volume = 27 | issue = 1 | pages = 27–39 | pmid = 15038246 | url = http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&amp;amp;db=pubmed&amp;amp;list_uids=15038246&amp;amp;dopt=ExternalLink}}&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Variants==&lt;br /&gt;
Status epilepticus can be divided into two categories&amp;amp;mdash;convulsive and nonconvulsive, the latter of which is underdiagnosed.&lt;br /&gt;
===Convulsive===&lt;br /&gt;
[[Epilepsia partialis continua]] is a variant involving hour, day, or even week-long jerking. It is a consequence of [[vascular disease]], [[tumour]]s, or [[encephalitis]], and is drug-resistant.&lt;br /&gt;
&lt;br /&gt;
Generalized [[myoclonus]] is commonly seen in [[coma]]tose patients following [[CPR]] and is seen by some as an indication of catastrophic damage to the [[neocortex]].&amp;lt;ref name=&amp;quot;gen-myo-se&amp;quot;&amp;gt;{{cite journal | first = Eelco F. M. | last = Wijdicks | coauthors = Parisi JE, Sharbrough FW | month = February | year = 1994 | title = Prognostic value of myoclonus status in comatose survivors of cardiac arrest | journal = Annals of Neurology | volume = 35 | issue = 2 | pages = 239–43 | pmid =8109907}}&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
===Nonconvulsive===&lt;br /&gt;
&lt;br /&gt;
[[Complex partial status epilepticus]], or CPSE, and absence status epilepticus are rare forms of the condition which are marked by nonconvulsive seizures. In the case of CPSE, the seizure is confined to a small area of the brain, normally the temporal lobe. But the latter, absence status epilepticus, is marked by a generalised seizure affecting the whole brain, and an [[Electroencephalogram|EEG]] is needed to differentiate between the two conditions. This results in episodes characterized by a long-lasting stupor, staring and unresponsiveness.&lt;br /&gt;
&lt;br /&gt;
==Treatments==&lt;br /&gt;
&lt;br /&gt;
===Benzodiazepines===&lt;br /&gt;
&lt;br /&gt;
Shortly after it was introduced in 1963, [[diazepam]] became the first choice for SE. Even though other [[benzodiazepine]]s such as [[clonazepam]] were useful, diazepam was relied upon almost exclusively. This began to change in 1975 with a preliminary study on [[lorazepam]] conducted by &lt;br /&gt;
Waltregny and Dargent, who found that its pharmacological effects were longer lasting than those of an equal dose of diazepam.&amp;lt;ref name=&amp;quot;waltdar&amp;quot;&amp;gt;{{cite journal | first = Alain | last = Waltregny | coauthors = Jérôme Dargent | month = September/October | year = 1975 | title = Preliminary study of parenteral lorazepam in status epilepticus | journal = Acta Neurologica Belgica | volume = 75 | issue = 5 | pages = 219–29 | pmid = 3939}}&amp;lt;/ref&amp;gt; This meant it did not have to be repeatedly injected like diazepam,&amp;lt;ref name=&amp;quot;lorazepam1979&amp;quot;&amp;gt;{{cite journal | first = JE | last = Walker | coauthors = RW Homan, MR Vasko, IL Crawford, RD Bell, WG Tasker | month = September | year = 1979 | title = Lorazepam in status epilepticus | journal = Annals of Neurology | volume = 6 | issue = 3 | pages = 207–13 | pmid = 43112}}&amp;lt;/ref&amp;gt; the effects of which would wear off 5–15 minutes later in spite of its 30-hour [[half-life]] (due to extensive redistribution of diazepam outside the vascular compartment as diazepam is highly lipid soluble). It has also been found that patients who were first tried on diazepam were much more likely to require [[tracheotomy|endotracheal tubing]] than patients who were first tried on [[phenobarbital]], [[phenytoin]],&amp;lt;ref name=&amp;quot;vspbandpht&amp;quot;&amp;gt;{{cite journal | first = Richard A. | last = Orr | coauthors = Robert J. Dimand, Shekhar T. Venkataraman, Valerie A. Karr, Kathleen J. Kennedy | month = September | year = 1991 | title = Diazepam and intubation in emergency treatment of seizures in children | journal = Annals of Emergency Medicine | volume = 20 | issue = 9 | pages = 1009–13 | pmid = 1877765 |  doi = 10.1016/S0196-0644(05)82981-6 | url = http://www.sciencedirect.com/science?_ob=ArticleURL&amp;amp;_udi=B6WB0-4G82KTB-G&amp;amp;_coverDate=09%2F30%2F1991&amp;amp;_alid=434858892&amp;amp;_rdoc=1&amp;amp;_fmt=&amp;amp;_orig=search&amp;amp;_qd=1&amp;amp;_cdi=6696&amp;amp;_sort=d&amp;amp;view=c&amp;amp;_acct=C000050221&amp;amp;_version=1&amp;amp;_urlVersion=0&amp;amp;_userid=10&amp;amp;md5=fab697f11c8e05b7fe0405b1d34a6f7d}}&amp;lt;/ref&amp;gt; or lorazepam.&amp;lt;ref name=&amp;quot;vslorazepam&amp;quot;&amp;gt;{{cite journal | first = Richard | last = Appleton | coauthors = A. Sweeney, Imti Choonara, Joan Robson, Elizabeth Molyneux. | month = August | year = 1995 | title = Lorazepam versus diazepam in the acute treatment of epileptic seizures and status epilepticus | journal = Developmental Medicine and Child Neurology | volume = 37 | issue = 8 | pages = 682–8 | pmid = 7672465}}&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
Today, the benzodiazepine of choice is [[lorazepam]] 0.02-0.03mg/kg IV, for initial treatment due to its long (2–8 hour) duration of action and rapid onset of action, thought to be due to its high affinity for GABA receptors and to its low lipid solubility which causes it to remain in the vascular compartment.  If lorazepam is not available, then diazepam 0.1mg/kg IV or [[midazolam]] 0.05mg/kg IV should be given.&amp;lt;ref name=&amp;quot;benzo-of-choice&amp;quot;&amp;gt;{{cite journal | first = Trudy | last = Pang | coauthors = Lawrence J. Hirsch | month = July | year = 2005 | title = Treatment of Convulsive and Nonconvulsive Status Epilepticus | journal = Current Treatment Options in Neurology | volume = 7 | issue = 4 | pages = 247–259 | pmid = 15967088 | url = http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&amp;amp;db=pubmed&amp;amp;list_uids=15967088&amp;amp;dopt=ExternalLink}}&amp;lt;/ref&amp;gt; If IV access cannot be obtained, [[midazolam]] 10mg (if wt&amp;gt;40kg) or 5mg (if wt&amp;lt;40kg) can be administered via IM route&amp;lt;ref name=&amp;quot;pmid22335736&amp;quot;&amp;gt;{{cite journal| author=Silbergleit R, Durkalski V, Lowenstein D, Conwit R, Pancioli A, Palesch Y et al.| title=Intramuscular versus intravenous therapy for prehospital status epilepticus. | journal=N Engl J Med | year= 2012 | volume= 366 | issue= 7 | pages= 591-600 | pmid=22335736 | doi=10.1056/NEJMoa1107494 | pmc=PMC3307101 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;amp;tool=sumsearch.org/cite&amp;amp;retmode=ref&amp;amp;cmd=prlinks&amp;amp;id=22335736  }} &amp;lt;/ref&amp;gt;. Sometimes, the failure of lorazepam alone is considered to be enough to classify a case of SE as [[Wiktionary:refractory|refractory]].&lt;br /&gt;
&lt;br /&gt;
===Phenytoin and fosphenytoin===&lt;br /&gt;
&lt;br /&gt;
Phenytoin was once another first-line therapy, although the [[prodrug]] [[fosphenytoin]] can be administered three times as fast and with far fewer injection site reactions. If these or any other [[hydantoin|hydantoin derivative]]s are used, then cardiac monitoring is a must if they are administered intravenously. Because the hydantoins take 15–30 minutes to work, a benzodiazepine or barbiturate is often co-administered. Because of diazepam&#039;s short duration of action, they were often administered together anyway.&lt;br /&gt;
&lt;br /&gt;
===Barbiturates===&lt;br /&gt;
&lt;br /&gt;
Before the benzodiazepines were invented, there were the barbiturates, which are still used today if benzodiazepines or the hydantoins are not an option. These are used to induce a  [[barbiturate|barbituric]] coma. The barbiturate most commonly used for this is phenobarbital. [[Thiopental]] or [[pentobarbital]] may also be used for that purpose if the seizures have to be stopped immediately or if the patient has already been compromised by the underlying illness or toxic/metabolic-induced seizures; however, in those situations, thiopental is the agent of choice.&lt;br /&gt;
&lt;br /&gt;
The failure of phenobarbital therapy does not preclude the success of a lengthy comatose state induced by a stronger barbiturate such as [[secobarbital]]. Such was the case for Ohori, Fujioka, and Ohta ca. 1998, when they induced a 10-month long coma (or &amp;quot;anesthesia&amp;quot; as they called it) in a 26-year-old woman suffering from refractory status epilepticus secondary to [[encephalitis|viral encephalitis]] and then tapered her off the secobarbital very slowly while using [[zonisamide]] at the same time.&amp;lt;ref name=&amp;quot;secobarbitalofo&amp;quot;&amp;gt;{{cite journal | first = Nobuhira | last = Ohori | coauthors = Fujioka Y, Ohta M. | month = May | year = 1998 | title = [Experience in managing refractory status epilepticus caused by viral encephalitis under long-term anesthesia with barbiturate: a case report] | journal = Rinsho Shinkeigaku | volume = 38 | issue = 5 | pages = 474–7 | pmid = 9806000}} (Japanese)&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
===General anesthetics===&lt;br /&gt;
&lt;br /&gt;
If this proves ineffective or if barbiturates cannot be used for some reason, then a [[general anesthetic]] such as [[propofol]]&amp;lt;ref name=&amp;quot;propofol&amp;quot;&amp;gt;{{cite journal | first = X | last = Pourrat | coauthors = JM Serekian, D Antier, J. Grassin | title = [Generalized tonic-clonic status epilepticus: therapeutic strategy] | journal = Presse Médicale | volume = 30 | issue = | date = June 9, 2001 | pages = 1031–6 | pmid = 11433696}} (French).&amp;lt;/ref&amp;gt; is tried; sometimes it is used second after the failure of [[lorazepam]].&amp;lt;ref name=&amp;quot;propofol2&amp;quot;&amp;gt;{{cite journal | first = Paul E. | last = Marik | coauthors = Joseph Varon | title = The management of status epilepticus | journal = Chest | year = 2004 | volume = 126 | issue = 2 | pages = 582–91 | pmid = 15302747 | url = http://www.chestjournal.org/cgi/content/full/126/2/582}}&amp;lt;/ref&amp;gt; This also means putting the patient on artificial respiration. Propofol has been shown to be effective in suppressing the jerks seen in myoclonus status epilepticus, but as of 2002, there have been no cases of anyone going into myoclonus status epilepticus, undergoing propofol treatment, and then not dying anyway.&amp;lt;ref name=&amp;quot;propofolmse&amp;quot;&amp;gt;{{cite journal | first = Eelco F.M. | last = Wijdicks | year = 2002 | month = July | title = Propofol in myoclonus status epilepticus in comatose patients following cardiac resuscitation | journal = Journal of Neurology Neurosurgery and Psychiatry | volume = 73 | issue = 1 | pages = 94–5 | pmid = 12082068 | url = http://jnnp.bmjjournals.com/cgi/content/full/73/1/94}}&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
===Lidocaine===&lt;br /&gt;
&lt;br /&gt;
The use of [[lidocaine]] in status epilepticus was first reported in 1955 by Bernhard, Boem and Hojeberg.&amp;lt;ref name=&amp;quot;lidocaine1955&amp;quot;&amp;gt;{{cite journal | first = CG | last = Bernhard | coauthors = Bohm E, Hojeberg S | month = August | year = 1955 | title = A new treatment of status epilepticus; intravenous injections of a local anesthetic (lidocaine) | journal = AMA Archives of Neurology and  Psychiatry | volume = 74 | issue = 2 | page = 208–14 | pmid = 14397899}}&amp;lt;/ref&amp;gt; Since then, it has been used in cases refractory to phenobarbital, diazepam, and phenytoin, and has been studied as an alternative to barbiturates and general anesthetics.&amp;lt;ref name=&amp;quot;lidocainepro&amp;quot;&amp;gt;{{cite journal | first = Praveen | last = Aggarwal | coauthors = Jyoti Prakash Wali | month = May | year = 1993 | title = Lidocaine in refractory status epilepticus: a forgotten drug in the emergency department | journal = American Journal of Emergency Medicine | volume = 11 | issue = 3 | pages = 243–4 | pmid = 93257009 | doi = 10.1016/0735-6757(93)90135-X | url = http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&amp;amp;db=pubmed&amp;amp;list_uids=8489668&amp;amp;dopt=ExternalLink}}&amp;lt;/ref&amp;gt;&amp;lt;ref name=&amp;quot;lidocainepro2&amp;quot;&amp;gt;{{cite journal | first = N | last = Sugiyama | coauthors = Hamano S, Mochizuki M, Tanaka M, Eto Y | month = November | year = 2004 | title = [Efficacy of lidocaine on seizures by intravenous and intravenous-drip infusion] | journal = No To Hattatsu | volume = 36 | issue = 6 | pages = 451–4 | pmid = 15560386}} (Japanese)&amp;lt;/ref&amp;gt; Lidocaine is a [[sodium channel]] blocker and has been used where sodium channel dysfunction was suspected.&amp;lt;ref name=&amp;quot;sodium-channel-dysfunction&amp;quot;&amp;gt;{{cite journal | author = Sawaishi Yukio | coauthors = Yano Tamami, Enoki Masamichi, and Takada Goro | month = February | year = 2002 | title = Lidocaine-dependent early infantile status epilepticus with highly suppressed EEG | journal = Epilepsia | volume = 43 | issue = 2 | pages = 201–4 | pmid = 11903470 | doi = 10.1046/j.1528-1157.2002.25301.x}}&amp;lt;/ref&amp;gt; However, in some studies, it was either ineffective or even harmful for most patients.&amp;lt;ref name=&amp;quot;lidocainecon&amp;quot;&amp;gt;{{cite journal | author = Tanabe Takuya | coauthors = Suzuki Shuuhei, Shimakawa Shuichi, Yamashiro Kuniteru&amp;lt;!--The original kanji for &amp;quot;Kuniteru(?)&amp;quot; were 國暉. Please find the actual pronunciation if that is incorrect!--&amp;gt;, Tamai Hiroshi | month = January | year = 1999 | title = Problems of intravenous lidocaine treatment in status epilepticus or clustering seizures in childhood | journal = [http://www.meteo-intergate.com/journal/journal-archive_cl1nohat.html No To Hattatsu] | volume = 31 | issue = 1 | pages = 14–20 | pmid = 10025129}} (Japanese)&amp;lt;/ref&amp;gt; The last is not so surprising in light of the fact that lidocaine has been known to cause seizures in humans and laboratory animals at doses greater than 15&amp;amp;nbsp;µg/mL&amp;lt;ref name=&amp;quot;pro-and-anticonvulsant&amp;quot;&amp;gt;{{cite journal | first = John C. | last = DeToledo | month = June | year = 2000 | title = Lidocaine and Seizures | journal = Therapeutic Drug Monitoring | volume = 22 | issue = 3 | pages = 320–322 | pmid = 10850400}}&amp;lt;/ref&amp;gt; or 2–3&amp;amp;nbsp;mg/kg.&amp;lt;ref name=&amp;quot;pro-and-anticonvulsant2&amp;quot;&amp;gt;{{cite web | author=Steven C. Schachter | title=Lidocaine | url=http://professionals.epilepsy.com/page/local_lidocaine.html | publisher=epilepsy.com/professionals}} Adapted from: {{cite book | author=Najjar S, Devinsky O, Rosenberg AD, et al | editor=ed. Ettinger AB and Devinsky O | title=Managing epilepsy and co-existing disorders | chapter=Procedures in epilepsy  patients | year=2002 | pages=499–513 | publisher=Butterworth-Heinemann | location=Boston | isbn=0-7506-7241-2}}&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==References==&lt;br /&gt;
{{Reflist|2}}&lt;br /&gt;
{{-}}&lt;br /&gt;
{{Diseases of the nervous system}}&lt;br /&gt;
{{SIB}}&lt;br /&gt;
&lt;br /&gt;
[[Category:Neurology]]&lt;br /&gt;
[[Category:Medical emergencies]]&lt;br /&gt;
[[Category:Epilepsy]]&lt;br /&gt;
[[Category:Emergency medicine]]&lt;br /&gt;
[[Category:Overview complete]]&lt;br /&gt;
[[de:status epilepticus]]&lt;br /&gt;
[[nl:Status epilepticus]]&lt;br /&gt;
[[ru:Эпилептический статус]]&lt;br /&gt;
[[fi:Status epilepticus]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
{{WH}}&lt;br /&gt;
{{WS}}&lt;/div&gt;</summary>
		<author><name>Varun Kumar</name></author>
	</entry>
	<entry>
		<id>https://www.wikidoc.org/index.php?title=Tietze_costochondritis&amp;diff=648046</id>
		<title>Tietze costochondritis</title>
		<link rel="alternate" type="text/html" href="https://www.wikidoc.org/index.php?title=Tietze_costochondritis&amp;diff=648046"/>
		<updated>2012-06-07T14:44:05Z</updated>

		<summary type="html">&lt;p&gt;Varun Kumar: ←Redirected page to Tietze&amp;#039;s syndrome&lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;#redirect [[Tietze&#039;s syndrome]]&lt;/div&gt;</summary>
		<author><name>Varun Kumar</name></author>
	</entry>
	<entry>
		<id>https://www.wikidoc.org/index.php?title=Quaternary_syphilis&amp;diff=648045</id>
		<title>Quaternary syphilis</title>
		<link rel="alternate" type="text/html" href="https://www.wikidoc.org/index.php?title=Quaternary_syphilis&amp;diff=648045"/>
		<updated>2012-06-07T14:43:02Z</updated>

		<summary type="html">&lt;p&gt;Varun Kumar: ←Redirected page to Syphilis&lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;#redirect [[syphilis]]&lt;/div&gt;</summary>
		<author><name>Varun Kumar</name></author>
	</entry>
	<entry>
		<id>https://www.wikidoc.org/index.php?title=Prinzmetal_angina&amp;diff=648044</id>
		<title>Prinzmetal angina</title>
		<link rel="alternate" type="text/html" href="https://www.wikidoc.org/index.php?title=Prinzmetal_angina&amp;diff=648044"/>
		<updated>2012-06-07T14:42:04Z</updated>

		<summary type="html">&lt;p&gt;Varun Kumar: ←Redirected page to Prinzmetal&amp;#039;s angina&lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;#redirect [[Prinzmetal&#039;s angina]]&lt;/div&gt;</summary>
		<author><name>Varun Kumar</name></author>
	</entry>
	<entry>
		<id>https://www.wikidoc.org/index.php?title=Esophageal_foreign_body&amp;diff=648043</id>
		<title>Esophageal foreign body</title>
		<link rel="alternate" type="text/html" href="https://www.wikidoc.org/index.php?title=Esophageal_foreign_body&amp;diff=648043"/>
		<updated>2012-06-07T14:40:07Z</updated>

		<summary type="html">&lt;p&gt;Varun Kumar: ←Redirected page to Foreign body&lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;#redirect [[Foreign body]]&lt;/div&gt;</summary>
		<author><name>Varun Kumar</name></author>
	</entry>
	<entry>
		<id>https://www.wikidoc.org/index.php?title=Esophageal_foreign_body&amp;diff=648042</id>
		<title>Esophageal foreign body</title>
		<link rel="alternate" type="text/html" href="https://www.wikidoc.org/index.php?title=Esophageal_foreign_body&amp;diff=648042"/>
		<updated>2012-06-07T14:39:56Z</updated>

		<summary type="html">&lt;p&gt;Varun Kumar: Created page with &amp;quot;# redirect Foreign body&amp;quot;&lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;# redirect [[Foreign body]]&lt;/div&gt;</summary>
		<author><name>Varun Kumar</name></author>
	</entry>
	<entry>
		<id>https://www.wikidoc.org/index.php?title=Lymphangiomyomatosis&amp;diff=648041</id>
		<title>Lymphangiomyomatosis</title>
		<link rel="alternate" type="text/html" href="https://www.wikidoc.org/index.php?title=Lymphangiomyomatosis&amp;diff=648041"/>
		<updated>2012-06-07T14:39:02Z</updated>

		<summary type="html">&lt;p&gt;Varun Kumar: Created page with &amp;quot;{{SI}} {{CMG}}; {{AOEIC}} {{VK}}  ==Overview== Lymphangiomyocytosis is defined as a multifocal neoplasm with differentiation of the perivascular epithelioid cell and has a fem...&amp;quot;&lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;{{SI}}&lt;br /&gt;
{{CMG}}; {{AOEIC}} {{VK}}&lt;br /&gt;
&lt;br /&gt;
==Overview==&lt;br /&gt;
Lymphangiomyocytosis is defined as a multifocal neoplasm with differentiation of the perivascular epithelioid cell and has a female prepondrance, especially females of child-bearing age. &lt;br /&gt;
&lt;br /&gt;
==Characteristic Features==&lt;br /&gt;
Lymphangiomyocytosis is characterized by the presence of smooth muscle and epithelioid cells and by the proliferation of lymphatic vessels. &lt;br /&gt;
&lt;br /&gt;
==Sites of Involvement==&lt;br /&gt;
*Lungs,&lt;br /&gt;
*Mediastinum, and &lt;br /&gt;
*Retroperitoneum. &lt;br /&gt;
&lt;br /&gt;
==Presentation==&lt;br /&gt;
It usually presents with [[pleural effusion|chylous pleural effusion]] or [[ascites]].&lt;br /&gt;
&lt;br /&gt;
==Reference==&lt;br /&gt;
{{reflist|2}}&lt;br /&gt;
&lt;br /&gt;
[[Category: Disease]]&lt;br /&gt;
[[Category: Oncology]]&lt;br /&gt;
[[Category: Hematology]]&lt;br /&gt;
&lt;br /&gt;
{{WH}}&lt;br /&gt;
{{WS}}&lt;/div&gt;</summary>
		<author><name>Varun Kumar</name></author>
	</entry>
	<entry>
		<id>https://www.wikidoc.org/index.php?title=Glycogenosis_type_7&amp;diff=648040</id>
		<title>Glycogenosis type 7</title>
		<link rel="alternate" type="text/html" href="https://www.wikidoc.org/index.php?title=Glycogenosis_type_7&amp;diff=648040"/>
		<updated>2012-06-07T14:34:17Z</updated>

		<summary type="html">&lt;p&gt;Varun Kumar: ←Redirected page to Phosphofructokinase deficiency&lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;#redirect [[phosphofructokinase deficiency]]&lt;/div&gt;</summary>
		<author><name>Varun Kumar</name></author>
	</entry>
	<entry>
		<id>https://www.wikidoc.org/index.php?title=Phosphofructokinase_deficiency&amp;diff=648039</id>
		<title>Phosphofructokinase deficiency</title>
		<link rel="alternate" type="text/html" href="https://www.wikidoc.org/index.php?title=Phosphofructokinase_deficiency&amp;diff=648039"/>
		<updated>2012-06-07T14:32:59Z</updated>

		<summary type="html">&lt;p&gt;Varun Kumar: &lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;{{Infobox_Disease |&lt;br /&gt;
  Name           = {{PAGENAME}} |&lt;br /&gt;
  Image          = |&lt;br /&gt;
  Caption        = |&lt;br /&gt;
  DiseasesDB     = 5314 |&lt;br /&gt;
  ICD10          = {{ICD10|E|74|0|e|70}} |&lt;br /&gt;
  ICD9           = {{ICD9|271.0}} |&lt;br /&gt;
  ICDO           = |&lt;br /&gt;
  OMIM           = 232800 |&lt;br /&gt;
  MedlinePlus    = |&lt;br /&gt;
  MeshID         = D006014 |&lt;br /&gt;
}}&lt;br /&gt;
{{SI}}&lt;br /&gt;
{{CMG}}&lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;&#039;&#039;Synonyms and Keywords:&#039;&#039;&#039;&#039;&#039; Glycogenosis type 7 or Tarui disease or Glycogen storage disease type 7.&lt;br /&gt;
&lt;br /&gt;
==Overview==&lt;br /&gt;
Phosphofructokinase deficiency, also known as &#039;&#039;&#039;Glycogen storage disease type VII&#039;&#039;&#039; or &#039;&#039;&#039;Tarui&#039;s disease&#039;&#039;&#039;&amp;lt;ref&amp;gt;{{WhoNamedIt|synd|3022}}&amp;lt;/ref&amp;gt;, is a [[metabolic disorder]] with [[autosomal recessive]] inheritance, in which deficiency of the M subunit of the [[phosphofructokinase]] [[enzyme]] impairs the ability of cells such as [[erythrocytes]] and [[Skeletal muscle|rhabdomyocyte]]s to use [[carbohydrate]]s (such as [[glucose]]) for energy. It may affects humans as well as other mammals (especially dogs).  In humans it is the least common type of [[glycogen storage disease]].&lt;br /&gt;
&lt;br /&gt;
==Presentation==&lt;br /&gt;
The disease presents with exercise-induced [[muscle cramps]] and [[weakness]] (sometimes [[rhabdomyolysis]]), as well as with [[hemolytic anemia]] causing dark urine a few hours later.&lt;br /&gt;
&lt;br /&gt;
==References==&lt;br /&gt;
{{reflist|2}}&lt;br /&gt;
&lt;br /&gt;
{{WikiDoc Help Menu}}&lt;br /&gt;
{{WikiDoc Sources}}&lt;br /&gt;
&lt;br /&gt;
[[Category:Disease]]&lt;br /&gt;
[[Category:Endocrinology]]&lt;br /&gt;
[[Category:Inborn errors of metabolism]]&lt;/div&gt;</summary>
		<author><name>Varun Kumar</name></author>
	</entry>
	<entry>
		<id>https://www.wikidoc.org/index.php?title=Somatoform_disorder&amp;diff=648038</id>
		<title>Somatoform disorder</title>
		<link rel="alternate" type="text/html" href="https://www.wikidoc.org/index.php?title=Somatoform_disorder&amp;diff=648038"/>
		<updated>2012-06-07T14:30:17Z</updated>

		<summary type="html">&lt;p&gt;Varun Kumar: &lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;&#039;&#039;&#039;For patient information click [[Somatoform disorder (patient information)|here]]&#039;&#039;&#039;&lt;br /&gt;
&lt;br /&gt;
{{Infobox_Disease |&lt;br /&gt;
  Name           = {{PAGENAME}} |&lt;br /&gt;
  Image          = |&lt;br /&gt;
  Caption        = |&lt;br /&gt;
  DiseasesDB     = 1645 |&lt;br /&gt;
  ICD10          = {{ICD10|F|45||f|40}} |&lt;br /&gt;
  ICD9           = {{ICD9|300.8}} |&lt;br /&gt;
  ICDO           = |&lt;br /&gt;
  OMIM           = |&lt;br /&gt;
  MedlinePlus    = 000955|&lt;br /&gt;
  eMedicineSubj  = |&lt;br /&gt;
  eMedicineTopic = |&lt;br /&gt;
  MeshID         = D013001 |&lt;br /&gt;
}}&lt;br /&gt;
{{SI}}&lt;br /&gt;
{{CMG}}&lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;&#039;&#039;Synonyms and Keywords:&#039;&#039;&#039;&#039;&#039; Functional disorders or Psychophysiological disorder or Psychosomatic disorders or Somatization disorders or Briquet syndrome or CFS or Chronic fatigue syndromes or Conversion disorder.&lt;br /&gt;
&lt;br /&gt;
==Overview==&lt;br /&gt;
&#039;&#039;&#039;Somatoform disorders&#039;&#039;&#039; are physical ailments (such as [[Pain and nociception|pain]], [[nausea]], [[Clinical depression|depression]], [[dizziness]]) or concerns for which no adequate medical explanation has been found. Somatoform disorders are physical symptoms that seem as if they are part of a general medical condition. However, no general medical condition, other mental disorder, or substance is present. &lt;br /&gt;
The complaints are serious enough to cause significant emotional distress and impairment of social and/or occupational functioning.&lt;br /&gt;
&lt;br /&gt;
A diagnosis of a somatoform disorder implies that psychological factors are a large contributor to the symptoms&#039; onset, severity and duration. It is important to note that somatoform disorders are not the result of conscious [[malingering]] or [[factitious disorders]].&lt;br /&gt;
&lt;br /&gt;
==Recognized somatoform disorders==&lt;br /&gt;
The somatoform disorders recognized by the [[Diagnostic and Statistical Manual of Mental Disorders]] of the [[American Psychiatric Association]]  are:&lt;br /&gt;
*[[Conversion disorder]] &lt;br /&gt;
*[[Somatization disorder]] &lt;br /&gt;
*[[Hypochondriasis]] &lt;br /&gt;
*[[Body dysmorphic disorder]]&lt;br /&gt;
*[[Pain disorder]]&lt;br /&gt;
*[[Undifferentiated somatoform disorder]] - only one unexplained symptom is required for at least 6 months&lt;br /&gt;
*[[Somatoform disorder NOS]]&lt;br /&gt;
&lt;br /&gt;
==Proposed somatoform disorders==&lt;br /&gt;
Additional proposed somatoform disorders are:&lt;br /&gt;
* [[Abridged somatization disorder]]&amp;lt;ref name=&amp;quot;pmid2918297&amp;quot;&amp;gt;{{cite journal |author=Escobar JI, Rubio-Stipec M, Canino G, Karno M |title=Somatic symptom index (SSI): a new and abridged somatization construct. Prevalence and epidemiological correlates in two large community samples |journal=J. Nerv. Ment. Dis. |volume=177 |issue=3 |pages=140-6 |year=1989 |pmid=2918297 |doi=}}&amp;lt;/ref&amp;gt; - at least 4 unexplained somatic complaints in men and 6 in women &lt;br /&gt;
* [[Multisomatoform disorder]]&amp;lt;ref name=&amp;quot;pmid9107152&amp;quot;&amp;gt;{{cite journal |author=Kroenke K, Spitzer RL, deGruy FV, &#039;&#039;et al&#039;&#039; |title=Multisomatoform disorder. An alternative to undifferentiated somatoform disorder for the somatizing patient in primary care |journal=Arch. Gen. Psychiatry |volume=54 |issue=4 |pages=352-8 |year=1997 |pmid=9107152 |doi=}}&amp;lt;/ref&amp;gt; - at least 3 unexplained somatic complaints from the [[PRIME-MD]] scale for at least 2 years of active symptoms&lt;br /&gt;
&lt;br /&gt;
These disorders have been proposed because the recognized somatoform disorders are either too restrictive or too broad. In a study of 119 primary care patients, the following prevalences were found&amp;lt;ref name=&amp;quot;pmid15014690&amp;quot;&amp;gt;{{cite journal |author=Lynch DJ, McGrady A, Nagel R, Zsembik C |title=Somatization in Family Practice: Comparing 5 Methods of Classification |journal= |volume=1 |issue=3 |pages=85-89 |year=1999 |pmid=15014690 |doi=}}&amp;lt;/ref&amp;gt;:&lt;br /&gt;
* [[Somatization disorder]] - 1%&lt;br /&gt;
* [[Abridged somatization disorder]] - 6%&lt;br /&gt;
* [[Multisomatoform disorder]] - 24%&lt;br /&gt;
* [[Undifferentiated somatoform disorder]] - 79%&lt;br /&gt;
&lt;br /&gt;
==References==&lt;br /&gt;
{{reflist|2}}&lt;br /&gt;
&lt;br /&gt;
[[Category:Psychiatry]]&lt;br /&gt;
[[Category:Somatoform disorders]]&lt;br /&gt;
&lt;br /&gt;
[[Category:Overview complete]]&lt;br /&gt;
 &lt;br /&gt;
[[he: הפרעה סומטופורמית]]&lt;br /&gt;
[[is:Geðvefrænir sjúkdómar]]&lt;br /&gt;
[[nl:Somatoforme stoornis]]&lt;br /&gt;
[[pl:Zaburzenia somatoformiczne]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
{{WikiDoc Sources}}&lt;br /&gt;
{{WH}}&lt;/div&gt;</summary>
		<author><name>Varun Kumar</name></author>
	</entry>
	<entry>
		<id>https://www.wikidoc.org/index.php?title=Somatoform_disorder&amp;diff=648037</id>
		<title>Somatoform disorder</title>
		<link rel="alternate" type="text/html" href="https://www.wikidoc.org/index.php?title=Somatoform_disorder&amp;diff=648037"/>
		<updated>2012-06-07T14:29:42Z</updated>

		<summary type="html">&lt;p&gt;Varun Kumar: &lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;&#039;&#039;&#039;For patient information click [[Somatoform disorder (patient information)|here]]&#039;&#039;&#039;&lt;br /&gt;
&lt;br /&gt;
{{Infobox_Disease |&lt;br /&gt;
  Name           = {{PAGENAME}} |&lt;br /&gt;
  Image          = |&lt;br /&gt;
  Caption        = |&lt;br /&gt;
  DiseasesDB     = 1645 |&lt;br /&gt;
  ICD10          = {{ICD10|F|45||f|40}} |&lt;br /&gt;
  ICD9           = {{ICD9|300.8}} |&lt;br /&gt;
  ICDO           = |&lt;br /&gt;
  OMIM           = |&lt;br /&gt;
  MedlinePlus    = 000955|&lt;br /&gt;
  eMedicineSubj  = |&lt;br /&gt;
  eMedicineTopic = |&lt;br /&gt;
  MeshID         = D013001 |&lt;br /&gt;
}}&lt;br /&gt;
{{SI}}&lt;br /&gt;
{{CMG}}&lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;&#039;&#039;Synonyms and Keywords:&#039;&#039;&#039;&#039;&#039; Functional disorders or Psychophysiological disorder or Psychosomatic disorders or Somatization disorders or Briquet syndrome or CFS or Chronic fatigue syndromes or Conversion disorder.&lt;br /&gt;
&lt;br /&gt;
==Overview==&lt;br /&gt;
&#039;&#039;&#039;Somatoform disorders&#039;&#039;&#039; are physical ailments (such as [[Pain and nociception|pain]], [[nausea]], [[Clinical depression|depression]], [[dizziness]]) or concerns for which no adequate medical explanation has been found. Somatoform disorders are physical symptoms that seem as if they are part of a general medical condition. However, no general medical condition, other mental disorder, or substance is present. &lt;br /&gt;
The complaints are serious enough to cause significant emotional distress and impairment of social and/or occupational functioning.&lt;br /&gt;
&lt;br /&gt;
A diagnosis of a somatoform disorder implies that psychological factors are a large contributor to the symptoms&#039; onset, severity and duration. It is important to note that somatoform disorders are not the result of conscious [[malingering]] or [[factitious disorders]].&lt;br /&gt;
&lt;br /&gt;
==Recognized somatoform disorders==&lt;br /&gt;
The somatoform disorders recognized by the [[Diagnostic and Statistical Manual of Mental Disorders]] of the [[American Psychiatric Association]]  are:&lt;br /&gt;
*[[Conversion disorder]] &lt;br /&gt;
*[[Somatization disorder]] &lt;br /&gt;
*[[Hypochondriasis]] &lt;br /&gt;
*[[Body dysmorphic disorder]]&lt;br /&gt;
*[[Pain disorder]]&lt;br /&gt;
*[[Undifferentiated somatoform disorder]] - only one unexplained symptom is required for at least 6 months&lt;br /&gt;
*[[Somatoform disorder NOS]]&lt;br /&gt;
&lt;br /&gt;
==Proposed somatoform disorders==&lt;br /&gt;
Additional proposed somatoform disorders are:&lt;br /&gt;
* [[Abridged somatization disorder]]&amp;lt;ref name=&amp;quot;pmid2918297&amp;quot;&amp;gt;{{cite journal |author=Escobar JI, Rubio-Stipec M, Canino G, Karno M |title=Somatic symptom index (SSI): a new and abridged somatization construct. Prevalence and epidemiological correlates in two large community samples |journal=J. Nerv. Ment. Dis. |volume=177 |issue=3 |pages=140-6 |year=1989 |pmid=2918297 |doi=}}&amp;lt;/ref&amp;gt; - at least 4 unexplained somatic complaints in men and 6 in women &lt;br /&gt;
* [[Multisomatoform disorder]]&amp;lt;ref name=&amp;quot;pmid9107152&amp;quot;&amp;gt;{{cite journal |author=Kroenke K, Spitzer RL, deGruy FV, &#039;&#039;et al&#039;&#039; |title=Multisomatoform disorder. An alternative to undifferentiated somatoform disorder for the somatizing patient in primary care |journal=Arch. Gen. Psychiatry |volume=54 |issue=4 |pages=352-8 |year=1997 |pmid=9107152 |doi=}}&amp;lt;/ref&amp;gt; - at least 3 unexplained somatic complaints from the [[PRIME-MD]] scale for at least 2 years of active symptoms&lt;br /&gt;
&lt;br /&gt;
These disorders have been proposed because the recognized somatoform disorders are either too restrictive or too broad. In a study of 119 primary care patients, the following prevalences were found&amp;lt;ref name=&amp;quot;pmid15014690&amp;quot;&amp;gt;{{cite journal |author=Lynch DJ, McGrady A, Nagel R, Zsembik C |title=Somatization in Family Practice: Comparing 5 Methods of Classification |journal= |volume=1 |issue=3 |pages=85-89 |year=1999 |pmid=15014690 |doi=}}&amp;lt;/ref&amp;gt;:&lt;br /&gt;
* [[Somatization disorder]] - 1%&lt;br /&gt;
* [[Abridged somatization disorder]] - 6%&lt;br /&gt;
* [[Multisomatoform disorder]] - 24%&lt;br /&gt;
* [[Undifferentiated somatoform disorder]] - 79%&lt;br /&gt;
&lt;br /&gt;
==References==&lt;br /&gt;
{{reflist|2}}&lt;br /&gt;
&lt;br /&gt;
{{Mental and behavioural disorders}}&lt;br /&gt;
{{Mental-health-stub}}&lt;br /&gt;
&lt;br /&gt;
[[Category:Psychiatry]]&lt;br /&gt;
[[Category:Somatoform disorders]]&lt;br /&gt;
[[Category:Overview complete]]&lt;br /&gt;
 &lt;br /&gt;
[[he: הפרעה סומטופורמית]]&lt;br /&gt;
[[is:Geðvefrænir sjúkdómar]]&lt;br /&gt;
[[nl:Somatoforme stoornis]]&lt;br /&gt;
[[pl:Zaburzenia somatoformiczne]]&lt;br /&gt;
{{WikiDoc Sources}}&lt;/div&gt;</summary>
		<author><name>Varun Kumar</name></author>
	</entry>
	<entry>
		<id>https://www.wikidoc.org/index.php?title=Functional_disorders&amp;diff=648036</id>
		<title>Functional disorders</title>
		<link rel="alternate" type="text/html" href="https://www.wikidoc.org/index.php?title=Functional_disorders&amp;diff=648036"/>
		<updated>2012-06-07T14:28:26Z</updated>

		<summary type="html">&lt;p&gt;Varun Kumar: ←Redirected page to Somatoform disorder&lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;#redirect [[Somatoform disorder]]&lt;/div&gt;</summary>
		<author><name>Varun Kumar</name></author>
	</entry>
	<entry>
		<id>https://www.wikidoc.org/index.php?title=Esophageal_cyst&amp;diff=648035</id>
		<title>Esophageal cyst</title>
		<link rel="alternate" type="text/html" href="https://www.wikidoc.org/index.php?title=Esophageal_cyst&amp;diff=648035"/>
		<updated>2012-06-07T14:27:15Z</updated>

		<summary type="html">&lt;p&gt;Varun Kumar: Created page with &amp;quot;{{SI}} {{CMG}}  ==Overview== Esophageal cyst is defined as any fluid-filled closed cavity or sac that is lined by an epithelium and found in the esophageal region.  ==Related ...&amp;quot;&lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;{{SI}}&lt;br /&gt;
{{CMG}}&lt;br /&gt;
&lt;br /&gt;
==Overview==&lt;br /&gt;
Esophageal cyst is defined as any fluid-filled closed cavity or sac that is lined by an epithelium and found in the esophageal region.&lt;br /&gt;
&lt;br /&gt;
==Related Chapter==&lt;br /&gt;
*[[Cyst]]&lt;br /&gt;
&lt;br /&gt;
==References==&lt;br /&gt;
{{reflist|2}}&lt;br /&gt;
&lt;br /&gt;
[[Category: Disease]]&lt;br /&gt;
&lt;br /&gt;
{{WH}}&lt;br /&gt;
{{WS}}&lt;/div&gt;</summary>
		<author><name>Varun Kumar</name></author>
	</entry>
	<entry>
		<id>https://www.wikidoc.org/index.php?title=Dressler_syndrome&amp;diff=648034</id>
		<title>Dressler syndrome</title>
		<link rel="alternate" type="text/html" href="https://www.wikidoc.org/index.php?title=Dressler_syndrome&amp;diff=648034"/>
		<updated>2012-06-07T14:23:25Z</updated>

		<summary type="html">&lt;p&gt;Varun Kumar: #REDIRECT&lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;#REDIRECT [[Dressler&#039;s syndrome]]&lt;/div&gt;</summary>
		<author><name>Varun Kumar</name></author>
	</entry>
	<entry>
		<id>https://www.wikidoc.org/index.php?title=ST_elevation_myocardial_infarction_differential_diagnosis&amp;diff=648033</id>
		<title>ST elevation myocardial infarction differential diagnosis</title>
		<link rel="alternate" type="text/html" href="https://www.wikidoc.org/index.php?title=ST_elevation_myocardial_infarction_differential_diagnosis&amp;diff=648033"/>
		<updated>2012-06-07T14:21:58Z</updated>

		<summary type="html">&lt;p&gt;Varun Kumar: &lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;{{DiseaseDisorder infobox |&lt;br /&gt;
  DiseasesDB     = 16537 |&lt;br /&gt;
}}&lt;br /&gt;
{{ST elevation myocardial infarction}}&lt;br /&gt;
{{CMG}}; {{AOEIC}} {{CZ}}&lt;br /&gt;
&lt;br /&gt;
==Overview==&lt;br /&gt;
ST segment myocardial infarction can be broadly categorized, from a patient perspective, as chest pain. In addition, ST segment myocardial infarction diagnosis can be influence by both, the absence and presence of myonecrosis. A thorough differential diagnosis is necessary to eliminate extraneous causation within a patient diagnosis.&lt;br /&gt;
&lt;br /&gt;
==Complete Differential Diagnosis of Chest Pain==&lt;br /&gt;
====By Organ System====&lt;br /&gt;
{|style=&amp;quot;width:60%; height:100px&amp;quot; border=&amp;quot;1&amp;quot;&lt;br /&gt;
|style=&amp;quot;height:100px&amp;quot;; style=&amp;quot;width:25%&amp;quot; border=&amp;quot;1&amp;quot; bgcolor=&amp;quot;LightSteelBlue&amp;quot; | &#039;&#039;&#039;Cardiovascular&#039;&#039;&#039;&lt;br /&gt;
|style=&amp;quot;height:100px&amp;quot;; style=&amp;quot;width:75%&amp;quot; border=&amp;quot;1&amp;quot; bgcolor=&amp;quot;Beige&amp;quot; | • [[Aortic Dissection|Acute Aortic Dissection]] • [[Acute Coronary Syndrome]] • ([[unstable angina]]) • ([[non ST elevation MI]]) • ([[ST elevation MI]]) • [[Aortic Aneurysm]] • [[Aortic Stenosis]] • [[Arryhthmias]] • [[Bland-White-Garland Syndrome]] • [[Chronic Stable Angina]] • [[Cor pulmonale]] • [[Coronary Heart Disease]] • [[Dressler&#039;s syndrome | Dressler&#039;s syndrome (postpericardiotomy)]] • [[Cardiomyopathy|Hypertrophic Cardiomyopathy]] • [[Mitral valve prolapse]] • [[STEMI|Myocardial infarction]] • [[Myocarditis]] • [[tamponade|Pericardial tamponade]] • [[Pericarditis]] • [[Takotsubos cardiomyopathy]] • [[Stress cardiomyopathy]]&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Chemical / poisoning&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes &lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Dermatologic&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| [[Herpes zoster]]&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Drug Side Effect&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| Drugs to treat [[migraine headache]]&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Ear Nose Throat&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| • [[Retropharyngeal abscess]] &lt;br /&gt;
|- &lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Endocrine&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| • [[Acromegaly]]  &lt;br /&gt;
|- &lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Environmental&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes &lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Gastroenterologic&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| • [[Achalasia]] • [[Abdominal distension]] • [[Barret’s esophagus]] • [[Carcinoma]] • [[Cholecystitis]] • [[Cholelithiasis]] • [[Diverticulitis]] • [[Duodenitis]] • [[Esophageal rupture]] • [[Esophageal spasm]] • [[Esophagitis]] • [[Foreign body]] • [[Gastritis]] • [[Gastroesophageal reflux]] ([[GERD]]) • [[Hiatus Hernia]] • [[Impacted stone]] • [[Liver abscess]] • [[Mallory-Weiss Syndrome]] • [[Neoplasm]] • [[nutcracker&#039;s esophagus|Nutcracker&#039;s esophagus]] • [[Pancreatitis]] • [[Peptic ulcer disease]] • [[Perforated ulcer]] • [[Plummer-Vinson Syndrome]] • [[Pneumoperitoneum]] • [[Splenomegaly|Splenic enlargement]] • [[Splenic infarction]] • Subdiaphragmatic abcsess • [[Subphrenic abscess]] • [[Whipple&#039;s Disease]] &lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Genetic&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes &lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Hematologic&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes  &lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Iatrogenic&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes &lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Infectious Disease&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| • [[Bornholm disease]] • [[Hepatitis]] • [[HIV|HIV infection]] • [[Herpes Zoster]] &lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Musculoskeletal / Ortho&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| • [[Bechterew&#039;s Disease]] • [[Bone tumor]] • Chest wall injuries • Chest wall pain syndrome • [[Costochondritis]] • Chosto condral tendinitis • Chosto sternal tendinitis • [[Tietze&#039;s syndrome]] • CS/TS osteochondrosis • [[Fibromyalgia]] • [[Fractured rib]] • [[Intercostal muscle spasm]] • Interstitial fibrosis • [[Intercostal neuralgia]] • [[Muscle strain or spasm]] • Myofascial pain • [[Myostitis]] • [[Neuritis]] • [[Radiculitis]] • [[Periostitis]] • [[Precordial catch syndrome]] • [[bursitis|Shoulder bursitis]] • [[tendinitis|Shoulder tendinitis]] • [[tumor|Soft tissue sarcoma or tumor]] • Sternoclavicular arthritis • Strain of pectoralis muscle • [[Thoracic Outlet Syndrome]] • [[Trauma]] • Vertebrogenic thoracic pain&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Neurologic&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| • [[Tabes dorsalis]] &lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Nutritional / Metabolic&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes  &lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Oncologic&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| • [[Liver cancer]] • [[Mesothelioma]] • [[Metastatic tumor]] • [[Neurofibroma]] • [[Pheochromocytoma]] &lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Opthalmologic&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes &lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Overdose / Toxicity&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes  &lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Psychiatric&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| • [[Anxiety|Anxiety disorders]] • [[Affective disorders]] (e.g., [[depression]]) • [[Da costa&#039;s syndrome]] • Thought disorders (e.g., [[delusions|fixed delusions]]) • [[Hyperventilation syndrome]] • [[Hypochondria]] • [[Factitious disorders]] (e.g. [[Münchausen syndrome]] • [[Fabricated or induced illness]] • Hospital addiction syndrome) • [[Panic attack]] • [[Somatoform disorder]]s •  [[Somatization disorder]] &lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Pulmonary&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| • [[Asthma]] • [[Bronchial carcinoma]] • [[Bronchiectasis]] • [[Bronchogenic carcinoma]] • [[Carcinomatous]] • [[Pleural Effusion]] • [[Chronic Obstructive Pulmonary Disease]] ([[COPD]]) • [[Empyema]] • [[Hemothorax]] • [[Lung Abscess]] • [[Lung Cancer]] • [[Lymphoma]] • [[Mediastinitis]] • [[Pleuritis]] • [[Pleurodynia]] • [[Pneumomediastinum]] • [[Pneumonia]] • [[Pneumothorax]] • [[Pulmonary Embolism]] • [[Pulmonary Infarction]] • [[pneumothorax|Tension pneumothorax]] • [[Thymoma]] • Tracheoesophageal abscess • [[Tuberculosis]]   &lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Renal / Electrolyte&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes &lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Rheum / Immune / Allergy&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes  &lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Trauma&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes  &lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Miscellaneous&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| • Collagen vascular disease with pleuritis • [[Conn&#039;s Syndrome]] • Degenerative changes of cervical spine • [[Familial Mediterranean Fever]] • [[Peritonitis]] • [[Pott&#039;s Disease]] • Xyphodenia &lt;br /&gt;
|-&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
====By Alphabetical Order====&lt;br /&gt;
*[[Actinomycosis]]&lt;br /&gt;
*[[Acute intermittent porphyria]]&lt;br /&gt;
*[[Adenosine]]&lt;br /&gt;
*[[Amonafide]]&lt;br /&gt;
*[[Anemia]]&lt;br /&gt;
*[[Ankylosing spondylitis]]&lt;br /&gt;
*[[Aortic valve stenosis]]&lt;br /&gt;
*[[Arsenic trioxide]]&lt;br /&gt;
*[[Arsenicals]]&lt;br /&gt;
*[[Blood transfusion]] and complications&lt;br /&gt;
*[[Bornholm disease]]&lt;br /&gt;
*[[Bronchogenic cyst]]&lt;br /&gt;
*[[Carbon monoxide toxicity]]&lt;br /&gt;
*[[Cardiomyopathy]]&lt;br /&gt;
*[[HOCM|Familial hypertrophic cardiomyopathy]] &lt;br /&gt;
*[[CPR|Cardiopulmonary resuscitation]]&lt;br /&gt;
*[[Coronary artery dissection]]&lt;br /&gt;
*[[Diffuse esophageal spasm]]&lt;br /&gt;
*[[Dissecting aortic aneurysm]]&lt;br /&gt;
*[[Dressler syndrome]]&lt;br /&gt;
*[[Empyema|Pleural empyema]]&lt;br /&gt;
*[[Esophageal achalasia]]&lt;br /&gt;
*[[Esophageal cyst]]&lt;br /&gt;
*[[Fabry disease]]&lt;br /&gt;
*[[Functional disorders]]&lt;br /&gt;
*[[Gastric ulcer]]&lt;br /&gt;
*[[Gastroesophageal reflux]]&lt;br /&gt;
*[[Gemeprost]]&lt;br /&gt;
*[[Glatiramer acetate]]&lt;br /&gt;
*[[Glycogenosis type 7]]&lt;br /&gt;
*[[Ischaemic heart disease]]&lt;br /&gt;
*[[Kawasaki disease]]&lt;br /&gt;
*[[Left ventricular hypertrophy]]&lt;br /&gt;
*[[Lymphangiomyomatosis]]&lt;br /&gt;
*[[Mediastinitis]]&lt;br /&gt;
*[[Mesothelioma]]&lt;br /&gt;
*[[Mitral valve prolapse]]&lt;br /&gt;
*[[Myocardial infarction]]&lt;br /&gt;
*[[Myocarditis]]&lt;br /&gt;
*[[Naratriptan]]&lt;br /&gt;
*[[Nylidrin]]&lt;br /&gt;
*[[Esophageal foreign body]]&lt;br /&gt;
*[[Esophageal rupture]]&lt;br /&gt;
*[[Esophagitis]]&lt;br /&gt;
*[[Pericarditis]]&lt;br /&gt;
*[[Pleural effusion]]&lt;br /&gt;
*[[Pleural fibroma]]&lt;br /&gt;
*[[Pleuritis]]&lt;br /&gt;
*[[Pneumonia]]&lt;br /&gt;
*[[Pneumothorax]]&lt;br /&gt;
*[[Porfimer]]&lt;br /&gt;
*[[Prinzmetal angina]]&lt;br /&gt;
*[[Pulmonary embolism]]&lt;br /&gt;
*[[Pulmonary infarction]]&lt;br /&gt;
*[[Quaternary syphilis]]&lt;br /&gt;
*[[Recurrent hereditary polyserositis]]&lt;br /&gt;
*[[Regadenoson]]&lt;br /&gt;
*[[Respiratory alkalosis]]&lt;br /&gt;
*[[Rib fracture]]&lt;br /&gt;
*[[Rib pain]]&lt;br /&gt;
*[[Rizatriptan]]&lt;br /&gt;
*[[Rumination disorder]]&lt;br /&gt;
*[[SAPHO syndrome]]&lt;br /&gt;
*[[Shingles]]&lt;br /&gt;
*[[Sickle cell crisis]] (thrombotic)&lt;br /&gt;
*[[Sickle cell disease]]&lt;br /&gt;
*[[Spinal cord injury|Acute spinal cord injury]]&lt;br /&gt;
*[[Subdiaphragmatic abscess]]&lt;br /&gt;
*[[Sumatriptan]]&lt;br /&gt;
*[[Syndrome X]]&lt;br /&gt;
*[[Tabes dorsalis]]&lt;br /&gt;
*[[Takotsubo cardiomyopathy]]&lt;br /&gt;
*[[Tension pneumothorax]]&lt;br /&gt;
*[[Thallium]]&lt;br /&gt;
*[[Thyroiditis]]&lt;br /&gt;
*[[Tietze costochondritis]]&lt;br /&gt;
*[[Trichinella spiralis]]&lt;br /&gt;
*[[Unstable angina]]&lt;br /&gt;
*[[Varicella-zoster virus]]&lt;br /&gt;
*[[Wegener granulomatosis]]&lt;br /&gt;
*[[Zolmitriptan]]&lt;br /&gt;
&lt;br /&gt;
==Differential Diagnosis of Causes of ST Segment Elevation in the Absence of Myonecrosis==&lt;br /&gt;
Acute epicardial artery occlusion by [[thrombus]] is certainly one cause of ST segment elevation, but other causes of ST segment elevation which are not associated with myonecrosis include the following:&amp;lt;ref name=&amp;quot;pmid14645641&amp;quot;&amp;gt;{{cite journal |author=Wang K, Asinger RW, Marriott HJ |title=ST-segment elevation in conditions other than acute myocardial infarction |journal=N. Engl. J. Med. |volume=349 |issue=22 |pages=2128–35 |year=2003 |month=November |pmid=14645641 |doi=10.1056/NEJMra022580 |url=}}&amp;lt;/ref&amp;gt;&amp;lt;ref name=&amp;quot;pmid15014192&amp;quot;&amp;gt;{{cite journal |author=Ako J, Honda Y, Fitzgerald PJ |title=Conditions associated with ST-segment elevation |journal=N. Engl. J. Med. |volume=350 |issue=11 |pages=1152–5; author reply 1152–5 |year=2004 |month=March |pmid=15014192 |doi=10.1056/NEJM200403113501118 |url=}}&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
====Listed in Alphabetical Order====&lt;br /&gt;
&lt;br /&gt;
* [[Aneurysm]] of the ventricle can result in persistent ST segment elevation that can be exacerbated with tachycardia.&lt;br /&gt;
&lt;br /&gt;
* [[Arrhythmogenic right ventricular cardiomyopathy]]&lt;br /&gt;
&lt;br /&gt;
* Balloon inflation in a coronary artery during percutaneous coronary intervention&lt;br /&gt;
&lt;br /&gt;
* [[Brugada syndrome]]&lt;br /&gt;
&lt;br /&gt;
* [[Cardioversion|Transthoracic cardioversion]]&lt;br /&gt;
&lt;br /&gt;
* [[Coronary artery]] rupture during percutaneous coronary intervention&lt;br /&gt;
&lt;br /&gt;
* [[Early repolarization]] is a normal variant that can result in ST segment elevation. It is more common in males of younger age. The ST elevation is exacerbated by [[bradycardia]].&lt;br /&gt;
&lt;br /&gt;
* [[Hyperkalemia]] known as the &amp;quot;dialyzable current of njury&amp;quot; hyperkalemia may cause hyperacute ECG changes due to changes in membrane polarity&lt;br /&gt;
&lt;br /&gt;
* [[Left bundle branch block]] is associated with ST segment elevation in those leads that are discordant to the QRS. Stated differently, if the QRS is predominantly of a negative deflection, it is normal to observe ST segment elevation in the same leads. The presence of ST elevation in leads where the QRS deflection is upright (concordance) may be a marker of myocardial injury.&lt;br /&gt;
&lt;br /&gt;
* [[Myopericarditis]] can cause injury to the subepicardial myocytes and ST segment elevation.&lt;br /&gt;
&lt;br /&gt;
* [[Myocarditis]] can cause injury to the subepicardial myocytes and ST segment elevation.&lt;br /&gt;
&lt;br /&gt;
* [[Pericardiocentesis]] when the needle comes into contact with the myocardium, there can be ST segment elevation reflecting local injury of the myocardium.&lt;br /&gt;
&lt;br /&gt;
* [[Pericarditis]] can cause injury to the subepicardial myocytes and ST elevation.&lt;br /&gt;
&lt;br /&gt;
* [[Pulmonary Embolism]]&lt;br /&gt;
&lt;br /&gt;
* [[Prinzmetal&#039;s angina]] is associated with ST segment elevation due to transient epicardial coronary artery spasm either in the absence or presence of atherosclerosis. If the condition persists long enough, myonecrosis can be observed.&lt;br /&gt;
&lt;br /&gt;
* [[Stroke]] [[Intracranial hemorrhage]] can in some cases cause ST segment elevation due to direct [[myocyte]] injury from a hyperadrenergic stimulation emanating from the central nervous system.&lt;br /&gt;
&lt;br /&gt;
==Differential Diagnosis of Causes of ST Segment Elevation in the Presence of Myonecrosis (STEMI)==&lt;br /&gt;
&lt;br /&gt;
While plaque rupture is the most common cause of ST segment elevation MI, other conditions can cause ST elevation and myocardial necrosis. In order to expeditiously treat an alternate underlying cause of myonecrosis, it is important to rapidly identify conditions other than plaque rupture that may also cause ST elevation and myonecrosis. Indeed, the management of some of these conditions might be differ substantially from that of plaque rupture: [[cocaine]] induced STEMI would not be treated with [[beta-blocker]]s, and [[myocardial contusion]] would not be treated with an [[antithrombin]]. These conditions include the following:&lt;br /&gt;
&lt;br /&gt;
====By Organ System====&lt;br /&gt;
&lt;br /&gt;
{|style=&amp;quot;width:75%; height:100px&amp;quot; border=&amp;quot;1&amp;quot;&lt;br /&gt;
|style=&amp;quot;height:100px&amp;quot;; style=&amp;quot;width:25%&amp;quot; border=&amp;quot;1&amp;quot; bgcolor=&amp;quot;LightSteelBlue&amp;quot; | &#039;&#039;&#039;Cardiovascular&#039;&#039;&#039;&lt;br /&gt;
|style=&amp;quot;height:100px&amp;quot;; style=&amp;quot;width:75%&amp;quot; border=&amp;quot;1&amp;quot; bgcolor=&amp;quot;Beige&amp;quot; | [[Aortic dissection]] more often extends to occlude the ostium of the [[right coronary artery]]&lt;br /&gt;
&lt;br /&gt;
[[Aortic stenosis]] can cause subendocardial ischemia and infarction if demand grossly exceeds supply&lt;br /&gt;
&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Chemical / poisoning&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| [[Carbon monoxide poisoning]]&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Dermatologic&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Drug Side Effect&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| [[Oral contraceptive pills]], particularly among women who smoke&lt;br /&gt;
&lt;br /&gt;
[[Anabolic steroids]]&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Ear Nose Throat&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| A recent [[upper respiratory tract infection]]s has been associated with a 4.9 fold rise in the risk of [[trigger of MI|MI]]&lt;br /&gt;
|- &lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Endocrine&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| [[Thyrotoxicosis]]&lt;br /&gt;
|- &lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Environmental&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| Blizzards and snow shoveling, and inhalation of fine particulate matter in areas with air pollution and high traffic have been identified as [[triggers of MI]].&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Gastroenterologic&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| A heavy meal has been associated with a 4 fold rise in the risk of [[trigger of MI|MI]], and it is not clear if this is mediated by hyperadrenergic tone&amp;lt;ref name=&amp;quot;pmid15609883&amp;quot;&amp;gt;{{cite journal |author=Lipovetzky N, Hod H, Roth A, Kishon Y, Sclarovsky S, Green MS |title=Heavy meals as a trigger for a first event of the acute coronary syndrome: a case-crossover study |journal=Isr. Med. Assoc. J. |volume=6 |issue=12 |pages=728–31 |year=2004 |month=December |pmid=15609883 |doi= |url=}}&amp;lt;/ref&amp;gt;;&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Genetic&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| [[Familial hypercholesterolemia]]&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Hematologic&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| [[Disseminated intravascular coagulation]] ([[DIC]])&lt;br /&gt;
&lt;br /&gt;
[[Hypercoagulable states]]&lt;br /&gt;
&lt;br /&gt;
[[Polycythemia vera]]&lt;br /&gt;
&lt;br /&gt;
[[Thrombocytosis]]&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Iatrogenic&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| [[Epinephrine]] overdose&lt;br /&gt;
&lt;br /&gt;
Sudden withdrawal of [[Beta blockers]] or [[nitrates]]&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Infectious Disease&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| A recent [[upper respiratory tract infection]]s has been associated with a 4.9 fold rise in the risk of [[trigger of MI|MI]]&lt;br /&gt;
&lt;br /&gt;
[[Infectious endocarditis]] may STEMI as a result of embolization&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Musculoskeletal / Ortho&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Neurologic&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Nutritional / Metabolic&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| A heavy meal has been associated with a 4 fold rise in the risk of [[trigger of MI|MI]] and it is not clear if this is mediated by hyperadrenergic tone&amp;lt;ref name=&amp;quot;pmid15609883&amp;quot;&amp;gt;{{cite journal |author=Lipovetzky N, Hod H, Roth A, Kishon Y, Sclarovsky S, Green MS |title=Heavy meals as a trigger for a first event of the acute coronary syndrome: a case-crossover study |journal=Isr. Med. Assoc. J. |volume=6 |issue=12 |pages=728–31 |year=2004 |month=December |pmid=15609883 |doi= |url=}}&amp;lt;/ref&amp;gt;;&lt;br /&gt;
&lt;br /&gt;
[[Amyloidosis]]&lt;br /&gt;
&lt;br /&gt;
[[Fabry disease]]&lt;br /&gt;
&lt;br /&gt;
[[Homocystinuria]]&lt;br /&gt;
&lt;br /&gt;
[[Mucopolysaccharidoses]] or [[Hurler disease]]&lt;br /&gt;
&lt;br /&gt;
[[Pseudoxanthoma elasticum]]&lt;br /&gt;
&lt;br /&gt;
[[Thiamine deficiency]] has been associated with ST elevation and myonecrosis &amp;lt;ref name=&amp;quot;pmid16020883&amp;quot;&amp;gt;{{cite journal |author=Kawano H, Koide Y, Toda G, Yano K |title=ST-segment elevation of electrocardiogram in a patient with Shoshin beriberi |journal=Intern. Med. |volume=44 |issue=6 |pages=578–85 |year=2005 |month=June |pmid=16020883 |doi= |url=http://joi.jlc.jst.go.jp/JST.JSTAGE/internalmedicine/44.578?from=PubMed}}&amp;lt;/ref&amp;gt; &amp;lt;ref&amp;gt;Hundley JM, Ashburn LL, Sebrell WH. The electrocardiogram in chronic thiamine deficiency in rats. Am J Physiol 144: 404–414, 1954. &amp;lt;/ref&amp;gt;  &amp;lt;ref name=&amp;quot;pmid7197132&amp;quot;&amp;gt;{{cite journal |author=Read DH, Harrington DD |title=Experimentally induced thiamine deficiency in beagle dogs: clinical observations |journal=Am. J. Vet. Res. |volume=42 |issue=6 |pages=984–91 |year=1981 |month=June |pmid=7197132 |doi= |url=}}&amp;lt;/ref&amp;gt;&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Obstetric/Gynecologic&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| Spontaneous coronary [[dissection]] in the setting of [[pregnancy]]&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Oncologic&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| [[Radiation therapy]] can accelerate atherosclerosis particularly in the distribution of the left anterior descending artery; &lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Opthalmologic&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Overdose / Toxicity&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| [[Cocaine]] ingestion which may result in direct myocyte injury due to an adrendergic surge, vasoconstriction of the microvasculature or plaque rupture and thrombus formation; &lt;br /&gt;
&lt;br /&gt;
[[Marijuana]] ingestion has been identified as a [[trigger of MI]].&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Psychiatric&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| Anger, [[anxiety]], [[bereavement]], work-related stress, earthquakes, bombings and other psychosocial stressors have been identified as [[triggers of MI]], and it is not clear if the mechanism is plaque rupture or hyperadrenergic tone; &lt;br /&gt;
&lt;br /&gt;
[[Stress cardiomyopathy]] or [[Broken heart syndrome]] causes ST segment elevation most often in the anterior precordium and is thought to be due to direct [[myocyte]] injury from a hyperadrenergic stimulation emanating from the central nervous system.&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Pulmonary&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| A recent [[upper respiratory tract infection]]s has been associated with a 4.9 fold rise in the risk of [[trigger of MI|MI]]&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Renal / Electrolyte&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| [[Homocystinuria]]&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Rheum / Immune / Allergy&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| Takayasus&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Sexual&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| Sexual activity has been identified as a [[trigger of MI]]&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Trauma&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| Both penetrating and non-penetrating trauma to the heart or [[myocardial contusion]], [[commotio cordis]] can be associated with ST elevation and myonecrosis.&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Urologic&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Miscellaneous&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| [[Hypotension]] particularly if it is prolonged&lt;br /&gt;
|-&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
==References==&lt;br /&gt;
{{reflist|2}}&lt;br /&gt;
&lt;br /&gt;
[[Category:Cardiology]]&lt;br /&gt;
[[Category:Emergency medicine]]&lt;br /&gt;
[[Category:Intensive care medicine]]&lt;br /&gt;
&lt;br /&gt;
{{WikiDoc Help Menu}}&lt;br /&gt;
{{WikiDoc Sources}}&lt;/div&gt;</summary>
		<author><name>Varun Kumar</name></author>
	</entry>
	<entry>
		<id>https://www.wikidoc.org/index.php?title=Category:Grammar&amp;diff=644943</id>
		<title>Category:Grammar</title>
		<link rel="alternate" type="text/html" href="https://www.wikidoc.org/index.php?title=Category:Grammar&amp;diff=644943"/>
		<updated>2012-05-04T14:17:38Z</updated>

		<summary type="html">&lt;p&gt;Varun Kumar: Created page with &amp;quot;{{CMG}}&amp;quot;&lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;{{CMG}}&lt;/div&gt;</summary>
		<author><name>Varun Kumar</name></author>
	</entry>
	<entry>
		<id>https://www.wikidoc.org/index.php?title=User:Lakshmi_Gopalakrishnan&amp;diff=644564</id>
		<title>User:Lakshmi Gopalakrishnan</title>
		<link rel="alternate" type="text/html" href="https://www.wikidoc.org/index.php?title=User:Lakshmi_Gopalakrishnan&amp;diff=644564"/>
		<updated>2012-04-27T00:16:50Z</updated>

		<summary type="html">&lt;p&gt;Varun Kumar: &lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;__NOTOC__&lt;br /&gt;
==Lakshmi Gopalakrishnan==&lt;br /&gt;
&lt;br /&gt;
Contact: [mailto:lgopalakrishnan@perfuse.org, lgopalakrishnan@perfuse.org]&lt;br /&gt;
&lt;br /&gt;
==Current Position==&lt;br /&gt;
*Research fellow at PERFUSE Study Group, Beth Israel Deaconess Medical Center, Harvard Medical School.&lt;br /&gt;
*Deputy Editor-In-Chief for WikiDoc.org&lt;br /&gt;
*Asociate Editor-In-Chief for several WikiDoc pages.&lt;br /&gt;
&lt;br /&gt;
==Education==&lt;br /&gt;
M.B.B.S degree from M.S.Ramaiah Medical College, The Rajiv Gandhi University of Health Sciences, Bangalore, India.&lt;/div&gt;</summary>
		<author><name>Varun Kumar</name></author>
	</entry>
	<entry>
		<id>https://www.wikidoc.org/index.php?title=User:Varun_Kumar&amp;diff=644563</id>
		<title>User:Varun Kumar</title>
		<link rel="alternate" type="text/html" href="https://www.wikidoc.org/index.php?title=User:Varun_Kumar&amp;diff=644563"/>
		<updated>2012-04-27T00:15:15Z</updated>

		<summary type="html">&lt;p&gt;Varun Kumar: &lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;__NOTOC__&lt;br /&gt;
==Varun Kumar==&lt;br /&gt;
[[Image:Varun Kumar.jpg|right]]&lt;br /&gt;
&lt;br /&gt;
Contact : [mailto:vkumar@perfuse.org, vkumar@perfuse.org]&lt;br /&gt;
&lt;br /&gt;
==Current Position==&lt;br /&gt;
*Research fellow at PERFUSE Study Group, Beth Israel Deaconess Medical Center, Harvard Medical School.&lt;br /&gt;
*Deputy Editor-In-Chief for WikiDoc.org&lt;br /&gt;
*Associate Editor-In-Chief for several WikiDoc pages.&lt;br /&gt;
&lt;br /&gt;
==Education==&lt;br /&gt;
M.B.B.S degree from M.S.Ramaiah Medical College, The Rajiv Gandhi University of Health Sciences, Bangalore, India.&lt;/div&gt;</summary>
		<author><name>Varun Kumar</name></author>
	</entry>
	<entry>
		<id>https://www.wikidoc.org/index.php?title=User:Lakshmi_Gopalakrishnan&amp;diff=643661</id>
		<title>User:Lakshmi Gopalakrishnan</title>
		<link rel="alternate" type="text/html" href="https://www.wikidoc.org/index.php?title=User:Lakshmi_Gopalakrishnan&amp;diff=643661"/>
		<updated>2012-04-23T04:14:58Z</updated>

		<summary type="html">&lt;p&gt;Varun Kumar: &lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;__NOTOC__&lt;br /&gt;
==Lakshmi Gopalakrishnan==&lt;br /&gt;
&lt;br /&gt;
Contact: lgopalakrishnan@perfuse.org [mailto:lgopalakrishnan@perfuse.org]&lt;br /&gt;
&lt;br /&gt;
==Current Position==&lt;br /&gt;
*&#039;&#039;&#039;Research fellow&#039;&#039;&#039; at PERFUSE Study Group, Beth Israel Deaconess Medical Center, Harvard Medical School.&lt;br /&gt;
*&#039;&#039;&#039;Deputy Editor-In-Chief&#039;&#039;&#039; for WikiDoc.org&lt;br /&gt;
*&#039;&#039;&#039;Associate Editor-In-Chief&#039;&#039;&#039; for several WikiDoc pages.&lt;br /&gt;
&lt;br /&gt;
==Education==&lt;br /&gt;
&#039;&#039;&#039;M.B.B.S&#039;&#039;&#039; degree from  M.S.Ramaiah Medical College, The Rajiv Gandhi University of Health Sciences, Bangalore, India.&lt;br /&gt;
&lt;br /&gt;
==Previous Research work==&lt;br /&gt;
&lt;br /&gt;
Research coordinator for Phase III Randomized Multi Center Study for Terminal Breast Cancer at Kidwai Memorial Institute of Oncology, Bangalore, India, Supervisor : Dr.Vijayalakshmi Deshmane.&lt;br /&gt;
&lt;br /&gt;
Presented a paper on the Cross-section study of Health status of 4704 school children from 36 schools coming under the mid-day meal program, at  2nd  National Conference on Student’s medical research, Trivandrum Medical College, India, Supervisor : Dr Dinesh Rajaram &amp;amp; Dr. Shalini.&lt;/div&gt;</summary>
		<author><name>Varun Kumar</name></author>
	</entry>
	<entry>
		<id>https://www.wikidoc.org/index.php?title=User:Varun_Kumar&amp;diff=643660</id>
		<title>User:Varun Kumar</title>
		<link rel="alternate" type="text/html" href="https://www.wikidoc.org/index.php?title=User:Varun_Kumar&amp;diff=643660"/>
		<updated>2012-04-23T04:14:15Z</updated>

		<summary type="html">&lt;p&gt;Varun Kumar: &lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;__NOTOC__&lt;br /&gt;
==Varun Kumar==&lt;br /&gt;
[[Image:Varun Kumar.jpg|right]]&lt;br /&gt;
&lt;br /&gt;
Contact : vkumar@perfuse.org[mailto:vkumar@perfuse.org]&lt;br /&gt;
&lt;br /&gt;
==Current Position==&lt;br /&gt;
*&#039;&#039;&#039;Research fellow&#039;&#039;&#039; at PERFUSE Study Group, Beth Israel Deaconess Medical Center, Harvard Medical School.&lt;br /&gt;
*&#039;&#039;&#039;Deputy Editor-In-Chief&#039;&#039;&#039; for WikiDoc.org&lt;br /&gt;
*&#039;&#039;&#039;Associate Editor-In-Chief&#039;&#039;&#039; for several WikiDoc pages.&lt;br /&gt;
&lt;br /&gt;
==Education==&lt;br /&gt;
&#039;&#039;&#039;M.B.B.S&#039;&#039;&#039; degree from  M.S.Ramaiah Medical College, The Rajiv Gandhi University of Health Sciences, Bangalore, India.&lt;br /&gt;
&lt;br /&gt;
==Previous Research work==&lt;br /&gt;
Research coordinator for Phase III Randomized Multi Center Study for Terminal Breast Cancer at Kidwai Memorial Institute of Oncology, Bangalore, India, Supervisor : Dr.Vijayalakshmi Deshmane.&lt;br /&gt;
&lt;br /&gt;
Presented a paper as a first author, on the Cross-section study of Health status of 4704 school children from 36 schools coming under the mid-day meal program, at  2nd  National Conference on Student’s medical research, Trivandrum Medical College, India, Supervisor : Dr Dinesh Rajaram &amp;amp; Dr. Shalini.&lt;br /&gt;
&lt;br /&gt;
Presented Science models at state level and national level science exhibition at Jawaharlal Nehru Planetarium and Indian Space Research Organization (ISRO) respectively.&lt;/div&gt;</summary>
		<author><name>Varun Kumar</name></author>
	</entry>
	<entry>
		<id>https://www.wikidoc.org/index.php?title=Left_atrial_enlargement_electrocardiogram&amp;diff=642809</id>
		<title>Left atrial enlargement electrocardiogram</title>
		<link rel="alternate" type="text/html" href="https://www.wikidoc.org/index.php?title=Left_atrial_enlargement_electrocardiogram&amp;diff=642809"/>
		<updated>2012-04-17T18:03:54Z</updated>

		<summary type="html">&lt;p&gt;Varun Kumar: /* See Also */&lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;{{Infobox_Disease |&lt;br /&gt;
  Name           = {{PAGENAME}} |&lt;br /&gt;
  Image          =  LAE.png|&lt;br /&gt;
  Caption        =  |&lt;br /&gt;
  Width          = 200px |&lt;br /&gt;
  DiseasesDB     =  |&lt;br /&gt;
  ICD10          =  |&lt;br /&gt;
  ICD9           =  |&lt;br /&gt;
  ICDO           =  |&lt;br /&gt;
  OMIM           =  |&lt;br /&gt;
  MedlinePlus    =  |&lt;br /&gt;
  eMedicineSubj  = med |&lt;br /&gt;
  eMedicineTopic = |&lt;br /&gt;
  MeshName       = Left+Atrial+Enlargement |&lt;br /&gt;
  MeshNumber     = |&lt;br /&gt;
}}&lt;br /&gt;
{{SI}}&lt;br /&gt;
&lt;br /&gt;
{{CMG}}; &#039;&#039;&#039;Associate Editor-In-Chief:&#039;&#039;&#039; {{CZ}}&lt;br /&gt;
&lt;br /&gt;
==Overview==&lt;br /&gt;
Left atrial enlargement may be observed among patients with pressure or volume overload of the [[left atrium]].&lt;br /&gt;
&lt;br /&gt;
== Differential Diagnosis of Left Atrial Enlargement==&lt;br /&gt;
* Atrial aneurysm&lt;br /&gt;
* [[Infective endocarditis]]&lt;br /&gt;
* [[Left heart failure]]&lt;br /&gt;
* [[Mitral regurgitation]]&lt;br /&gt;
* [[Mitral stenosis]]&lt;br /&gt;
* [[Mitral valve prolapse]]&lt;br /&gt;
* [[Myxedema]]&lt;br /&gt;
* [[Patent Ductus Arteriosus]]&lt;br /&gt;
* [[Ventricular septal defect]]&lt;br /&gt;
&lt;br /&gt;
==EKG in Left Atrial Enlargement==&lt;br /&gt;
&#039;&#039;&#039;1.&#039;&#039;&#039; [[LA enlargement]]: [[Left atrial enlargement]] produces a broad, bifid [[P wave]] in lead II (&#039;&#039;&#039;P mitrale&#039;&#039;&#039;) and enlarges the terminal negative portion of the P wave in VI.&lt;br /&gt;
&lt;br /&gt;
In &#039;&#039;&#039;lead I and/or II&#039;&#039;&#039; following may be seen:&lt;br /&gt;
*Bifid [[P wave]] with &amp;gt; 40 ms between the two peaks&lt;br /&gt;
*Total [[P wave]] duration &amp;gt; 110 ms &lt;br /&gt;
[[Image:P mitrale.gif|200px]]&lt;br /&gt;
&lt;br /&gt;
In &#039;&#039;&#039;lead V1&#039;&#039;&#039;, the following may be seen:&lt;br /&gt;
*Biphasic [[P wave]] with terminal negative portion &amp;gt; 40 ms duration (&amp;gt;0.04 sec or 1 small square)&lt;br /&gt;
*Biphasic [[P wave]] with terminal negative portion &amp;gt; 1mm deep &lt;br /&gt;
&lt;br /&gt;
[[Image:LAE-v1.png|Left atrial enlargement as seen in lead V1|400px]]&lt;br /&gt;
&lt;br /&gt;
==Examples of Left Atrial Enlargement on EKG==&lt;br /&gt;
&amp;lt;div align=&amp;quot;left&amp;quot;&amp;gt;&lt;br /&gt;
&amp;lt;gallery heights=&amp;quot;175&amp;quot; widths=&amp;quot;150&amp;quot;&amp;gt;&lt;br /&gt;
Image:left_atrial_enlargement.jpg|Left atrial enlargement&lt;br /&gt;
Image:LAE.png|12 lead EKG: Left atrial enlargement&lt;br /&gt;
&amp;lt;/gallery&amp;gt;&lt;br /&gt;
&amp;lt;/div&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&amp;lt;div align=&amp;quot;left&amp;quot;&amp;gt;&lt;br /&gt;
&amp;lt;gallery heights=&amp;quot;175&amp;quot; widths=&amp;quot;150&amp;quot;&amp;gt;&lt;br /&gt;
Image:LAE-v1.png|Left atrial enlargement as seen in lead V1.&lt;br /&gt;
Image:LAE_12lead.jpg|Left atrial enlargement, a 12 lead ECG&lt;br /&gt;
&amp;lt;/gallery&amp;gt;&lt;br /&gt;
&amp;lt;/div&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==See Also==&lt;br /&gt;
*[[Left atrial enlargement chest x-ray]]&lt;br /&gt;
*[[Left atrial enlargement causes]]&lt;br /&gt;
{{Circulatory system pathology}}&lt;br /&gt;
{{Electrocardiography}}&lt;br /&gt;
&lt;br /&gt;
[[Category:Electrophysiology]]&lt;br /&gt;
[[Category:Cardiology]]&lt;br /&gt;
&lt;br /&gt;
{{WikiDoc Help Menu}}&lt;br /&gt;
{{WikiDoc Sources}}&lt;/div&gt;</summary>
		<author><name>Varun Kumar</name></author>
	</entry>
	<entry>
		<id>https://www.wikidoc.org/index.php?title=Aortic_regurgitation_causes&amp;diff=642802</id>
		<title>Aortic regurgitation causes</title>
		<link rel="alternate" type="text/html" href="https://www.wikidoc.org/index.php?title=Aortic_regurgitation_causes&amp;diff=642802"/>
		<updated>2012-04-17T17:57:54Z</updated>

		<summary type="html">&lt;p&gt;Varun Kumar: /* By Organ System */&lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;{{Aortic insufficiency}}&lt;br /&gt;
&lt;br /&gt;
{{CMG}}; &#039;&#039;&#039;Associate Editor-In-Chief:&#039;&#039;&#039; {{CZ}}; [[Varun Kumar]], M.B.B.S.; [[Lakshmi Gopalakrishnan]], M.B.B.S.&lt;br /&gt;
&lt;br /&gt;
==Overview==&lt;br /&gt;
Aortic insufficiency can be an acute illness or a chronic illness and the causes differ depending upon the acuity of the disease.  In general, aortic insufficiency is due to abnormalities of the aortic valve itself or the aortic root.  Aortic regurgitation secondary to dilation of the ascending aorta has overtaken valvular aortic disease as the most common cause of aortic regurgitation.&lt;br /&gt;
&lt;br /&gt;
==Common Causes==&lt;br /&gt;
*Worldwide the most common cause of aortic insufficiency is [[rheumatic heart disease]].&lt;br /&gt;
*In the United States, senile degenerative calcific aortic valve disease and bicuspid aortic valve disease are the most common causes.&lt;br /&gt;
*Aortic regurgitation secondary to dilation of the ascending aorta has overtaken valvular aortic disease as the most common cause of aortic regurgitation.&lt;br /&gt;
&lt;br /&gt;
==Differential Diagnosis of the Causes of Aortic Insufficiency==&lt;br /&gt;
===By Organ System===&lt;br /&gt;
&lt;br /&gt;
{|height:100px&amp;quot; border=&amp;quot;1&amp;quot;&lt;br /&gt;
|style=&amp;quot;height:100px&amp;quot;; style=&amp;quot;width:25%&amp;quot; border=&amp;quot;1&amp;quot; bgcolor=&amp;quot;LightSteelBlue&amp;quot; | &#039;&#039;&#039;Cardiovascular&#039;&#039;&#039;&lt;br /&gt;
|style=&amp;quot;height:100px&amp;quot;; style=&amp;quot;width:75%&amp;quot; border=&amp;quot;1&amp;quot; bgcolor=&amp;quot;Beige&amp;quot; | After [[aortic valvuloplasty]]&amp;lt;ref name=&amp;quot;pmid2016464&amp;quot;&amp;gt;{{cite journal |author=Isner JM |title=Acute catastrophic complications of balloon aortic valvuloplasty. The Mansfield Scientific Aortic Valvuloplasty Registry Investigators |journal=[[Journal of the American College of Cardiology]] |volume=17 |issue=6 |pages=1436–44 |year=1991 |month=May |pmid=2016464 |doi= |url= |accessdate=2011-03-28}}&amp;lt;/ref&amp;gt;, [[Aortic dissection]], [[Arteriosclerosis]], [[Bacterial Endocarditis]], [[Bicuspid aortic valve]], [[Prosthetic valve]] dysfunction&amp;lt;ref&amp;gt;Friedman T, Mani A, Elefteriades JA. Bicuspid aortic valve: clinical approach and scientific review of a common clinical entity. Expert Rev Cardiovasc Ther. Feb 2008;6(2):235-48.&amp;lt;/ref&amp;gt;, [[Hypertension]], [[Myxomatous]] aortic valve, [[Rheumatic Fever]], Senile aortic ectasia and dilation, Senile or degenerative calcific aortic valve disease, [[Sinus of Valsalva Aneurysm]], [[Ventricular Septal Defect]]&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Chemical / poisoning&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Dermatologic&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| [[Psoriatic arthritis]]&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Drug Side Effect&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| [[Fenfluramine]] and [[Dexfenfluramine]]: These drugs have been associated with degeneration of the aortic valve.&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Ear Nose Throat&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes&lt;br /&gt;
|- &lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Endocrine&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes&lt;br /&gt;
|- &lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Environmental&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Gastroenterologic&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| [[Ulcerative colitis]], [[Whipple disease]]&amp;lt;ref&amp;gt;Jeserich M, Ihling C, Holubarsch C. Aortic valve endocarditis with Whipple disease. Ann Intern Med. Jun 1 1997;126(11):920.&amp;lt;/ref&amp;gt;&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Genetic&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| [[Ankylosing Spondylitis]]&amp;lt;ref&amp;gt;Palazzi C, D&#039; Angelo S, Lubrano E, Olivieri I. Aortic involvement in ankylosing spondylitis. Clin Exp Rheumatol. May-Jun 2008;26(3 Suppl 49):S131-4.&amp;lt;/ref&amp;gt;, [[Ehlers-Danlos Syndrome]], [[Marfan Syndrome]], [[Osteogenesis imperfecta]], [[Pseudoxanthoma Elasticum]], [[Reiter&#039;s Syndrome]], [[Rheumatoid Arthritis]]&amp;lt;ref&amp;gt;Chand EM, Freant LJ, Rubin JW. Aortic valve rheumatoid nodules producing clinical aortic regurgitation and a review of the literature. Cardiovasc Pathol. Nov-Dec 1999;8(6):333-8.&amp;lt;/ref&amp;gt;, [[Systemic Lupus Erythematosus]], [[Takayasu arteritis]], [[Turner&#039;s Syndrome]]&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Hematologic&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Iatrogenic&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| After [[aortic valvuloplasty]]&amp;lt;ref name=&amp;quot;pmid2016464&amp;quot;&amp;gt;{{cite journal |author=Isner JM |title=Acute catastrophic complications of balloon aortic valvuloplasty. The Mansfield Scientific Aortic Valvuloplasty Registry Investigators |journal=[[Journal of the American College of Cardiology]] |volume=17 |issue=6 |pages=1436–44 |year=1991 |month=May |pmid=2016464 |doi= |url= |accessdate=2011-03-28}}&amp;lt;/ref&amp;gt;, [[Prosthetic valve]] dysfunction&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Infectious Disease&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| [[Bacterial Endocarditis]], [[Rheumatic Fever]], [[Syphilis]]&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Musculoskeletal / Ortho&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| [[Ankylosing Spondylitis]], [[Collagen vascular disease]], [[Ehlers-Danlos Syndrome]], [[Osteogenesis imperfecta]], [[Psoriatic arthritis]], [[Reiter&#039;s Syndrome]], [[Relapsing polychondritis]], [[Rheumatoid Arthritis]]&amp;lt;ref&amp;gt;Chand EM, Freant LJ, Rubin JW. Aortic valve rheumatoid nodules producing clinical aortic regurgitation and a review of the literature. Cardiovasc Pathol. Nov-Dec 1999;8(6):333-8.&amp;lt;/ref&amp;gt;, [[Spondyloarthropathy]], [[Systemic Lupus Erythematosus]]&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Neurologic&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Nutritional / Metabolic&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Obstetric/Gynecologic&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Oncologic&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Opthalmologic&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Overdose / Toxicity&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Psychiatric&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Pulmonary&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Renal / Electrolyte&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Rheum / Immune / Allergy&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| [[Ankylosing Spondylitis]]&amp;lt;ref&amp;gt;Palazzi C, D&#039; Angelo S, Lubrano E, Olivieri I. Aortic involvement in ankylosing spondylitis. Clin Exp Rheumatol. May-Jun 2008;26(3 Suppl 49):S131-4.&amp;lt;/ref&amp;gt;, [[Bechterew&#039;s Disease]], [[Behcet disease]], [[Collagen vascular disease]], [[Cystic medial necrosis]], [[Ehlers-Danlos Syndrome]], [[Giant cell arteritis]], [[Marfan Syndrome]], [[Myxomatous]] aortic valve: The valvular structure can degenerate, [[Osteogenesis imperfecta]], [[Polymyalgia Rheumatica]], [[Pseudoxanthoma Elasticum]], [[Psoriatic arthritis]], [[Reiter&#039;s Syndrome]], [[Rheumatic Fever]], [[Rheumatoid Arthritis]]&amp;lt;ref&amp;gt;Chand EM, Freant LJ, Rubin JW. Aortic valve rheumatoid nodules producing clinical aortic regurgitation and a review of the literature. Cardiovasc Pathol. Nov-Dec 1999;8(6):333-8.&amp;lt;/ref&amp;gt;, [[Spondyloarthropathy]], [[Systemic Lupus Erythematosus]], [[Takayasu arteritis]], [[Ulcerative colitis]], [[Whipple disease]]&amp;lt;ref&amp;gt;Jeserich M, Ihling C, Holubarsch C. Aortic valve endocarditis with Whipple disease. Ann Intern Med. Jun 1 1997;126(11):920.&amp;lt;/ref&amp;gt;&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Sexual&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| [[Syphilis]]&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Trauma&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| Blunt [[chest trauma]] disrupting the supporting apparatus of the aortic valve.&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Urologic&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Miscellaneous&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| [[Myxomatous]] aortic valve&lt;br /&gt;
|-&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
==Differential Diagnosis of the Causes of Acute Aortic Insufficiency==&lt;br /&gt;
In alphabetical order:&lt;br /&gt;
* After [[aortic valvuloplasty]]&amp;lt;ref name=&amp;quot;pmid2016464&amp;quot;&amp;gt;{{cite journal |author=Isner JM |title=Acute catastrophic complications of balloon aortic valvuloplasty. The Mansfield Scientific Aortic Valvuloplasty Registry Investigators |journal=[[Journal of the American College of Cardiology]] |volume=17 |issue=6 |pages=1436–44 |year=1991 |month=May |pmid=2016464 |doi= |url= |accessdate=2011-03-28}}&amp;lt;/ref&amp;gt;&lt;br /&gt;
* [[Aortic dissection]]: A type A dissection may disrupt the integrity of the valve leaflets causing malcoaptation of the aortic leaflets.&lt;br /&gt;
* [[Bacterial Endocarditis]]: The infection can erode the valve, can cause a leaflet to become flail, or a vegetation can prevent coaptation of the leaflets.&lt;br /&gt;
* Blunt [[chest trauma]]: Trauma can disrupt the supporting apparatus of the aortic valve.&lt;br /&gt;
* [[Myxomatous]] aortic valve: The valvular structure can degenerate&lt;br /&gt;
* [[Prosthetic valve]] dysfunction&lt;br /&gt;
* [[Rheumatic Fever]]&lt;br /&gt;
&lt;br /&gt;
==Differential Diagnosis of the Causes of Chronic Aortic Insufficiency==&lt;br /&gt;
In alphabetical order:&lt;br /&gt;
* [[Ankylosing Spondylitis]]: Ankylosing spondylitis can be associated with inflammation of the aorta ([[aortitis]]).&amp;lt;ref&amp;gt;Palazzi C, D&#039; Angelo S, Lubrano E, Olivieri I. Aortic involvement in ankylosing spondylitis. Clin Exp Rheumatol. May-Jun 2008;26(3 Suppl 49):S131-4.&amp;lt;/ref&amp;gt;  The inflammatory process can also involve the septum and cause [[conduction disease]].&lt;br /&gt;
* [[Aortic Dissection]]: A type A dissection may disrupt the integrity of the valve leaflets causing malcoaptation of the aortic leaflets.&lt;br /&gt;
* [[Arteriosclerosis]]&lt;br /&gt;
* [[Bechterew&#039;s Disease]]:  Ankylosing spondylitis can be associated with inflammation of the aorta ([[aortitis]]).&amp;lt;ref&amp;gt;Palazzi C, D&#039; Angelo S, Lubrano E, Olivieri I. Aortic involvement in ankylosing spondylitis. Clin Exp Rheumatol. May-Jun 2008;26(3 Suppl 49):S131-4.&amp;lt;/ref&amp;gt;  The inflammatory process can also involve the septum and cause [[conduction disease]].&lt;br /&gt;
* [[Behcet disease]]: Rarely, in 5% of Behcet&#039;s cases there is an [[aortitis]] that involves the ascending aorta and in some cases the [[coronary arteries]].&lt;br /&gt;
* [[Bicuspid aortic valve]]: This is the most common congenital abnormality of the ehart.  It is the most common cause of isolated aortic insufficiency requiring surgical repair.  Bicuspid aortic valve is also associated with inflammation of the aorta (an aortopathy) which may lead to dilation of the aorta and or aortic dissection that can worsen the aortic insufficiency.&amp;lt;ref&amp;gt;Friedman T, Mani A, Elefteriades JA. Bicuspid aortic valve: clinical approach and scientific review of a common clinical entity. Expert Rev Cardiovasc Ther. Feb 2008;6(2):235-48.&amp;lt;/ref&amp;gt;&lt;br /&gt;
* [[Cystic medial necrosis]] of the aorta&lt;br /&gt;
* [[Ehlers-Danlos Syndrome]]&lt;br /&gt;
* [[Giant cell arteritis]]: [[GCA]] may also be associated with an [[aortitis]] as well as [[coronary artery disease]].&amp;lt;ref&amp;gt;Eberhardt RT, Dhadly M. Giant cell arteritis: diagnosis, management, and cardiovascular implications. Cardiol Rev. Mar-Apr 2007;15(2):55-61.&amp;lt;/ref&amp;gt;&lt;br /&gt;
* [[Hypertension]]&lt;br /&gt;
* [[Marfan Syndrome]]&lt;br /&gt;
* [[Myxomatous]] aortic valve&lt;br /&gt;
* [[Polymyalgia Rheumatica]]&lt;br /&gt;
* [[Pseudoxanthoma Elasticum]]&lt;br /&gt;
* [[Reiter&#039;s Syndrome]]&lt;br /&gt;
* [[Rheumatic Fever]]: Rheumatic fever remains a cause of AS in the Middle East, Northern Africa and Asia as well as some immigrant populations in the United States.  It less prevalent in the US than it was in the 20th century. AR occurs as a result of fibrosis of the valve that is associated with thickening and retraction of the leaflets of the aortic valve.  This retraction results in regurgitation in the center of the valve.  At the same time, there may also be fusion of the aortic leaflets which results in concurrent aortic stenosis.  It should be noted that rheumatic disease of the mitral valve is usually present in the same patient.&lt;br /&gt;
* [[Rheumatoid Arthritis]]: [[RA]] rarely causes symptomatic AR, but can as a result of [[granulomatous]] nodules that may form on the aortic leaflets.&amp;lt;ref&amp;gt;Chand EM, Freant LJ, Rubin JW. Aortic valve rheumatoid nodules producing clinical aortic regurgitation and a review of the literature. Cardiovasc Pathol. Nov-Dec 1999;8(6):333-8.&amp;lt;/ref&amp;gt;&lt;br /&gt;
* [[Sinus of Valsalva Aneurysm]]&lt;br /&gt;
* [[Syphilis]]&lt;br /&gt;
* [[Systemic Lupus Erythematosus]]: There are tow mechanisms by which [[SLE]] can cause AR. SLE can cause inflammation and fibrosis of the aortic leaflets leading to their damage and retraction.&amp;lt;ref&amp;gt;Jain D, Halushka MK. Cardiac pathology of systemic lupus erythematosus. J Clin Pathol. Jul 2009;62(7):584-92.&amp;lt;/ref&amp;gt; SLE can also be associated with the development of sterile verrucous vegetations on the valves called [[Libman-Sacks endocarditis]].&amp;lt;ref&amp;gt;Moyssakis I, Tektonidou MG, Vasilliou VA, Samarkos M, Votteas V, Moutsopoulos HM. Libman-Sacks endocarditis in systemic lupus erythematosus: prevalence, associations, and evolution. Am J Med. Jul 2007;120(7):636-42.&amp;lt;/ref&amp;gt;&amp;lt;ref&amp;gt;Lee JL, Naguwa SM, Cheema GS, Gershwin ME. Revisiting Libman-Sacks endocarditis: a historical review and update. Clin Rev Allergy Immunol. Jun 2009;36(2-3):126-30.&amp;lt;/ref&amp;gt;&lt;br /&gt;
* [[Takayasu arteritis]]: [[Takayasu arteritis]] can involve the aorta in an [[aortitis]], the aortic valve itself, and the [[coronary arteries]].&amp;lt;ref&amp;gt;Adachi O, Saiki Y, Akasaka J, Oda K, Iguchi A, Tabayashi K. Surgical management of aortic regurgitation associated with takayasu arteritis and other forms of aortitis. Ann Thorac Surg. Dec 2007;84(6):1950-3.&amp;lt;/ref&amp;gt;&lt;br /&gt;
* [[Turner&#039;s Syndrome]]&lt;br /&gt;
* [[Ventricular Septal Defect]]&lt;br /&gt;
* [[Weight loss]] medications including [[fenfluramine]] and [[dexfenfluramine]] (a.k.a. [[Phen-Fen]]). These drugs have been associated with degeneration of the aortic valve.&lt;br /&gt;
* [[Whipple disease]]: Can involve the aortic valve.&amp;lt;ref&amp;gt;Jeserich M, Ihling C, Holubarsch C. Aortic valve endocarditis with Whipple disease. Ann Intern Med. Jun 1 1997;126(11):920.&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Differential Diagnosis Based Upon Aortic Valvular Causes==&lt;br /&gt;
*[[Bicuspid aortic valve]]&lt;br /&gt;
*[[Collagen vascular disease]]&lt;br /&gt;
*Senile or degenerative calcific aortic valve disease&lt;br /&gt;
*[[Endocarditis]]&lt;br /&gt;
* [[Myxomatous]] aortic valve&lt;br /&gt;
*[[Rheumatic fever]]&lt;br /&gt;
*[[Rheumatoid arthritis]]&lt;br /&gt;
*[[Sinus of Valsalva Aneurysm]]&lt;br /&gt;
*[[Systemic Lupus Erythematosus]]&lt;br /&gt;
*[[Trauma]]&lt;br /&gt;
*[[Turner&#039;s Syndrome]]&lt;br /&gt;
*[[Ventricular Septal Defect]]&lt;br /&gt;
*[[Weight loss]] medications&lt;br /&gt;
&lt;br /&gt;
==Differential Diagnosis Based Upon Abnormalities of the Ascending Aorta==&lt;br /&gt;
*[[Ankylosing spondylitis]]&lt;br /&gt;
*[[Aortic dissection]]&lt;br /&gt;
*[[Arteriosclerosis]]&lt;br /&gt;
* [[Bechterew&#039;s Disease]]&lt;br /&gt;
*[[Behcet&#039;s syndrome]]&lt;br /&gt;
*[[Cystic medial necrosis]] of the [[aorta]]&lt;br /&gt;
*[[Ehlers-Danlos Syndrome]]&lt;br /&gt;
*[[Giant cell arteritis]]&lt;br /&gt;
*[[Hypertension]]&lt;br /&gt;
*Idiopathic dilation of the [[ascending aorta]]&lt;br /&gt;
*[[Marfan syndrome]]&lt;br /&gt;
*[[Osteogenesis imperfecta]]&lt;br /&gt;
*[[Polymyalgia Rheumatica]]&lt;br /&gt;
*[[Pseudoxanthoma Elasticum]]&lt;br /&gt;
*[[Psoriatic arthritis]]&lt;br /&gt;
*[[Reiter&#039;s syndrome]]&lt;br /&gt;
*[[Relapsing polychondritis]]&lt;br /&gt;
*Senile aortic ectasia and dilation&lt;br /&gt;
*[[Spondyloarthropathy]]&lt;br /&gt;
*[[Syphilitic]] aortitis&lt;br /&gt;
*[[Takayasu arteritis]]&lt;br /&gt;
*[[Trauma]]&lt;br /&gt;
*[[Ulcerative colitis]]&lt;br /&gt;
*[[Whipple&#039;s disease]]&lt;br /&gt;
&lt;br /&gt;
==References==&lt;br /&gt;
{{reflist|2}}&lt;br /&gt;
&lt;br /&gt;
[[Category:Valvular heart disease]]&lt;br /&gt;
[[Category:Cardiology]]&lt;br /&gt;
[[Category:Mature chapter]]&lt;br /&gt;
[[Category:Cardiac surgery]]&lt;br /&gt;
[[Category:Surgery]]&lt;br /&gt;
&lt;br /&gt;
{{WH}}&lt;br /&gt;
{{WS}}&lt;/div&gt;</summary>
		<author><name>Varun Kumar</name></author>
	</entry>
	<entry>
		<id>https://www.wikidoc.org/index.php?title=Aortic_regurgitation_causes&amp;diff=642797</id>
		<title>Aortic regurgitation causes</title>
		<link rel="alternate" type="text/html" href="https://www.wikidoc.org/index.php?title=Aortic_regurgitation_causes&amp;diff=642797"/>
		<updated>2012-04-17T17:00:03Z</updated>

		<summary type="html">&lt;p&gt;Varun Kumar: /* By Organ System */&lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;{{Aortic insufficiency}}&lt;br /&gt;
&lt;br /&gt;
{{CMG}}; &#039;&#039;&#039;Associate Editor-In-Chief:&#039;&#039;&#039; {{CZ}}; [[Varun Kumar]], M.B.B.S.; [[Lakshmi Gopalakrishnan]], M.B.B.S.&lt;br /&gt;
&lt;br /&gt;
==Overview==&lt;br /&gt;
Aortic insufficiency can be an acute illness or a chronic illness and the causes differ depending upon the acuity of the disease.  In general, aortic insufficiency is due to abnormalities of the aortic valve itself or the aortic root.  Aortic regurgitation secondary to dilation of the ascending aorta has overtaken valvular aortic disease as the most common cause of aortic regurgitation.&lt;br /&gt;
&lt;br /&gt;
==Common Causes==&lt;br /&gt;
*Worldwide the most common cause of aortic insufficiency is [[rheumatic heart disease]].&lt;br /&gt;
*In the United States, senile degenerative calcific aortic valve disease and bicuspid aortic valve disease are the most common causes.&lt;br /&gt;
*Aortic regurgitation secondary to dilation of the ascending aorta has overtaken valvular aortic disease as the most common cause of aortic regurgitation.&lt;br /&gt;
&lt;br /&gt;
==Differential Diagnosis of the Causes of Aortic Insufficiency==&lt;br /&gt;
===By Organ System===&lt;br /&gt;
&lt;br /&gt;
{|height:100px&amp;quot; border=&amp;quot;1&amp;quot;&lt;br /&gt;
|style=&amp;quot;height:100px&amp;quot;; style=&amp;quot;width:25%&amp;quot; border=&amp;quot;1&amp;quot; bgcolor=&amp;quot;LightSteelBlue&amp;quot; | &#039;&#039;&#039;Cardiovascular&#039;&#039;&#039;&lt;br /&gt;
|style=&amp;quot;height:100px&amp;quot;; style=&amp;quot;width:75%&amp;quot; border=&amp;quot;1&amp;quot; bgcolor=&amp;quot;Beige&amp;quot; | After [[aortic valvuloplasty]]&amp;lt;ref name=&amp;quot;pmid2016464&amp;quot;&amp;gt;{{cite journal |author=Isner JM |title=Acute catastrophic complications of balloon aortic valvuloplasty. The Mansfield Scientific Aortic Valvuloplasty Registry Investigators |journal=[[Journal of the American College of Cardiology]] |volume=17 |issue=6 |pages=1436–44 |year=1991 |month=May |pmid=2016464 |doi= |url= |accessdate=2011-03-28}}&amp;lt;/ref&amp;gt;, [[Aortic dissection]], [[Arteriosclerosis]], [[Bacterial Endocarditis]], [[Bicuspid aortic valve]], [[Prosthetic valve]] dysfunction&amp;lt;ref&amp;gt;Friedman T, Mani A, Elefteriades JA. Bicuspid aortic valve: clinical approach and scientific review of a common clinical entity. Expert Rev Cardiovasc Ther. Feb 2008;6(2):235-48.&amp;lt;/ref&amp;gt;, [[Hypertension]], [[Myxomatous]] aortic valve, [[Rheumatic Fever]], [[Sinus of Valsalva Aneurysm]], [[Ventricular Septal Defect]]&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Chemical / poisoning&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Dermatologic&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Drug Side Effect&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| [[Fenfluramine]] and [[Dexfenfluramine]]: These drugs have been associated with degeneration of the aortic valve.&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Ear Nose Throat&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes&lt;br /&gt;
|- &lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Endocrine&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes&lt;br /&gt;
|- &lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Environmental&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Gastroenterologic&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| [[Whipple disease]]&amp;lt;ref&amp;gt;Jeserich M, Ihling C, Holubarsch C. Aortic valve endocarditis with Whipple disease. Ann Intern Med. Jun 1 1997;126(11):920.&amp;lt;/ref&amp;gt;&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Genetic&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| [[Ankylosing Spondylitis]]&amp;lt;ref&amp;gt;Palazzi C, D&#039; Angelo S, Lubrano E, Olivieri I. Aortic involvement in ankylosing spondylitis. Clin Exp Rheumatol. May-Jun 2008;26(3 Suppl 49):S131-4.&amp;lt;/ref&amp;gt;, [[Ehlers-Danlos Syndrome]], [[Marfan Syndrome]], [[Pseudoxanthoma Elasticum]], [[Reiter&#039;s Syndrome]], [[Rheumatoid Arthritis]]&amp;lt;ref&amp;gt;Chand EM, Freant LJ, Rubin JW. Aortic valve rheumatoid nodules producing clinical aortic regurgitation and a review of the literature. Cardiovasc Pathol. Nov-Dec 1999;8(6):333-8.&amp;lt;/ref&amp;gt;, [[Systemic Lupus Erythematosus]], [[Takayasu arteritis]], [[Turner&#039;s Syndrome]]&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Hematologic&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Iatrogenic&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| After [[aortic valvuloplasty]]&amp;lt;ref name=&amp;quot;pmid2016464&amp;quot;&amp;gt;{{cite journal |author=Isner JM |title=Acute catastrophic complications of balloon aortic valvuloplasty. The Mansfield Scientific Aortic Valvuloplasty Registry Investigators |journal=[[Journal of the American College of Cardiology]] |volume=17 |issue=6 |pages=1436–44 |year=1991 |month=May |pmid=2016464 |doi= |url= |accessdate=2011-03-28}}&amp;lt;/ref&amp;gt;, [[Prosthetic valve]] dysfunction&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Infectious Disease&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| [[Bacterial Endocarditis]], [[Rheumatic Fever]], [[Syphilis]]&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Musculoskeletal / Ortho&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| [[Ankylosing Spondylitis]], [[Ehlers-Danlos Syndrome]], [[Reiter&#039;s Syndrome]], [[Rheumatoid Arthritis]]&amp;lt;ref&amp;gt;Chand EM, Freant LJ, Rubin JW. Aortic valve rheumatoid nodules producing clinical aortic regurgitation and a review of the literature. Cardiovasc Pathol. Nov-Dec 1999;8(6):333-8.&amp;lt;/ref&amp;gt;, [[Systemic Lupus Erythematosus]]&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Neurologic&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Nutritional / Metabolic&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Obstetric/Gynecologic&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Oncologic&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Opthalmologic&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Overdose / Toxicity&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Psychiatric&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Pulmonary&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Renal / Electrolyte&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Rheum / Immune / Allergy&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| [[Ankylosing Spondylitis]]&amp;lt;ref&amp;gt;Palazzi C, D&#039; Angelo S, Lubrano E, Olivieri I. Aortic involvement in ankylosing spondylitis. Clin Exp Rheumatol. May-Jun 2008;26(3 Suppl 49):S131-4.&amp;lt;/ref&amp;gt;, [[Bechterew&#039;s Disease]], [[Behcet disease]], [[Cystic medial necrosis]], [[Ehlers-Danlos Syndrome]], [[Giant cell arteritis]], [[Marfan Syndrome]], [[Myxomatous]] aortic valve: The valvular structure can degenerate, [[Polymyalgia Rheumatica]], [[Pseudoxanthoma Elasticum]], [[Reiter&#039;s Syndrome]], [[Rheumatic Fever]], [[Rheumatoid Arthritis]]&amp;lt;ref&amp;gt;Chand EM, Freant LJ, Rubin JW. Aortic valve rheumatoid nodules producing clinical aortic regurgitation and a review of the literature. Cardiovasc Pathol. Nov-Dec 1999;8(6):333-8.&amp;lt;/ref&amp;gt;, [[Systemic Lupus Erythematosus]], [[Takayasu arteritis]], [[Whipple disease]]&amp;lt;ref&amp;gt;Jeserich M, Ihling C, Holubarsch C. Aortic valve endocarditis with Whipple disease. Ann Intern Med. Jun 1 1997;126(11):920.&amp;lt;/ref&amp;gt;&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Sexual&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| [[Syphilis]]&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Trauma&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| Blunt [[chest trauma]] disrupting the supporting apparatus of the aortic valve.&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Urologic&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Miscellaneous&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| [[Myxomatous]] aortic valve&lt;br /&gt;
|-&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
==Differential Diagnosis of the Causes of Acute Aortic Insufficiency==&lt;br /&gt;
In alphabetical order:&lt;br /&gt;
* After [[aortic valvuloplasty]]&amp;lt;ref name=&amp;quot;pmid2016464&amp;quot;&amp;gt;{{cite journal |author=Isner JM |title=Acute catastrophic complications of balloon aortic valvuloplasty. The Mansfield Scientific Aortic Valvuloplasty Registry Investigators |journal=[[Journal of the American College of Cardiology]] |volume=17 |issue=6 |pages=1436–44 |year=1991 |month=May |pmid=2016464 |doi= |url= |accessdate=2011-03-28}}&amp;lt;/ref&amp;gt;&lt;br /&gt;
* [[Aortic dissection]]: A type A dissection may disrupt the integrity of the valve leaflets causing malcoaptation of the aortic leaflets.&lt;br /&gt;
* [[Bacterial Endocarditis]]: The infection can erode the valve, can cause a leaflet to become flail, or a vegetation can prevent coaptation of the leaflets.&lt;br /&gt;
* Blunt [[chest trauma]]: Trauma can disrupt the supporting apparatus of the aortic valve.&lt;br /&gt;
* [[Myxomatous]] aortic valve: The valvular structure can degenerate&lt;br /&gt;
* [[Prosthetic valve]] dysfunction&lt;br /&gt;
* [[Rheumatic Fever]]&lt;br /&gt;
&lt;br /&gt;
==Differential Diagnosis of the Causes of Chronic Aortic Insufficiency==&lt;br /&gt;
In alphabetical order:&lt;br /&gt;
* [[Ankylosing Spondylitis]]: Ankylosing spondylitis can be associated with inflammation of the aorta ([[aortitis]]).&amp;lt;ref&amp;gt;Palazzi C, D&#039; Angelo S, Lubrano E, Olivieri I. Aortic involvement in ankylosing spondylitis. Clin Exp Rheumatol. May-Jun 2008;26(3 Suppl 49):S131-4.&amp;lt;/ref&amp;gt;  The inflammatory process can also involve the septum and cause [[conduction disease]].&lt;br /&gt;
* [[Aortic Dissection]]: A type A dissection may disrupt the integrity of the valve leaflets causing malcoaptation of the aortic leaflets.&lt;br /&gt;
* [[Arteriosclerosis]]&lt;br /&gt;
* [[Bechterew&#039;s Disease]]:  Ankylosing spondylitis can be associated with inflammation of the aorta ([[aortitis]]).&amp;lt;ref&amp;gt;Palazzi C, D&#039; Angelo S, Lubrano E, Olivieri I. Aortic involvement in ankylosing spondylitis. Clin Exp Rheumatol. May-Jun 2008;26(3 Suppl 49):S131-4.&amp;lt;/ref&amp;gt;  The inflammatory process can also involve the septum and cause [[conduction disease]].&lt;br /&gt;
* [[Behcet disease]]: Rarely, in 5% of Behcet&#039;s cases there is an [[aortitis]] that involves the ascending aorta and in some cases the [[coronary arteries]].&lt;br /&gt;
* [[Bicuspid aortic valve]]: This is the most common congenital abnormality of the ehart.  It is the most common cause of isolated aortic insufficiency requiring surgical repair.  Bicuspid aortic valve is also associated with inflammation of the aorta (an aortopathy) which may lead to dilation of the aorta and or aortic dissection that can worsen the aortic insufficiency.&amp;lt;ref&amp;gt;Friedman T, Mani A, Elefteriades JA. Bicuspid aortic valve: clinical approach and scientific review of a common clinical entity. Expert Rev Cardiovasc Ther. Feb 2008;6(2):235-48.&amp;lt;/ref&amp;gt;&lt;br /&gt;
* [[Cystic medial necrosis]] of the aorta&lt;br /&gt;
* [[Ehlers-Danlos Syndrome]]&lt;br /&gt;
* [[Giant cell arteritis]]: [[GCA]] may also be associated with an [[aortitis]] as well as [[coronary artery disease]].&amp;lt;ref&amp;gt;Eberhardt RT, Dhadly M. Giant cell arteritis: diagnosis, management, and cardiovascular implications. Cardiol Rev. Mar-Apr 2007;15(2):55-61.&amp;lt;/ref&amp;gt;&lt;br /&gt;
* [[Hypertension]]&lt;br /&gt;
* [[Marfan Syndrome]]&lt;br /&gt;
* [[Myxomatous]] aortic valve&lt;br /&gt;
* [[Polymyalgia Rheumatica]]&lt;br /&gt;
* [[Pseudoxanthoma Elasticum]]&lt;br /&gt;
* [[Reiter&#039;s Syndrome]]&lt;br /&gt;
* [[Rheumatic Fever]]: Rheumatic fever remains a cause of AS in the Middle East, Northern Africa and Asia as well as some immigrant populations in the United States.  It less prevalent in the US than it was in the 20th century. AR occurs as a result of fibrosis of the valve that is associated with thickening and retraction of the leaflets of the aortic valve.  This retraction results in regurgitation in the center of the valve.  At the same time, there may also be fusion of the aortic leaflets which results in concurrent aortic stenosis.  It should be noted that rheumatic disease of the mitral valve is usually present in the same patient.&lt;br /&gt;
* [[Rheumatoid Arthritis]]: [[RA]] rarely causes symptomatic AR, but can as a result of [[granulomatous]] nodules that may form on the aortic leaflets.&amp;lt;ref&amp;gt;Chand EM, Freant LJ, Rubin JW. Aortic valve rheumatoid nodules producing clinical aortic regurgitation and a review of the literature. Cardiovasc Pathol. Nov-Dec 1999;8(6):333-8.&amp;lt;/ref&amp;gt;&lt;br /&gt;
* [[Sinus of Valsalva Aneurysm]]&lt;br /&gt;
* [[Syphilis]]&lt;br /&gt;
* [[Systemic Lupus Erythematosus]]: There are tow mechanisms by which [[SLE]] can cause AR. SLE can cause inflammation and fibrosis of the aortic leaflets leading to their damage and retraction.&amp;lt;ref&amp;gt;Jain D, Halushka MK. Cardiac pathology of systemic lupus erythematosus. J Clin Pathol. Jul 2009;62(7):584-92.&amp;lt;/ref&amp;gt; SLE can also be associated with the development of sterile verrucous vegetations on the valves called [[Libman-Sacks endocarditis]].&amp;lt;ref&amp;gt;Moyssakis I, Tektonidou MG, Vasilliou VA, Samarkos M, Votteas V, Moutsopoulos HM. Libman-Sacks endocarditis in systemic lupus erythematosus: prevalence, associations, and evolution. Am J Med. Jul 2007;120(7):636-42.&amp;lt;/ref&amp;gt;&amp;lt;ref&amp;gt;Lee JL, Naguwa SM, Cheema GS, Gershwin ME. Revisiting Libman-Sacks endocarditis: a historical review and update. Clin Rev Allergy Immunol. Jun 2009;36(2-3):126-30.&amp;lt;/ref&amp;gt;&lt;br /&gt;
* [[Takayasu arteritis]]: [[Takayasu arteritis]] can involve the aorta in an [[aortitis]], the aortic valve itself, and the [[coronary arteries]].&amp;lt;ref&amp;gt;Adachi O, Saiki Y, Akasaka J, Oda K, Iguchi A, Tabayashi K. Surgical management of aortic regurgitation associated with takayasu arteritis and other forms of aortitis. Ann Thorac Surg. Dec 2007;84(6):1950-3.&amp;lt;/ref&amp;gt;&lt;br /&gt;
* [[Turner&#039;s Syndrome]]&lt;br /&gt;
* [[Ventricular Septal Defect]]&lt;br /&gt;
* [[Weight loss]] medications including [[fenfluramine]] and [[dexfenfluramine]] (a.k.a. [[Phen-Fen]]). These drugs have been associated with degeneration of the aortic valve.&lt;br /&gt;
* [[Whipple disease]]: Can involve the aortic valve.&amp;lt;ref&amp;gt;Jeserich M, Ihling C, Holubarsch C. Aortic valve endocarditis with Whipple disease. Ann Intern Med. Jun 1 1997;126(11):920.&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Differential Diagnosis Based Upon Aortic Valvular Causes==&lt;br /&gt;
*[[Bicuspid aortic valve]]&lt;br /&gt;
*[[Collagen vascular disease]]&lt;br /&gt;
*Senile or degenerative calcific aortic valve disease&lt;br /&gt;
*[[Endocarditis]]&lt;br /&gt;
* [[Myxomatous]] aortic valve&lt;br /&gt;
*[[Rheumatic fever]]&lt;br /&gt;
*[[Rheumatoid arthritis]]&lt;br /&gt;
*[[Sinus of Valsalva Aneurysm]]&lt;br /&gt;
*[[Systemic Lupus Erythematosus]]&lt;br /&gt;
*[[Trauma]]&lt;br /&gt;
*[[Turner&#039;s Syndrome]]&lt;br /&gt;
*[[Ventricular Septal Defect]]&lt;br /&gt;
*[[Weight loss]] medications&lt;br /&gt;
&lt;br /&gt;
==Differential Diagnosis Based Upon Abnormalities of the Ascending Aorta==&lt;br /&gt;
*[[Ankylosing spondylitis]]&lt;br /&gt;
*[[Aortic dissection]]&lt;br /&gt;
*[[Arteriosclerosis]]&lt;br /&gt;
* [[Bechterew&#039;s Disease]]&lt;br /&gt;
*[[Behcet&#039;s syndrome]]&lt;br /&gt;
*[[Cystic medial necrosis]] of the [[aorta]]&lt;br /&gt;
*[[Ehlers-Danlos Syndrome]]&lt;br /&gt;
*[[Giant cell arteritis]]&lt;br /&gt;
*[[Hypertension]]&lt;br /&gt;
*Idiopathic dilation of the [[ascending aorta]]&lt;br /&gt;
*[[Marfan syndrome]]&lt;br /&gt;
*[[Osteogenesis imperfecta]]&lt;br /&gt;
*[[Polymyalgia Rheumatica]]&lt;br /&gt;
*[[Pseudoxanthoma Elasticum]]&lt;br /&gt;
*[[Psoriatic arthritis]]&lt;br /&gt;
*[[Reiter&#039;s syndrome]]&lt;br /&gt;
*[[Relapsing polychondritis]]&lt;br /&gt;
*Senile aortic ectasia and dilation&lt;br /&gt;
*[[Spondyloarthropathy]]&lt;br /&gt;
*[[Syphilitic]] aortitis&lt;br /&gt;
*[[Takayasu arteritis]]&lt;br /&gt;
*[[Trauma]]&lt;br /&gt;
*[[Ulcerative colitis]]&lt;br /&gt;
*[[Whipple&#039;s disease]]&lt;br /&gt;
&lt;br /&gt;
==References==&lt;br /&gt;
{{reflist|2}}&lt;br /&gt;
&lt;br /&gt;
[[Category:Valvular heart disease]]&lt;br /&gt;
[[Category:Cardiology]]&lt;br /&gt;
[[Category:Mature chapter]]&lt;br /&gt;
[[Category:Cardiac surgery]]&lt;br /&gt;
[[Category:Surgery]]&lt;br /&gt;
&lt;br /&gt;
{{WH}}&lt;br /&gt;
{{WS}}&lt;/div&gt;</summary>
		<author><name>Varun Kumar</name></author>
	</entry>
	<entry>
		<id>https://www.wikidoc.org/index.php?title=Aortic_regurgitation_causes&amp;diff=642796</id>
		<title>Aortic regurgitation causes</title>
		<link rel="alternate" type="text/html" href="https://www.wikidoc.org/index.php?title=Aortic_regurgitation_causes&amp;diff=642796"/>
		<updated>2012-04-17T16:59:41Z</updated>

		<summary type="html">&lt;p&gt;Varun Kumar: /* Common Causes */&lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;{{Aortic insufficiency}}&lt;br /&gt;
&lt;br /&gt;
{{CMG}}; &#039;&#039;&#039;Associate Editor-In-Chief:&#039;&#039;&#039; {{CZ}}; [[Varun Kumar]], M.B.B.S.; [[Lakshmi Gopalakrishnan]], M.B.B.S.&lt;br /&gt;
&lt;br /&gt;
==Overview==&lt;br /&gt;
Aortic insufficiency can be an acute illness or a chronic illness and the causes differ depending upon the acuity of the disease.  In general, aortic insufficiency is due to abnormalities of the aortic valve itself or the aortic root.  Aortic regurgitation secondary to dilation of the ascending aorta has overtaken valvular aortic disease as the most common cause of aortic regurgitation.&lt;br /&gt;
&lt;br /&gt;
==Common Causes==&lt;br /&gt;
*Worldwide the most common cause of aortic insufficiency is [[rheumatic heart disease]].&lt;br /&gt;
*In the United States, senile degenerative calcific aortic valve disease and bicuspid aortic valve disease are the most common causes.&lt;br /&gt;
*Aortic regurgitation secondary to dilation of the ascending aorta has overtaken valvular aortic disease as the most common cause of aortic regurgitation.&lt;br /&gt;
&lt;br /&gt;
==Differential Diagnosis of the Causes of Aortic Insufficiency==&lt;br /&gt;
===By Organ System===&lt;br /&gt;
&lt;br /&gt;
{|style=&amp;quot;width:90%; height:100px&amp;quot; border=&amp;quot;1&amp;quot;&lt;br /&gt;
|style=&amp;quot;height:100px&amp;quot;; style=&amp;quot;width:25%&amp;quot; border=&amp;quot;1&amp;quot; bgcolor=&amp;quot;LightSteelBlue&amp;quot; | &#039;&#039;&#039;Cardiovascular&#039;&#039;&#039;&lt;br /&gt;
|style=&amp;quot;height:100px&amp;quot;; style=&amp;quot;width:75%&amp;quot; border=&amp;quot;1&amp;quot; bgcolor=&amp;quot;Beige&amp;quot; | After [[aortic valvuloplasty]]&amp;lt;ref name=&amp;quot;pmid2016464&amp;quot;&amp;gt;{{cite journal |author=Isner JM |title=Acute catastrophic complications of balloon aortic valvuloplasty. The Mansfield Scientific Aortic Valvuloplasty Registry Investigators |journal=[[Journal of the American College of Cardiology]] |volume=17 |issue=6 |pages=1436–44 |year=1991 |month=May |pmid=2016464 |doi= |url= |accessdate=2011-03-28}}&amp;lt;/ref&amp;gt;, [[Aortic dissection]], [[Arteriosclerosis]], [[Bacterial Endocarditis]], [[Bicuspid aortic valve]], [[Prosthetic valve]] dysfunction&amp;lt;ref&amp;gt;Friedman T, Mani A, Elefteriades JA. Bicuspid aortic valve: clinical approach and scientific review of a common clinical entity. Expert Rev Cardiovasc Ther. Feb 2008;6(2):235-48.&amp;lt;/ref&amp;gt;, [[Hypertension]], [[Myxomatous]] aortic valve, [[Rheumatic Fever]], [[Sinus of Valsalva Aneurysm]], [[Ventricular Septal Defect]]&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Chemical / poisoning&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Dermatologic&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Drug Side Effect&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| [[Fenfluramine]] and [[Dexfenfluramine]]: These drugs have been associated with degeneration of the aortic valve.&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Ear Nose Throat&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes&lt;br /&gt;
|- &lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Endocrine&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes&lt;br /&gt;
|- &lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Environmental&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Gastroenterologic&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| [[Whipple disease]]&amp;lt;ref&amp;gt;Jeserich M, Ihling C, Holubarsch C. Aortic valve endocarditis with Whipple disease. Ann Intern Med. Jun 1 1997;126(11):920.&amp;lt;/ref&amp;gt;&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Genetic&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| [[Ankylosing Spondylitis]]&amp;lt;ref&amp;gt;Palazzi C, D&#039; Angelo S, Lubrano E, Olivieri I. Aortic involvement in ankylosing spondylitis. Clin Exp Rheumatol. May-Jun 2008;26(3 Suppl 49):S131-4.&amp;lt;/ref&amp;gt;, [[Ehlers-Danlos Syndrome]], [[Marfan Syndrome]], [[Pseudoxanthoma Elasticum]], [[Reiter&#039;s Syndrome]], [[Rheumatoid Arthritis]]&amp;lt;ref&amp;gt;Chand EM, Freant LJ, Rubin JW. Aortic valve rheumatoid nodules producing clinical aortic regurgitation and a review of the literature. Cardiovasc Pathol. Nov-Dec 1999;8(6):333-8.&amp;lt;/ref&amp;gt;, [[Systemic Lupus Erythematosus]], [[Takayasu arteritis]], [[Turner&#039;s Syndrome]]&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Hematologic&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Iatrogenic&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| After [[aortic valvuloplasty]]&amp;lt;ref name=&amp;quot;pmid2016464&amp;quot;&amp;gt;{{cite journal |author=Isner JM |title=Acute catastrophic complications of balloon aortic valvuloplasty. The Mansfield Scientific Aortic Valvuloplasty Registry Investigators |journal=[[Journal of the American College of Cardiology]] |volume=17 |issue=6 |pages=1436–44 |year=1991 |month=May |pmid=2016464 |doi= |url= |accessdate=2011-03-28}}&amp;lt;/ref&amp;gt;, [[Prosthetic valve]] dysfunction&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Infectious Disease&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| [[Bacterial Endocarditis]], [[Rheumatic Fever]], [[Syphilis]]&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Musculoskeletal / Ortho&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| [[Ankylosing Spondylitis]], [[Ehlers-Danlos Syndrome]], [[Reiter&#039;s Syndrome]], [[Rheumatoid Arthritis]]&amp;lt;ref&amp;gt;Chand EM, Freant LJ, Rubin JW. Aortic valve rheumatoid nodules producing clinical aortic regurgitation and a review of the literature. Cardiovasc Pathol. Nov-Dec 1999;8(6):333-8.&amp;lt;/ref&amp;gt;, [[Systemic Lupus Erythematosus]]&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Neurologic&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Nutritional / Metabolic&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Obstetric/Gynecologic&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Oncologic&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Opthalmologic&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Overdose / Toxicity&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Psychiatric&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Pulmonary&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Renal / Electrolyte&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Rheum / Immune / Allergy&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| [[Ankylosing Spondylitis]]&amp;lt;ref&amp;gt;Palazzi C, D&#039; Angelo S, Lubrano E, Olivieri I. Aortic involvement in ankylosing spondylitis. Clin Exp Rheumatol. May-Jun 2008;26(3 Suppl 49):S131-4.&amp;lt;/ref&amp;gt;, [[Bechterew&#039;s Disease]], [[Behcet disease]], [[Cystic medial necrosis]], [[Ehlers-Danlos Syndrome]], [[Giant cell arteritis]], [[Marfan Syndrome]], [[Myxomatous]] aortic valve: The valvular structure can degenerate, [[Polymyalgia Rheumatica]], [[Pseudoxanthoma Elasticum]], [[Reiter&#039;s Syndrome]], [[Rheumatic Fever]], [[Rheumatoid Arthritis]]&amp;lt;ref&amp;gt;Chand EM, Freant LJ, Rubin JW. Aortic valve rheumatoid nodules producing clinical aortic regurgitation and a review of the literature. Cardiovasc Pathol. Nov-Dec 1999;8(6):333-8.&amp;lt;/ref&amp;gt;, [[Systemic Lupus Erythematosus]], [[Takayasu arteritis]], [[Whipple disease]]&amp;lt;ref&amp;gt;Jeserich M, Ihling C, Holubarsch C. Aortic valve endocarditis with Whipple disease. Ann Intern Med. Jun 1 1997;126(11):920.&amp;lt;/ref&amp;gt;&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Sexual&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| [[Syphilis]]&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Trauma&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| Blunt [[chest trauma]] disrupting the supporting apparatus of the aortic valve.&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Urologic&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Miscellaneous&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| [[Myxomatous]] aortic valve&lt;br /&gt;
|-&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
==Differential Diagnosis of the Causes of Acute Aortic Insufficiency==&lt;br /&gt;
In alphabetical order:&lt;br /&gt;
* After [[aortic valvuloplasty]]&amp;lt;ref name=&amp;quot;pmid2016464&amp;quot;&amp;gt;{{cite journal |author=Isner JM |title=Acute catastrophic complications of balloon aortic valvuloplasty. The Mansfield Scientific Aortic Valvuloplasty Registry Investigators |journal=[[Journal of the American College of Cardiology]] |volume=17 |issue=6 |pages=1436–44 |year=1991 |month=May |pmid=2016464 |doi= |url= |accessdate=2011-03-28}}&amp;lt;/ref&amp;gt;&lt;br /&gt;
* [[Aortic dissection]]: A type A dissection may disrupt the integrity of the valve leaflets causing malcoaptation of the aortic leaflets.&lt;br /&gt;
* [[Bacterial Endocarditis]]: The infection can erode the valve, can cause a leaflet to become flail, or a vegetation can prevent coaptation of the leaflets.&lt;br /&gt;
* Blunt [[chest trauma]]: Trauma can disrupt the supporting apparatus of the aortic valve.&lt;br /&gt;
* [[Myxomatous]] aortic valve: The valvular structure can degenerate&lt;br /&gt;
* [[Prosthetic valve]] dysfunction&lt;br /&gt;
* [[Rheumatic Fever]]&lt;br /&gt;
&lt;br /&gt;
==Differential Diagnosis of the Causes of Chronic Aortic Insufficiency==&lt;br /&gt;
In alphabetical order:&lt;br /&gt;
* [[Ankylosing Spondylitis]]: Ankylosing spondylitis can be associated with inflammation of the aorta ([[aortitis]]).&amp;lt;ref&amp;gt;Palazzi C, D&#039; Angelo S, Lubrano E, Olivieri I. Aortic involvement in ankylosing spondylitis. Clin Exp Rheumatol. May-Jun 2008;26(3 Suppl 49):S131-4.&amp;lt;/ref&amp;gt;  The inflammatory process can also involve the septum and cause [[conduction disease]].&lt;br /&gt;
* [[Aortic Dissection]]: A type A dissection may disrupt the integrity of the valve leaflets causing malcoaptation of the aortic leaflets.&lt;br /&gt;
* [[Arteriosclerosis]]&lt;br /&gt;
* [[Bechterew&#039;s Disease]]:  Ankylosing spondylitis can be associated with inflammation of the aorta ([[aortitis]]).&amp;lt;ref&amp;gt;Palazzi C, D&#039; Angelo S, Lubrano E, Olivieri I. Aortic involvement in ankylosing spondylitis. Clin Exp Rheumatol. May-Jun 2008;26(3 Suppl 49):S131-4.&amp;lt;/ref&amp;gt;  The inflammatory process can also involve the septum and cause [[conduction disease]].&lt;br /&gt;
* [[Behcet disease]]: Rarely, in 5% of Behcet&#039;s cases there is an [[aortitis]] that involves the ascending aorta and in some cases the [[coronary arteries]].&lt;br /&gt;
* [[Bicuspid aortic valve]]: This is the most common congenital abnormality of the ehart.  It is the most common cause of isolated aortic insufficiency requiring surgical repair.  Bicuspid aortic valve is also associated with inflammation of the aorta (an aortopathy) which may lead to dilation of the aorta and or aortic dissection that can worsen the aortic insufficiency.&amp;lt;ref&amp;gt;Friedman T, Mani A, Elefteriades JA. Bicuspid aortic valve: clinical approach and scientific review of a common clinical entity. Expert Rev Cardiovasc Ther. Feb 2008;6(2):235-48.&amp;lt;/ref&amp;gt;&lt;br /&gt;
* [[Cystic medial necrosis]] of the aorta&lt;br /&gt;
* [[Ehlers-Danlos Syndrome]]&lt;br /&gt;
* [[Giant cell arteritis]]: [[GCA]] may also be associated with an [[aortitis]] as well as [[coronary artery disease]].&amp;lt;ref&amp;gt;Eberhardt RT, Dhadly M. Giant cell arteritis: diagnosis, management, and cardiovascular implications. Cardiol Rev. Mar-Apr 2007;15(2):55-61.&amp;lt;/ref&amp;gt;&lt;br /&gt;
* [[Hypertension]]&lt;br /&gt;
* [[Marfan Syndrome]]&lt;br /&gt;
* [[Myxomatous]] aortic valve&lt;br /&gt;
* [[Polymyalgia Rheumatica]]&lt;br /&gt;
* [[Pseudoxanthoma Elasticum]]&lt;br /&gt;
* [[Reiter&#039;s Syndrome]]&lt;br /&gt;
* [[Rheumatic Fever]]: Rheumatic fever remains a cause of AS in the Middle East, Northern Africa and Asia as well as some immigrant populations in the United States.  It less prevalent in the US than it was in the 20th century. AR occurs as a result of fibrosis of the valve that is associated with thickening and retraction of the leaflets of the aortic valve.  This retraction results in regurgitation in the center of the valve.  At the same time, there may also be fusion of the aortic leaflets which results in concurrent aortic stenosis.  It should be noted that rheumatic disease of the mitral valve is usually present in the same patient.&lt;br /&gt;
* [[Rheumatoid Arthritis]]: [[RA]] rarely causes symptomatic AR, but can as a result of [[granulomatous]] nodules that may form on the aortic leaflets.&amp;lt;ref&amp;gt;Chand EM, Freant LJ, Rubin JW. Aortic valve rheumatoid nodules producing clinical aortic regurgitation and a review of the literature. Cardiovasc Pathol. Nov-Dec 1999;8(6):333-8.&amp;lt;/ref&amp;gt;&lt;br /&gt;
* [[Sinus of Valsalva Aneurysm]]&lt;br /&gt;
* [[Syphilis]]&lt;br /&gt;
* [[Systemic Lupus Erythematosus]]: There are tow mechanisms by which [[SLE]] can cause AR. SLE can cause inflammation and fibrosis of the aortic leaflets leading to their damage and retraction.&amp;lt;ref&amp;gt;Jain D, Halushka MK. Cardiac pathology of systemic lupus erythematosus. J Clin Pathol. Jul 2009;62(7):584-92.&amp;lt;/ref&amp;gt; SLE can also be associated with the development of sterile verrucous vegetations on the valves called [[Libman-Sacks endocarditis]].&amp;lt;ref&amp;gt;Moyssakis I, Tektonidou MG, Vasilliou VA, Samarkos M, Votteas V, Moutsopoulos HM. Libman-Sacks endocarditis in systemic lupus erythematosus: prevalence, associations, and evolution. Am J Med. Jul 2007;120(7):636-42.&amp;lt;/ref&amp;gt;&amp;lt;ref&amp;gt;Lee JL, Naguwa SM, Cheema GS, Gershwin ME. Revisiting Libman-Sacks endocarditis: a historical review and update. Clin Rev Allergy Immunol. Jun 2009;36(2-3):126-30.&amp;lt;/ref&amp;gt;&lt;br /&gt;
* [[Takayasu arteritis]]: [[Takayasu arteritis]] can involve the aorta in an [[aortitis]], the aortic valve itself, and the [[coronary arteries]].&amp;lt;ref&amp;gt;Adachi O, Saiki Y, Akasaka J, Oda K, Iguchi A, Tabayashi K. Surgical management of aortic regurgitation associated with takayasu arteritis and other forms of aortitis. Ann Thorac Surg. Dec 2007;84(6):1950-3.&amp;lt;/ref&amp;gt;&lt;br /&gt;
* [[Turner&#039;s Syndrome]]&lt;br /&gt;
* [[Ventricular Septal Defect]]&lt;br /&gt;
* [[Weight loss]] medications including [[fenfluramine]] and [[dexfenfluramine]] (a.k.a. [[Phen-Fen]]). These drugs have been associated with degeneration of the aortic valve.&lt;br /&gt;
* [[Whipple disease]]: Can involve the aortic valve.&amp;lt;ref&amp;gt;Jeserich M, Ihling C, Holubarsch C. Aortic valve endocarditis with Whipple disease. Ann Intern Med. Jun 1 1997;126(11):920.&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Differential Diagnosis Based Upon Aortic Valvular Causes==&lt;br /&gt;
*[[Bicuspid aortic valve]]&lt;br /&gt;
*[[Collagen vascular disease]]&lt;br /&gt;
*Senile or degenerative calcific aortic valve disease&lt;br /&gt;
*[[Endocarditis]]&lt;br /&gt;
* [[Myxomatous]] aortic valve&lt;br /&gt;
*[[Rheumatic fever]]&lt;br /&gt;
*[[Rheumatoid arthritis]]&lt;br /&gt;
*[[Sinus of Valsalva Aneurysm]]&lt;br /&gt;
*[[Systemic Lupus Erythematosus]]&lt;br /&gt;
*[[Trauma]]&lt;br /&gt;
*[[Turner&#039;s Syndrome]]&lt;br /&gt;
*[[Ventricular Septal Defect]]&lt;br /&gt;
*[[Weight loss]] medications&lt;br /&gt;
&lt;br /&gt;
==Differential Diagnosis Based Upon Abnormalities of the Ascending Aorta==&lt;br /&gt;
*[[Ankylosing spondylitis]]&lt;br /&gt;
*[[Aortic dissection]]&lt;br /&gt;
*[[Arteriosclerosis]]&lt;br /&gt;
* [[Bechterew&#039;s Disease]]&lt;br /&gt;
*[[Behcet&#039;s syndrome]]&lt;br /&gt;
*[[Cystic medial necrosis]] of the [[aorta]]&lt;br /&gt;
*[[Ehlers-Danlos Syndrome]]&lt;br /&gt;
*[[Giant cell arteritis]]&lt;br /&gt;
*[[Hypertension]]&lt;br /&gt;
*Idiopathic dilation of the [[ascending aorta]]&lt;br /&gt;
*[[Marfan syndrome]]&lt;br /&gt;
*[[Osteogenesis imperfecta]]&lt;br /&gt;
*[[Polymyalgia Rheumatica]]&lt;br /&gt;
*[[Pseudoxanthoma Elasticum]]&lt;br /&gt;
*[[Psoriatic arthritis]]&lt;br /&gt;
*[[Reiter&#039;s syndrome]]&lt;br /&gt;
*[[Relapsing polychondritis]]&lt;br /&gt;
*Senile aortic ectasia and dilation&lt;br /&gt;
*[[Spondyloarthropathy]]&lt;br /&gt;
*[[Syphilitic]] aortitis&lt;br /&gt;
*[[Takayasu arteritis]]&lt;br /&gt;
*[[Trauma]]&lt;br /&gt;
*[[Ulcerative colitis]]&lt;br /&gt;
*[[Whipple&#039;s disease]]&lt;br /&gt;
&lt;br /&gt;
==References==&lt;br /&gt;
{{reflist|2}}&lt;br /&gt;
&lt;br /&gt;
[[Category:Valvular heart disease]]&lt;br /&gt;
[[Category:Cardiology]]&lt;br /&gt;
[[Category:Mature chapter]]&lt;br /&gt;
[[Category:Cardiac surgery]]&lt;br /&gt;
[[Category:Surgery]]&lt;br /&gt;
&lt;br /&gt;
{{WH}}&lt;br /&gt;
{{WS}}&lt;/div&gt;</summary>
		<author><name>Varun Kumar</name></author>
	</entry>
	<entry>
		<id>https://www.wikidoc.org/index.php?title=Left_atrial_enlargement_causes&amp;diff=642786</id>
		<title>Left atrial enlargement causes</title>
		<link rel="alternate" type="text/html" href="https://www.wikidoc.org/index.php?title=Left_atrial_enlargement_causes&amp;diff=642786"/>
		<updated>2012-04-17T16:29:10Z</updated>

		<summary type="html">&lt;p&gt;Varun Kumar: &lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;{{CMG}}; {{AOEIC}} {{VK}}&lt;br /&gt;
&lt;br /&gt;
==Overview==&lt;br /&gt;
In the general population, [[obesity]] appears to be the most important [[risk factor]] for left atrial enlargement.&amp;lt;ref name=&#039;Stritzke2009&#039;&amp;gt;{{cite journal|title=The Aging Process of the Heart: Obesity Is the Main Risk Factor for Left Atrial Enlargement During Aging: The MONICA/KORA (Monitoring of Trends and Determinations in Cardiovascular Disease/Cooperative Research in the Region of Augsburg) Study |journal=Journal of the American College of Cardiology|date=2009-11-17|author=Stritzke J, Markus MRP, Duderstadt S, Lieb W, Luchner A, Döring A, Keil U, Hense H and Schunkert H|volume=54|issue=21|pages=1982–9|pmid=19909880  |doi=10.1016/j.jacc.2009.07.034 |url=http://content.onlinejacc.org/cgi/content/abstract/54/21/1982|format=|accessdate=2009-12-02 }}&amp;lt;/ref&amp;gt; Persistent [[atrial fibrillation]] results in retention of blood in the left atrium secondary to inadequate pumping of blood by the atrium into the left ventricle&amp;lt;ref name=&#039;Sanfilippo1990&#039;&amp;gt;{{cite journal|title=Atrial enlargement as a consequence of atrial fibrillation  A prospective echocardiographic study|journal=Circulation|year=1990|author=Sanfilippo AJ, Abascal VM, Sheehan M, Oertel LB, Harrigan P, Hughes RA and Weyman AE |volume=82|issue=3|pages=792–7|pmid= 2144217 |url=http://circ.ahajournals.org/cgi/content/abstract/82/3/792|format=|accessdate=2009-12-02|doi=10.1161/01.CIR.82.3.792}}&amp;lt;/ref&amp;gt;. Similar pathophysiologic process occurs in [[mitral stenosis]] resulting in subsequent left atrial enlargement. [[Aortic stenosis]], [[mitral regurgitation]], [[aortic insufficiency]] and other causes of [[left ventricular heart failure]] causes an increase in back pressure within the atrium resulting in subsequent left atrial enlargement.&lt;br /&gt;
==Differential Diagnosis of Causes of Left Atrial Enlargement==&lt;br /&gt;
===By Organ System===&lt;br /&gt;
{|style=&amp;quot;width:75%&amp;quot; height:100px&amp;quot; border=&amp;quot;1&amp;quot;&lt;br /&gt;
|style=&amp;quot;height:100px&amp;quot;; style=&amp;quot;width:25%&amp;quot; border=&amp;quot;1&amp;quot; bgcolor=&amp;quot;LightSteelBlue&amp;quot; | &#039;&#039;&#039;Cardiovascular&#039;&#039;&#039;&lt;br /&gt;
|style=&amp;quot;height:100px&amp;quot;; style=&amp;quot;width:75%&amp;quot; border=&amp;quot;1&amp;quot; bgcolor=&amp;quot;Beige&amp;quot; | [[Aortic regurgitation]], [[Aortic stenosis]], [[Atrial fibrillation]]&amp;lt;ref name=&#039;Sanfilippo1990&#039;&amp;gt;{{cite journal|title=Atrial enlargement as a consequence of atrial fibrillation  A prospective echocardiographic study|journal=Circulation|year=1990|author=Sanfilippo AJ, Abascal VM, Sheehan M, Oertel LB, Harrigan P, Hughes RA and Weyman AE |volume=82|issue=3|pages=792–7|pmid= 2144217 |url=http://circ.ahajournals.org/cgi/content/abstract/82/3/792|format=|accessdate=2009-12-02|doi=10.1161/01.CIR.82.3.792}}&amp;lt;/ref&amp;gt;, [[Atrial septal defect]], [[Cardiac amyloidosis]]&amp;lt;ref name=&amp;quot;pmid12413446&amp;quot;&amp;gt;{{cite journal |author=Dardas PS, Tsikaderis DD, Mezilis N, Geleris P, Boudoulas H |title=Echocardiographic evidence of atrial myopathy in amyloidosis: a case report |journal=[[European Journal of Echocardiography : the Journal of the Working Group on Echocardiography of the European Society of Cardiology]] |volume=3 |issue=4 |pages=303–5 |year=2002 |month=December |pmid=12413446 |doi= |url=http://ejechocard.oxfordjournals.org/cgi/pmidlookup?view=long&amp;amp;pmid=12413446 |accessdate=2012-04-17}}&amp;lt;/ref&amp;gt;, [[Coarctation of the aorta]], [[Congestive heart failure]], [[Coronary artery disease]], [[Hypertrophic cardiomyopathy]], Hypoplasia of mitral valve annulus which is a part of the spectrum of [[hypoplastic left heart syndrome]], [[Infective endocarditis]], [[Ischemic mitral regurgitation]], [[Left atrial myxoma]], [[Left bundle branch block]], [[Mitral regurgitation]], [[Mitral stenosis]], Mitral valve annular [[calcification]], Mitral valve commissural fusion, [[Mitral valve prolapse]], [[Papillary muscle rupture]], Parachute mitral valve, [[Prosthetic mitral valve]] stenosis, [[Rheumatic heart disease]], Supra-valve mitral membrane, [[Systemic hypertension]], Thickened [[chordae tendinae]], [[Thrombus]] (ball valve thrombus) in left atrium&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Chemical / poisoning&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Dermatologic&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Drug Side Effect&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| [[Chronic alcoholism]]&amp;lt;ref&amp;gt;Kabir J. Singh, Beth Cohen, Bee Ya Na, Mary A. Whooley, and Nelson B. Schiller. Predictors Of Increasing Left Atrial Volume Over Five Years In Coronary Artery Disease Patients: Results From The Heart And Soul Study. J.Am.Coll.Cardiol.2010;55;A91.E864 [http://content.onlinejacc.org/cgi/reprint/55/10_MeetingAbstracts/A91.E864.pdf]&amp;lt;/ref&amp;gt;&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Ear Nose Throat&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes&lt;br /&gt;
|- &lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Endocrine&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes&lt;br /&gt;
|- &lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Environmental&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Gastroenterologic&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Genetic&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| [[Cardiac amyloidosis]]&amp;lt;ref name=&amp;quot;pmid12413446&amp;quot;&amp;gt;{{cite journal |author=Dardas PS, Tsikaderis DD, Mezilis N, Geleris P, Boudoulas H |title=Echocardiographic evidence of atrial myopathy in amyloidosis: a case report |journal=[[European Journal of Echocardiography : the Journal of the Working Group on Echocardiography of the European Society of Cardiology]] |volume=3 |issue=4 |pages=303–5 |year=2002 |month=December |pmid=12413446 |doi= |url=http://ejechocard.oxfordjournals.org/cgi/pmidlookup?view=long&amp;amp;pmid=12413446 |accessdate=2012-04-17}}&amp;lt;/ref&amp;gt;, [[Hypertrophic cardiomyopathy]], [[Hypoplasia]] of mitral valve annulus which is a part of the spectrum of [[hypoplastic left heart syndrome]]&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Hematologic&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Iatrogenic&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Infectious Disease&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| [[Infective endocarditis]], [[Pneumonia]], [[Rheumatic heart disease]]&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Musculoskeletal / Ortho&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| [[Ankylosing spondylitis]]&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Neurologic&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Nutritional / Metabolic&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| [[Hypercholesterolemia]] accelerates the stenotic process of the valves via [[calcification]], [[Obesity]]&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Obstetric/Gynecologic&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Oncologic&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| [[Left atrial myxoma]]&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Opthalmologic&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Overdose / Toxicity&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| [[Chronic alcoholism]]&amp;lt;ref&amp;gt;Kabir J. Singh, Beth Cohen, Bee Ya Na, Mary A. Whooley, and Nelson B. Schiller. Predictors Of Increasing Left Atrial Volume Over Five Years In Coronary Artery Disease Patients: Results From The Heart And Soul Study. J.Am.Coll.Cardiol.2010;55;A91.E864 [http://content.onlinejacc.org/cgi/reprint/55/10_MeetingAbstracts/A91.E864.pdf]&amp;lt;/ref&amp;gt;&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Psychiatric&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Pulmonary&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| [[Emphysema]], [[Pneumonia]]&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Renal / Electrolyte&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Rheum / Immune / Allergy&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| [[Ankylosing spondylitis]], [[Cardiac amyloidosis]]&amp;lt;ref name=&amp;quot;pmid12413446&amp;quot;&amp;gt;{{cite journal |author=Dardas PS, Tsikaderis DD, Mezilis N, Geleris P, Boudoulas H |title=Echocardiographic evidence of atrial myopathy in amyloidosis: a case report |journal=[[European Journal of Echocardiography : the Journal of the Working Group on Echocardiography of the European Society of Cardiology]] |volume=3 |issue=4 |pages=303–5 |year=2002 |month=December |pmid=12413446 |doi= |url=http://ejechocard.oxfordjournals.org/cgi/pmidlookup?view=long&amp;amp;pmid=12413446 |accessdate=2012-04-17}}&amp;lt;/ref&amp;gt;, [[Rheumatic heart disease]]&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Sexual&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Trauma&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Urologic&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Miscellaneous&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| [[Thrombus]] (ball valve thrombus) in left atrium&lt;br /&gt;
|-&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
===In Alphabetical Order===&lt;br /&gt;
&lt;br /&gt;
*[[Ankylosing spondylitis]]&lt;br /&gt;
*[[Aortic regurgitation]]&lt;br /&gt;
*[[Aortic stenosis]]&lt;br /&gt;
*[[Atrial fibrillation]]&amp;lt;ref name=&#039;Sanfilippo1990&#039;&amp;gt;{{cite journal|title=Atrial enlargement as a consequence of atrial fibrillation  A prospective echocardiographic study|journal=Circulation|year=1990|author=Sanfilippo AJ, Abascal VM, Sheehan M, Oertel LB, Harrigan P, Hughes RA and Weyman AE |volume=82|issue=3|pages=792–7|pmid= 2144217 |url=http://circ.ahajournals.org/cgi/content/abstract/82/3/792|format=|accessdate=2009-12-02|doi=10.1161/01.CIR.82.3.792}}&amp;lt;/ref&amp;gt;&lt;br /&gt;
*[[Atrial septal defect]]&lt;br /&gt;
*[[Cardiac amyloidosis]]&amp;lt;ref name=&amp;quot;pmid12413446&amp;quot;&amp;gt;{{cite journal |author=Dardas PS, Tsikaderis DD, Mezilis N, Geleris P, Boudoulas H |title=Echocardiographic evidence of atrial myopathy in amyloidosis: a case report |journal=[[European Journal of Echocardiography : the Journal of the Working Group on Echocardiography of the European Society of Cardiology]] |volume=3 |issue=4 |pages=303–5 |year=2002 |month=December |pmid=12413446 |doi= |url=http://ejechocard.oxfordjournals.org/cgi/pmidlookup?view=long&amp;amp;pmid=12413446 |accessdate=2012-04-17}}&amp;lt;/ref&amp;gt;&lt;br /&gt;
*[[Chronic alcoholism]]&amp;lt;ref&amp;gt;Kabir J. Singh, Beth Cohen, Bee Ya Na, Mary A. Whooley, and Nelson B. Schiller. Predictors Of Increasing Left Atrial Volume Over Five Years In Coronary Artery Disease Patients: Results From The Heart And Soul Study. J.Am.Coll.Cardiol.2010;55;A91.E864 [http://content.onlinejacc.org/cgi/reprint/55/10_MeetingAbstracts/A91.E864.pdf]&amp;lt;/ref&amp;gt;&lt;br /&gt;
*[[Coarctation of the aorta]]&lt;br /&gt;
*[[Congestive heart failure]]&lt;br /&gt;
*[[Coronary artery disease]]&lt;br /&gt;
*[[Emphysema]]&lt;br /&gt;
*[[Hypertrophic cardiomyopathy]]&lt;br /&gt;
*[[Hypercholesterolemia]] accelerates the stenotic process of the valves via [[calcification]]&lt;br /&gt;
*Hypoplasia of mitral valve annulus which is a part of the spectrum of [[hypoplastic left heart syndrome]]&lt;br /&gt;
*[[Infective endocarditis]]&lt;br /&gt;
*[[Ischemic mitral regurgitation]]&lt;br /&gt;
*[[Left atrial myxoma]]&lt;br /&gt;
*[[Left bundle branch block]]&lt;br /&gt;
*[[Mitral regurgitation]]&lt;br /&gt;
*[[Mitral stenosis]]&lt;br /&gt;
*Mitral valve annular calcification&lt;br /&gt;
*Mitral valve commissural fusion&lt;br /&gt;
*[[Mitral valve prolapse]]&lt;br /&gt;
*[[Obesity]]&lt;br /&gt;
*[[Papillary muscle rupture]]&lt;br /&gt;
*Parachute mitral valve&lt;br /&gt;
*[[Pneumonia]]&lt;br /&gt;
*[[Prosthetic mitral valve]] stenosis&lt;br /&gt;
*[[Rheumatic heart disease]]&lt;br /&gt;
*Supra-valve mitral membrane&lt;br /&gt;
*[[Systemic hypertension]]&lt;br /&gt;
*Thickened [[chordae tendinae]]&lt;br /&gt;
*[[Thrombus]] (ball valve thrombus) in left atrium&lt;br /&gt;
&lt;br /&gt;
==References==&lt;br /&gt;
{{reflist|2}}&lt;br /&gt;
&lt;br /&gt;
[[Category:Cardiology]]&lt;br /&gt;
&lt;br /&gt;
{{WS}}&lt;br /&gt;
{{WH}}&lt;/div&gt;</summary>
		<author><name>Varun Kumar</name></author>
	</entry>
	<entry>
		<id>https://www.wikidoc.org/index.php?title=Left_atrial_enlargement_causes&amp;diff=642768</id>
		<title>Left atrial enlargement causes</title>
		<link rel="alternate" type="text/html" href="https://www.wikidoc.org/index.php?title=Left_atrial_enlargement_causes&amp;diff=642768"/>
		<updated>2012-04-17T15:40:10Z</updated>

		<summary type="html">&lt;p&gt;Varun Kumar: /* In alphabetical Order */&lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;{{CMG}}; {{AOEIC}} {{VK}}&lt;br /&gt;
&lt;br /&gt;
==Differential Diagnosis of Causes of Left Atrial Enlargement==&lt;br /&gt;
===In alphabetical Order===&lt;br /&gt;
&lt;br /&gt;
*[[Ankylosing spondylitis]]&lt;br /&gt;
*[[Aortic regurgitation]]&lt;br /&gt;
*[[Aortic stenosis]]&lt;br /&gt;
*[[Atrial fibrillation]]&lt;br /&gt;
*[[Atrial septal defect]]&lt;br /&gt;
*[[Chronic alcoholism]]&amp;lt;ref&amp;gt;Kabir J. Singh, Beth Cohen, Bee Ya Na, Mary A. Whooley, and Nelson B. Schiller. Predictors Of Increasing Left Atrial Volume Over Five Years In Coronary Artery Disease Patients: Results From The Heart And Soul Study. J.Am.Coll.Cardiol.2010;55;A91.E864 [http://content.onlinejacc.org/cgi/reprint/55/10_MeetingAbstracts/A91.E864.pdf]&amp;lt;/ref&amp;gt;&lt;br /&gt;
*[[Coarctation of the aorta]]&lt;br /&gt;
*[[Congestive heart failure]]&lt;br /&gt;
*[[Emphysema]]&lt;br /&gt;
*[[Hypertrophic cardiomyopathy]]&lt;br /&gt;
*[[Hypercholesterolemia]] accelerates the stenotic process of the valves via [[calcification]]&lt;br /&gt;
*Hypoplasia of mitral valve annulus which is a part of the spectrum of [[hypoplastic left heart syndrome]]&lt;br /&gt;
*[[Infective endocarditis]]&lt;br /&gt;
*[[Ischemic mitral regurgitation]]&lt;br /&gt;
*[[Left atrial myxoma]]&lt;br /&gt;
*[[Left bundle branch block]]&lt;br /&gt;
*[[Mitral regurgitation]]&lt;br /&gt;
*[[Mitral stenosis]]&lt;br /&gt;
*Mitral valve annular calcification&lt;br /&gt;
*Mitral valve commissural fusion&lt;br /&gt;
*[[Mitral valve prolapse]]&lt;br /&gt;
*[[Obesity]]&lt;br /&gt;
*[[Papillary muscle rupture]]&lt;br /&gt;
*Parachute mitral valve&lt;br /&gt;
*[[Pneumonia]]&lt;br /&gt;
*[[Prosthetic mitral valve]]&lt;br /&gt;
*[[Rheumatic heart disease]]&lt;br /&gt;
*Supra-valve mitral membrane&lt;br /&gt;
*[[Systemic hypertension]]&lt;br /&gt;
*Thickened [[chordae tendinae]]&lt;br /&gt;
*[[Thrombus]] (ball valve thrombus) in left atrium&lt;br /&gt;
&lt;br /&gt;
==References==&lt;br /&gt;
{{reflist|2}}&lt;br /&gt;
&lt;br /&gt;
[[Category:Cardiology]]&lt;br /&gt;
&lt;br /&gt;
{{WS}}&lt;br /&gt;
{{WH}}&lt;/div&gt;</summary>
		<author><name>Varun Kumar</name></author>
	</entry>
	<entry>
		<id>https://www.wikidoc.org/index.php?title=Left_atrial_enlargement_causes&amp;diff=642765</id>
		<title>Left atrial enlargement causes</title>
		<link rel="alternate" type="text/html" href="https://www.wikidoc.org/index.php?title=Left_atrial_enlargement_causes&amp;diff=642765"/>
		<updated>2012-04-17T15:28:26Z</updated>

		<summary type="html">&lt;p&gt;Varun Kumar: &lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;{{CMG}}; {{AOEIC}} {{VK}}&lt;br /&gt;
&lt;br /&gt;
==Differential Diagnosis of Causes of Left Atrial Enlargement==&lt;br /&gt;
===In alphabetical Order===&lt;br /&gt;
*[[Alcoholism]]&lt;br /&gt;
*[[Ankylosing spondylitis]]&lt;br /&gt;
*[[Aortic regurgitation]]&lt;br /&gt;
*[[Aortic stenosis]]&lt;br /&gt;
*[[Atrial fibrillation]]&lt;br /&gt;
*[[Atrial septal defect]]&lt;br /&gt;
*[[Coarctation of the aorta]]&lt;br /&gt;
*[[Congestive heart failure]]&lt;br /&gt;
*[[Emphysema]]&lt;br /&gt;
*[[Hypertrophic cardiomyopathy]]&lt;br /&gt;
*[[Hypercholesterolemia]] accelerates the stenotic process of the valves via [[calcification]]&lt;br /&gt;
*Hypoplasia of mitral valve annulus which is a part of the spectrum of [[hypoplastic left heart syndrome]]&lt;br /&gt;
*[[Infective endocarditis]]&lt;br /&gt;
*[[Ischemic mitral regurgitation]]&lt;br /&gt;
*[[Left atrial myxoma]]&lt;br /&gt;
*[[Left bundle branch block]]&lt;br /&gt;
*[[Mitral regurgitation]]&lt;br /&gt;
*[[Mitral stenosis]]&lt;br /&gt;
*Mitral valve annular calcification&lt;br /&gt;
*Mitral valve commissural fusion&lt;br /&gt;
*[[Mitral valve prolapse]]&lt;br /&gt;
*[[Obesity]]&lt;br /&gt;
*[[Papillary muscle rupture]]&lt;br /&gt;
*Parachute mitral valve&lt;br /&gt;
*[[Pneumonia]]&lt;br /&gt;
*[[Prosthetic mitral valve]]&lt;br /&gt;
*[[Rheumatic heart disease]]&lt;br /&gt;
*Supra-valve mitral membrane&lt;br /&gt;
*[[Systemic hypertension]]&lt;br /&gt;
*Thickened [[chordae tendinae]]&lt;br /&gt;
*[[Thrombus]] (ball valve thrombus) in left atrium&lt;br /&gt;
&lt;br /&gt;
==References==&lt;br /&gt;
{{reflist|2}}&lt;br /&gt;
&lt;br /&gt;
[[Category:Cardiology]]&lt;br /&gt;
&lt;br /&gt;
{{WS}}&lt;br /&gt;
{{WH}}&lt;/div&gt;</summary>
		<author><name>Varun Kumar</name></author>
	</entry>
	<entry>
		<id>https://www.wikidoc.org/index.php?title=Left_atrial_enlargement_causes&amp;diff=642764</id>
		<title>Left atrial enlargement causes</title>
		<link rel="alternate" type="text/html" href="https://www.wikidoc.org/index.php?title=Left_atrial_enlargement_causes&amp;diff=642764"/>
		<updated>2012-04-17T15:25:33Z</updated>

		<summary type="html">&lt;p&gt;Varun Kumar: /* In alphabetical Order */&lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;{{CMG}}; {{AOEIC}} {{VK}}&lt;br /&gt;
&lt;br /&gt;
==Differential Diagnosis of Causes of Left Atrial Enlargement==&lt;br /&gt;
===In alphabetical Order===&lt;br /&gt;
*[[Alcoholism]]&lt;br /&gt;
*[[Ankylosing spondylitis]]&lt;br /&gt;
*[[Aortic regurgitation]]&lt;br /&gt;
*[[Aortic stenosis]]&lt;br /&gt;
*[[Atrial fibrillation]]&lt;br /&gt;
*[[Atrial septal defect]]&lt;br /&gt;
*[[Coarctation of the aorta]]&lt;br /&gt;
*[[Congestive heart failure]]&lt;br /&gt;
*[[Emphysema]]&lt;br /&gt;
*[[Hypertrophic cardiomyopathy]]&lt;br /&gt;
*Hypoplasia of mitral valve annulus which is a part of the spectrum of [[hypoplastic left heart syndrome]]&lt;br /&gt;
*[[Infective endocarditis]]&lt;br /&gt;
*[[Ischemic mitral regurgitation]]&lt;br /&gt;
*[[Left atrial myxoma]]&lt;br /&gt;
*[[Left bundle branch block]]&lt;br /&gt;
*[[Mitral regurgitation]]&lt;br /&gt;
*[[Mitral stenosis]]&lt;br /&gt;
*Mitral valve annular calcification&lt;br /&gt;
*Mitral valve commissural fusion&lt;br /&gt;
*[[Mitral valve prolapse]]&lt;br /&gt;
*[[Obesity]]&lt;br /&gt;
*[[Papillary muscle rupture]]&lt;br /&gt;
*Parachute mitral valve&lt;br /&gt;
*[[Pneumonia]]&lt;br /&gt;
*[[Prosthetic mitral valve]]&lt;br /&gt;
*[[Rheumatic heart disease]]&lt;br /&gt;
*Supra-valve mitral membrane&lt;br /&gt;
*[[Systemic hypertension]]&lt;br /&gt;
*Thickened [[chordae tendinae]]&lt;br /&gt;
*[[Thrombus]] (ball valve thrombus) in left atrium&lt;br /&gt;
&lt;br /&gt;
==References==&lt;br /&gt;
{{reflist|2}}&lt;br /&gt;
&lt;br /&gt;
[[Category:Cardiology]]&lt;br /&gt;
&lt;br /&gt;
{{WS}}&lt;br /&gt;
{{WH}}&lt;/div&gt;</summary>
		<author><name>Varun Kumar</name></author>
	</entry>
	<entry>
		<id>https://www.wikidoc.org/index.php?title=Left_atrial_enlargement_causes&amp;diff=642755</id>
		<title>Left atrial enlargement causes</title>
		<link rel="alternate" type="text/html" href="https://www.wikidoc.org/index.php?title=Left_atrial_enlargement_causes&amp;diff=642755"/>
		<updated>2012-04-17T15:02:35Z</updated>

		<summary type="html">&lt;p&gt;Varun Kumar: &lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;{{CMG}}; {{AOEIC}} {{VK}}&lt;br /&gt;
&lt;br /&gt;
==Differential Diagnosis of Causes of Left Atrial Enlargement==&lt;br /&gt;
===In alphabetical Order===&lt;br /&gt;
*[[Alcoholism]]&lt;br /&gt;
*[[Ankylosing spondylitis]]&lt;br /&gt;
*[[Aortic regurgitation]]&lt;br /&gt;
*[[Aortic stenosis]]&lt;br /&gt;
*[[Atrial fibrillation]]&lt;br /&gt;
*[[Atrial septal defect]]&lt;br /&gt;
*[[Coarctation of the aorta]]&lt;br /&gt;
*[[Congestive heart failure]]&lt;br /&gt;
*[[Emphysema]]&lt;br /&gt;
*[[Hypertrophic cardiomyopathy]]&lt;br /&gt;
*Hypoplasia of mitral valve annulus which is a part of the spectrum of [[hypoplastic left heart syndrome]]&lt;br /&gt;
*[[Infective endocarditis]]&lt;br /&gt;
*[[Ischemic mitral regurgitation]]&lt;br /&gt;
*[[Left atrial myxoma]]&lt;br /&gt;
*[[Left bundle branch block]]&lt;br /&gt;
*[[Mitral regurgitation]]&lt;br /&gt;
*[[Mitral stenosis]]&lt;br /&gt;
*Mitral valve annular calcification&lt;br /&gt;
*Mitral valve commissural fusion&lt;br /&gt;
*[[Obesity]]&lt;br /&gt;
*[[Papillary muscle rupture]]&lt;br /&gt;
*Parachute mitral valve&lt;br /&gt;
*[[Pneumonia]]&lt;br /&gt;
*[[Prosthetic mitral valve]]&lt;br /&gt;
*[[Rheumatic heart disease]]&lt;br /&gt;
*Supra-valve mitral membrane&lt;br /&gt;
*[[Systemic hypertension]]&lt;br /&gt;
*Thickened [[chordae tendinae]]&lt;br /&gt;
*[[Thrombus]] (ball valve thrombus) in left atrium&lt;br /&gt;
&lt;br /&gt;
==References==&lt;br /&gt;
{{reflist|2}}&lt;br /&gt;
&lt;br /&gt;
[[Category:Cardiology]]&lt;br /&gt;
&lt;br /&gt;
{{WS}}&lt;br /&gt;
{{WH}}&lt;/div&gt;</summary>
		<author><name>Varun Kumar</name></author>
	</entry>
	<entry>
		<id>https://www.wikidoc.org/index.php?title=Left_atrial_enlargement_causes&amp;diff=642754</id>
		<title>Left atrial enlargement causes</title>
		<link rel="alternate" type="text/html" href="https://www.wikidoc.org/index.php?title=Left_atrial_enlargement_causes&amp;diff=642754"/>
		<updated>2012-04-17T15:01:45Z</updated>

		<summary type="html">&lt;p&gt;Varun Kumar: Created page with &amp;quot;{{CMG}}; {{AOEIC}} {{VK}}  ==Differential Diagnosis of Causes of Left Atrial Enlargement== ===In alphabetical Order=== *Alcoholism *Ankylosing spondylitis *[[Aortic re...&amp;quot;&lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;{{CMG}}; {{AOEIC}} {{VK}}&lt;br /&gt;
&lt;br /&gt;
==Differential Diagnosis of Causes of Left Atrial Enlargement==&lt;br /&gt;
===In alphabetical Order===&lt;br /&gt;
*[[Alcoholism]]&lt;br /&gt;
*[[Ankylosing spondylitis]]&lt;br /&gt;
*[[Aortic regurgitation]]&lt;br /&gt;
*[[Aortic stenosis]]&lt;br /&gt;
*[[Atrial fibrillation]]&lt;br /&gt;
*[[Atrial septal defect]]&lt;br /&gt;
*[[Coarctation of the aorta]]&lt;br /&gt;
*[[Congestive heart failure]]&lt;br /&gt;
*[[Emphysema]]&lt;br /&gt;
*[[Hypertrophic cardiomyopathy]]&lt;br /&gt;
*Hypoplasia of mitral valve annulus which is a part of the spectrum of [[hypoplastic left heart syndrome]]&lt;br /&gt;
*[[Infective endocarditis]]&lt;br /&gt;
*[[Ischemic mitral regurgitation]]&lt;br /&gt;
*[[Left atrial myxoma]]&lt;br /&gt;
*[[Left bundle branch block]]&lt;br /&gt;
*[[Mitral regurgitation]]&lt;br /&gt;
*[[Mitral stenosis]]&lt;br /&gt;
*Mitral valve annular calcification&lt;br /&gt;
*Mitral valve commissural fusion&lt;br /&gt;
*[[Obesity]]&lt;br /&gt;
*[[Papillary muscle rupture]]&lt;br /&gt;
*Parachute mitral valve&lt;br /&gt;
*[[Pneumonia]]&lt;br /&gt;
*[[Prosthetic mitral valve]]&lt;br /&gt;
*[[Rheumatic heart disease]]&lt;br /&gt;
*Supra-valve mitral membrane&lt;br /&gt;
*[[Systemic hypertension]]&lt;br /&gt;
*Thickened [[chordae tendinae]]&lt;br /&gt;
*[[Thrombus]] (ball valve thrombus) in left atrium&lt;/div&gt;</summary>
		<author><name>Varun Kumar</name></author>
	</entry>
	<entry>
		<id>https://www.wikidoc.org/index.php?title=Systemic_hypertension&amp;diff=642740</id>
		<title>Systemic hypertension</title>
		<link rel="alternate" type="text/html" href="https://www.wikidoc.org/index.php?title=Systemic_hypertension&amp;diff=642740"/>
		<updated>2012-04-17T14:45:59Z</updated>

		<summary type="html">&lt;p&gt;Varun Kumar: ←Redirected page to Hypertension&lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;#REDIRECT [[Hypertension]]&lt;/div&gt;</summary>
		<author><name>Varun Kumar</name></author>
	</entry>
	<entry>
		<id>https://www.wikidoc.org/index.php?title=EKG_in_left_atrial_enlargement&amp;diff=642738</id>
		<title>EKG in left atrial enlargement</title>
		<link rel="alternate" type="text/html" href="https://www.wikidoc.org/index.php?title=EKG_in_left_atrial_enlargement&amp;diff=642738"/>
		<updated>2012-04-17T14:34:15Z</updated>

		<summary type="html">&lt;p&gt;Varun Kumar: moved EKG in left atrial enlargement to Left atrial enlargement electrocardiogram over redirect&lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;#REDIRECT [[Left atrial enlargement electrocardiogram]]&lt;/div&gt;</summary>
		<author><name>Varun Kumar</name></author>
	</entry>
	<entry>
		<id>https://www.wikidoc.org/index.php?title=Left_atrial_enlargement_electrocardiogram&amp;diff=642737</id>
		<title>Left atrial enlargement electrocardiogram</title>
		<link rel="alternate" type="text/html" href="https://www.wikidoc.org/index.php?title=Left_atrial_enlargement_electrocardiogram&amp;diff=642737"/>
		<updated>2012-04-17T14:34:15Z</updated>

		<summary type="html">&lt;p&gt;Varun Kumar: moved EKG in left atrial enlargement to Left atrial enlargement electrocardiogram over redirect&lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;{{Infobox_Disease |&lt;br /&gt;
  Name           = {{PAGENAME}} |&lt;br /&gt;
  Image          =  LAE.png|&lt;br /&gt;
  Caption        =  |&lt;br /&gt;
  Width          = 200px |&lt;br /&gt;
  DiseasesDB     =  |&lt;br /&gt;
  ICD10          =  |&lt;br /&gt;
  ICD9           =  |&lt;br /&gt;
  ICDO           =  |&lt;br /&gt;
  OMIM           =  |&lt;br /&gt;
  MedlinePlus    =  |&lt;br /&gt;
  eMedicineSubj  = med |&lt;br /&gt;
  eMedicineTopic = |&lt;br /&gt;
  MeshName       = Left+Atrial+Enlargement |&lt;br /&gt;
  MeshNumber     = |&lt;br /&gt;
}}&lt;br /&gt;
{{SI}}&lt;br /&gt;
&lt;br /&gt;
{{CMG}}; &#039;&#039;&#039;Associate Editor-In-Chief:&#039;&#039;&#039; {{CZ}}&lt;br /&gt;
&lt;br /&gt;
==Overview==&lt;br /&gt;
Left atrial enlargement may be observed among patients with pressure or volume overload of the [[left atrium]].&lt;br /&gt;
&lt;br /&gt;
== Differential Diagnosis of Left Atrial Enlargement==&lt;br /&gt;
* Atrial aneurysm&lt;br /&gt;
* [[Infective endocarditis]]&lt;br /&gt;
* [[Left heart failure]]&lt;br /&gt;
* [[Mitral regurgitation]]&lt;br /&gt;
* [[Mitral stenosis]]&lt;br /&gt;
* [[Mitral valve prolapse]]&lt;br /&gt;
* [[Myxedema]]&lt;br /&gt;
* [[Patent Ductus Arteriosus]]&lt;br /&gt;
* [[Ventricular septal defect]]&lt;br /&gt;
&lt;br /&gt;
==EKG in Left Atrial Enlargement==&lt;br /&gt;
&#039;&#039;&#039;1.&#039;&#039;&#039; [[LA enlargement]]: [[Left atrial enlargement]] produces a broad, bifid [[P wave]] in lead II (&#039;&#039;&#039;P mitrale&#039;&#039;&#039;) and enlarges the terminal negative portion of the P wave in VI.&lt;br /&gt;
&lt;br /&gt;
In &#039;&#039;&#039;lead I and/or II&#039;&#039;&#039; following may be seen:&lt;br /&gt;
*Bifid [[P wave]] with &amp;gt; 40 ms between the two peaks&lt;br /&gt;
*Total [[P wave]] duration &amp;gt; 110 ms &lt;br /&gt;
[[Image:P mitrale.gif|200px]]&lt;br /&gt;
&lt;br /&gt;
In &#039;&#039;&#039;lead V1&#039;&#039;&#039;, the following may be seen:&lt;br /&gt;
*Biphasic [[P wave]] with terminal negative portion &amp;gt; 40 ms duration (&amp;gt;0.04 sec or 1 small square)&lt;br /&gt;
*Biphasic [[P wave]] with terminal negative portion &amp;gt; 1mm deep &lt;br /&gt;
&lt;br /&gt;
[[Image:LAE-v1.png|Left atrial enlargement as seen in lead V1|400px]]&lt;br /&gt;
&lt;br /&gt;
==Examples of Left Atrial Enlargement on EKG==&lt;br /&gt;
&amp;lt;div align=&amp;quot;left&amp;quot;&amp;gt;&lt;br /&gt;
&amp;lt;gallery heights=&amp;quot;175&amp;quot; widths=&amp;quot;150&amp;quot;&amp;gt;&lt;br /&gt;
Image:left_atrial_enlargement.jpg|Left atrial enlargement&lt;br /&gt;
Image:LAE.png|12 lead EKG: Left atrial enlargement&lt;br /&gt;
&amp;lt;/gallery&amp;gt;&lt;br /&gt;
&amp;lt;/div&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&amp;lt;div align=&amp;quot;left&amp;quot;&amp;gt;&lt;br /&gt;
&amp;lt;gallery heights=&amp;quot;175&amp;quot; widths=&amp;quot;150&amp;quot;&amp;gt;&lt;br /&gt;
Image:LAE-v1.png|Left atrial enlargement as seen in lead V1.&lt;br /&gt;
Image:LAE_12lead.jpg|Left atrial enlargement, a 12 lead ECG&lt;br /&gt;
&amp;lt;/gallery&amp;gt;&lt;br /&gt;
&amp;lt;/div&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==See Also==&lt;br /&gt;
*[[Left atrial enlargement chest x-ray]]&lt;br /&gt;
{{Circulatory system pathology}}&lt;br /&gt;
{{Electrocardiography}}&lt;br /&gt;
&lt;br /&gt;
[[Category:Electrophysiology]]&lt;br /&gt;
[[Category:Cardiology]]&lt;br /&gt;
&lt;br /&gt;
{{WikiDoc Help Menu}}&lt;br /&gt;
{{WikiDoc Sources}}&lt;/div&gt;</summary>
		<author><name>Varun Kumar</name></author>
	</entry>
	<entry>
		<id>https://www.wikidoc.org/index.php?title=Left_atrial_enlargement_electrocardiogram&amp;diff=642734</id>
		<title>Left atrial enlargement electrocardiogram</title>
		<link rel="alternate" type="text/html" href="https://www.wikidoc.org/index.php?title=Left_atrial_enlargement_electrocardiogram&amp;diff=642734"/>
		<updated>2012-04-17T14:30:00Z</updated>

		<summary type="html">&lt;p&gt;Varun Kumar: /* Examples of Left Atrial Enlargement on EKG */&lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;{{Infobox_Disease |&lt;br /&gt;
  Name           = {{PAGENAME}} |&lt;br /&gt;
  Image          =  LAE.png|&lt;br /&gt;
  Caption        =  |&lt;br /&gt;
  Width          = 200px |&lt;br /&gt;
  DiseasesDB     =  |&lt;br /&gt;
  ICD10          =  |&lt;br /&gt;
  ICD9           =  |&lt;br /&gt;
  ICDO           =  |&lt;br /&gt;
  OMIM           =  |&lt;br /&gt;
  MedlinePlus    =  |&lt;br /&gt;
  eMedicineSubj  = med |&lt;br /&gt;
  eMedicineTopic = |&lt;br /&gt;
  MeshName       = Left+Atrial+Enlargement |&lt;br /&gt;
  MeshNumber     = |&lt;br /&gt;
}}&lt;br /&gt;
{{SI}}&lt;br /&gt;
&lt;br /&gt;
{{CMG}}; &#039;&#039;&#039;Associate Editor-In-Chief:&#039;&#039;&#039; {{CZ}}&lt;br /&gt;
&lt;br /&gt;
==Overview==&lt;br /&gt;
Left atrial enlargement may be observed among patients with pressure or volume overload of the [[left atrium]].&lt;br /&gt;
&lt;br /&gt;
== Differential Diagnosis of Left Atrial Enlargement==&lt;br /&gt;
* Atrial aneurysm&lt;br /&gt;
* [[Infective endocarditis]]&lt;br /&gt;
* [[Left heart failure]]&lt;br /&gt;
* [[Mitral regurgitation]]&lt;br /&gt;
* [[Mitral stenosis]]&lt;br /&gt;
* [[Mitral valve prolapse]]&lt;br /&gt;
* [[Myxedema]]&lt;br /&gt;
* [[Patent Ductus Arteriosus]]&lt;br /&gt;
* [[Ventricular septal defect]]&lt;br /&gt;
&lt;br /&gt;
==EKG in Left Atrial Enlargement==&lt;br /&gt;
&#039;&#039;&#039;1.&#039;&#039;&#039; [[LA enlargement]]: [[Left atrial enlargement]] produces a broad, bifid [[P wave]] in lead II (&#039;&#039;&#039;P mitrale&#039;&#039;&#039;) and enlarges the terminal negative portion of the P wave in VI.&lt;br /&gt;
&lt;br /&gt;
In &#039;&#039;&#039;lead I and/or II&#039;&#039;&#039; following may be seen:&lt;br /&gt;
*Bifid [[P wave]] with &amp;gt; 40 ms between the two peaks&lt;br /&gt;
*Total [[P wave]] duration &amp;gt; 110 ms &lt;br /&gt;
[[Image:P mitrale.gif|200px]]&lt;br /&gt;
&lt;br /&gt;
In &#039;&#039;&#039;lead V1&#039;&#039;&#039;, the following may be seen:&lt;br /&gt;
*Biphasic [[P wave]] with terminal negative portion &amp;gt; 40 ms duration (&amp;gt;0.04 sec or 1 small square)&lt;br /&gt;
*Biphasic [[P wave]] with terminal negative portion &amp;gt; 1mm deep &lt;br /&gt;
&lt;br /&gt;
[[Image:LAE-v1.png|Left atrial enlargement as seen in lead V1|400px]]&lt;br /&gt;
&lt;br /&gt;
==Examples of Left Atrial Enlargement on EKG==&lt;br /&gt;
&amp;lt;div align=&amp;quot;left&amp;quot;&amp;gt;&lt;br /&gt;
&amp;lt;gallery heights=&amp;quot;175&amp;quot; widths=&amp;quot;150&amp;quot;&amp;gt;&lt;br /&gt;
Image:left_atrial_enlargement.jpg|Left atrial enlargement&lt;br /&gt;
Image:LAE.png|12 lead EKG: Left atrial enlargement&lt;br /&gt;
&amp;lt;/gallery&amp;gt;&lt;br /&gt;
&amp;lt;/div&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&amp;lt;div align=&amp;quot;left&amp;quot;&amp;gt;&lt;br /&gt;
&amp;lt;gallery heights=&amp;quot;175&amp;quot; widths=&amp;quot;150&amp;quot;&amp;gt;&lt;br /&gt;
Image:LAE-v1.png|Left atrial enlargement as seen in lead V1.&lt;br /&gt;
Image:LAE_12lead.jpg|Left atrial enlargement, a 12 lead ECG&lt;br /&gt;
&amp;lt;/gallery&amp;gt;&lt;br /&gt;
&amp;lt;/div&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==See Also==&lt;br /&gt;
*[[Left atrial enlargement chest x-ray]]&lt;br /&gt;
{{Circulatory system pathology}}&lt;br /&gt;
{{Electrocardiography}}&lt;br /&gt;
&lt;br /&gt;
[[Category:Electrophysiology]]&lt;br /&gt;
[[Category:Cardiology]]&lt;br /&gt;
&lt;br /&gt;
{{WikiDoc Help Menu}}&lt;br /&gt;
{{WikiDoc Sources}}&lt;/div&gt;</summary>
		<author><name>Varun Kumar</name></author>
	</entry>
	<entry>
		<id>https://www.wikidoc.org/index.php?title=Left_atrial_enlargement_electrocardiogram&amp;diff=642731</id>
		<title>Left atrial enlargement electrocardiogram</title>
		<link rel="alternate" type="text/html" href="https://www.wikidoc.org/index.php?title=Left_atrial_enlargement_electrocardiogram&amp;diff=642731"/>
		<updated>2012-04-17T14:28:09Z</updated>

		<summary type="html">&lt;p&gt;Varun Kumar: /* Chest X-ray in Left Atrial Enlargement */&lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;{{Infobox_Disease |&lt;br /&gt;
  Name           = {{PAGENAME}} |&lt;br /&gt;
  Image          =  LAE.png|&lt;br /&gt;
  Caption        =  |&lt;br /&gt;
  Width          = 200px |&lt;br /&gt;
  DiseasesDB     =  |&lt;br /&gt;
  ICD10          =  |&lt;br /&gt;
  ICD9           =  |&lt;br /&gt;
  ICDO           =  |&lt;br /&gt;
  OMIM           =  |&lt;br /&gt;
  MedlinePlus    =  |&lt;br /&gt;
  eMedicineSubj  = med |&lt;br /&gt;
  eMedicineTopic = |&lt;br /&gt;
  MeshName       = Left+Atrial+Enlargement |&lt;br /&gt;
  MeshNumber     = |&lt;br /&gt;
}}&lt;br /&gt;
{{SI}}&lt;br /&gt;
&lt;br /&gt;
{{CMG}}; &#039;&#039;&#039;Associate Editor-In-Chief:&#039;&#039;&#039; {{CZ}}&lt;br /&gt;
&lt;br /&gt;
==Overview==&lt;br /&gt;
Left atrial enlargement may be observed among patients with pressure or volume overload of the [[left atrium]].&lt;br /&gt;
&lt;br /&gt;
== Differential Diagnosis of Left Atrial Enlargement==&lt;br /&gt;
* Atrial aneurysm&lt;br /&gt;
* [[Infective endocarditis]]&lt;br /&gt;
* [[Left heart failure]]&lt;br /&gt;
* [[Mitral regurgitation]]&lt;br /&gt;
* [[Mitral stenosis]]&lt;br /&gt;
* [[Mitral valve prolapse]]&lt;br /&gt;
* [[Myxedema]]&lt;br /&gt;
* [[Patent Ductus Arteriosus]]&lt;br /&gt;
* [[Ventricular septal defect]]&lt;br /&gt;
&lt;br /&gt;
==EKG in Left Atrial Enlargement==&lt;br /&gt;
&#039;&#039;&#039;1.&#039;&#039;&#039; [[LA enlargement]]: [[Left atrial enlargement]] produces a broad, bifid [[P wave]] in lead II (&#039;&#039;&#039;P mitrale&#039;&#039;&#039;) and enlarges the terminal negative portion of the P wave in VI.&lt;br /&gt;
&lt;br /&gt;
In &#039;&#039;&#039;lead I and/or II&#039;&#039;&#039; following may be seen:&lt;br /&gt;
*Bifid [[P wave]] with &amp;gt; 40 ms between the two peaks&lt;br /&gt;
*Total [[P wave]] duration &amp;gt; 110 ms &lt;br /&gt;
[[Image:P mitrale.gif|200px]]&lt;br /&gt;
&lt;br /&gt;
In &#039;&#039;&#039;lead V1&#039;&#039;&#039;, the following may be seen:&lt;br /&gt;
*Biphasic [[P wave]] with terminal negative portion &amp;gt; 40 ms duration (&amp;gt;0.04 sec or 1 small square)&lt;br /&gt;
*Biphasic [[P wave]] with terminal negative portion &amp;gt; 1mm deep &lt;br /&gt;
&lt;br /&gt;
[[Image:LAE-v1.png|Left atrial enlargement as seen in lead V1|400px]]&lt;br /&gt;
&lt;br /&gt;
==Examples of Left Atrial Enlargement on EKG==&lt;br /&gt;
&amp;lt;div align=&amp;quot;left&amp;quot;&amp;gt;&lt;br /&gt;
&amp;lt;gallery heights=&amp;quot;175&amp;quot; widths=&amp;quot;150&amp;quot;&amp;gt;&lt;br /&gt;
Image:left_atrial_enlargement.jpg|Left atrial enlargement&lt;br /&gt;
Image:LAE.png|12 lead EKG: Left atrial enlargement&lt;br /&gt;
&amp;lt;/gallery&amp;gt;&lt;br /&gt;
&amp;lt;/div&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&amp;lt;div align=&amp;quot;left&amp;quot;&amp;gt;&lt;br /&gt;
&amp;lt;gallery heights=&amp;quot;175&amp;quot; widths=&amp;quot;150&amp;quot;&amp;gt;&lt;br /&gt;
Image:LAE-v1.png|Left atrial enlargement as seen in lead V1.&lt;br /&gt;
Image:LAE_12lead.jpg|Left atrial enlargement, a 12 lead ECG&lt;br /&gt;
&amp;lt;/gallery&amp;gt;&lt;br /&gt;
&amp;lt;/div&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
{{Circulatory system pathology}}&lt;br /&gt;
{{Electrocardiography}}&lt;br /&gt;
&lt;br /&gt;
[[Category:Electrophysiology]]&lt;br /&gt;
[[Category:Cardiology]]&lt;br /&gt;
&lt;br /&gt;
{{WikiDoc Help Menu}}&lt;br /&gt;
{{WikiDoc Sources}}&lt;/div&gt;</summary>
		<author><name>Varun Kumar</name></author>
	</entry>
	<entry>
		<id>https://www.wikidoc.org/index.php?title=Left_atrial_enlargement_chest_x-ray&amp;diff=642728</id>
		<title>Left atrial enlargement chest x-ray</title>
		<link rel="alternate" type="text/html" href="https://www.wikidoc.org/index.php?title=Left_atrial_enlargement_chest_x-ray&amp;diff=642728"/>
		<updated>2012-04-17T14:23:55Z</updated>

		<summary type="html">&lt;p&gt;Varun Kumar: &lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;{{CMG}}; {{AOEIC}} {{CZ}}; {{VK}}&lt;br /&gt;
==Chest X-Ray==&lt;br /&gt;
Chest x-ray findings of left atrial enlargement are:&lt;br /&gt;
*Double density sign: Occur when the right side of the left atrium pushes behind the right atrial border, appearing as a double density. If large enough it can actually reach beyond the border of the right atrium. &lt;br /&gt;
*Convex [[left atria appendage]]: usually reflect prior [[rheumatic heart disease]]&lt;br /&gt;
*Splaying of the [[carina]]&lt;br /&gt;
*Posterior displacement of the left main stem bronchus on lateral radiograph&lt;br /&gt;
*Superior displacement of the left main stem bronchus on frontal view&lt;br /&gt;
*Posterior displacement of a barium filled oesophagus or [[nasogastric tube]]&lt;br /&gt;
&lt;br /&gt;
Images shown below are courtesy of Radiopedia.com.&lt;br /&gt;
&lt;br /&gt;
&amp;lt;div align=&amp;quot;left&amp;quot;&amp;gt;&lt;br /&gt;
&amp;lt;gallery heights=&amp;quot;175&amp;quot; widths=&amp;quot;175&amp;quot;&amp;gt;&lt;br /&gt;
Image:Left-atrial-enlargement-001.jpg|Double density sign&lt;br /&gt;
Image:Left-atrial-enlargement-002.jpg|Same patient &amp;amp; the same image. Double density sign. Image&#039;s modified for more contrast and better visualization.&lt;br /&gt;
Image:Left atrial enlargement with splaying of carina.jpg|Aside from the dirty lung due to [[emphysema]] and pneumonic infiltration in the lower right field you can notice a marked enlargement of the left atrium with splaying of the carina.&lt;br /&gt;
&amp;lt;/gallery&amp;gt;&lt;br /&gt;
&amp;lt;/div&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==References==&lt;br /&gt;
{{reflist|2}}&lt;br /&gt;
&lt;br /&gt;
{{WS}}&lt;br /&gt;
{{WH}}&lt;br /&gt;
&lt;br /&gt;
[[Category:Cardiology]]&lt;br /&gt;
[[Category:Radiology]]&lt;/div&gt;</summary>
		<author><name>Varun Kumar</name></author>
	</entry>
	<entry>
		<id>https://www.wikidoc.org/index.php?title=File:Left_atrial_enlargement_with_splaying_of_carina.jpg&amp;diff=642727</id>
		<title>File:Left atrial enlargement with splaying of carina.jpg</title>
		<link rel="alternate" type="text/html" href="https://www.wikidoc.org/index.php?title=File:Left_atrial_enlargement_with_splaying_of_carina.jpg&amp;diff=642727"/>
		<updated>2012-04-17T14:22:44Z</updated>

		<summary type="html">&lt;p&gt;Varun Kumar: &lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;&lt;/div&gt;</summary>
		<author><name>Varun Kumar</name></author>
	</entry>
	<entry>
		<id>https://www.wikidoc.org/index.php?title=Left_atrial_enlargement_chest_x-ray&amp;diff=642718</id>
		<title>Left atrial enlargement chest x-ray</title>
		<link rel="alternate" type="text/html" href="https://www.wikidoc.org/index.php?title=Left_atrial_enlargement_chest_x-ray&amp;diff=642718"/>
		<updated>2012-04-17T14:00:37Z</updated>

		<summary type="html">&lt;p&gt;Varun Kumar: Created page with &amp;quot;{{CMG}}; {{AOEIC}} {{VK}} ==Chest X-Ray== Chest x-ray findings of left atrial enlargement are: *Double density sign: Occur when the right side of the left atrium pushes behind...&amp;quot;&lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;{{CMG}}; {{AOEIC}} {{VK}}&lt;br /&gt;
==Chest X-Ray==&lt;br /&gt;
Chest x-ray findings of left atrial enlargement are:&lt;br /&gt;
*Double density sign: Occur when the right side of the left atrium pushes behind the right atrial border, appearing as a double density. If large enough it can actually reach beyond the border of the right atrium. &lt;br /&gt;
*Convex [[left atria appendage]]: usually reflect prior [[rheumatic heart disease]]&lt;br /&gt;
*Splaying of the [[carina]]&lt;br /&gt;
*Posterior displacement of the left main stem bronchus on lateral radiograph&lt;br /&gt;
*Superior displacement of the left main stem bronchus on frontal view&lt;br /&gt;
*Posterior displacement of a barium filled oesophagus or [[nasogastric tube]]&lt;br /&gt;
&lt;br /&gt;
==References==&lt;br /&gt;
{{reflist|2}}&lt;br /&gt;
&lt;br /&gt;
{{WS}}&lt;br /&gt;
{{WH}}&lt;br /&gt;
&lt;br /&gt;
[[Category:Cardiology]]&lt;br /&gt;
[[Category:Radiology]]&lt;/div&gt;</summary>
		<author><name>Varun Kumar</name></author>
	</entry>
	<entry>
		<id>https://www.wikidoc.org/index.php?title=Carina&amp;diff=642714</id>
		<title>Carina</title>
		<link rel="alternate" type="text/html" href="https://www.wikidoc.org/index.php?title=Carina&amp;diff=642714"/>
		<updated>2012-04-17T13:56:23Z</updated>

		<summary type="html">&lt;p&gt;Varun Kumar: ←Redirected page to Carina of trachea&lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;#REDIRECT [[Carina of trachea]]&lt;/div&gt;</summary>
		<author><name>Varun Kumar</name></author>
	</entry>
	<entry>
		<id>https://www.wikidoc.org/index.php?title=Mitral_regurgitation_overview&amp;diff=642420</id>
		<title>Mitral regurgitation overview</title>
		<link rel="alternate" type="text/html" href="https://www.wikidoc.org/index.php?title=Mitral_regurgitation_overview&amp;diff=642420"/>
		<updated>2012-04-16T03:43:05Z</updated>

		<summary type="html">&lt;p&gt;Varun Kumar: &lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;{{Mitral regurgitation}}&lt;br /&gt;
{{CMG}}; &#039;&#039;&#039;Associate Editor-In-Chief:&#039;&#039;&#039; {{CZ}}; [[Varun Kumar]], M.B.B.S.; [[Lakshmi Gopalakrishnan]], M.B.B.S; [[User:Mohammed Sbeih|Mohammed A. Sbeih, M.D.]] [mailto:msbeih@perfuse.org].&lt;br /&gt;
==Overview==&lt;br /&gt;
&#039;&#039;&#039;Mitral regurgitation&#039;&#039;&#039; (&#039;&#039;&#039;MR&#039;&#039;&#039;), &#039;&#039;&#039;mitral insufficiency&#039;&#039;&#039; or &#039;&#039;&#039;mitral incompetence&#039;&#039;&#039; is  a disorder of the [[heart]] in which  the [[mitral valve]] does not close properly when the heart pumps out [[blood]].  It is the abnormal leaking of blood from the [[left ventricle]],  through the mitral valve,  and into the [[left atrium]], when the left ventricle contracts, i.e. there is [[Regurgitation (circulation)|regurgitation]] of blood back into the left atrium &amp;lt;ref&amp;gt;[http://www.mountsinai.org/Other/Diseases/Mitral%20valve%20regurgitation Mitral valve regurgitation] at [[Mount Sinai Hospital, New York|Mount Sinai Hospital]]&amp;lt;/ref&amp;gt;. MR is the most common form of [[valvular heart disease]] &amp;lt;ref name=&#039;MedlineMitChron2008&#039;&amp;gt;{{cite encyclopedia |last=Weinrauch |first=LA |author= |authorlink= |coauthors= |editor=|encyclopedia=Medline Plus Encyclopedia |title=Mitral regurgitation - chronic |url=http://www.nlm.nih.gov/medlineplus/ency/article/000176.htm |accessdate=2009-12-04 |edition=|date=2008-05-12 |year= |publisher=U.S. National Library of Medicine and National Institutes of Health |volume= |location= |id= |doi= |pages= |quote= }}&amp;lt;/ref&amp;gt;.&lt;br /&gt;
Diseases that weaken or damage the valve or the heart tissue around the valve cause mitral regurgitation.&lt;br /&gt;
After age 55, some degree of mitral regurgitation is found in almost 20% of men and women who have an echocardiogram.&lt;br /&gt;
[[Image:Mitral Regurgitation.png|thumb|left|200px|&#039;&#039;&#039;Mitral regurgitation (schematic drawing)&#039;&#039;&#039;&amp;lt;br/&amp;gt;During systole, contraction of the left ventricle causes abnormal backflow (arrow) into the left atrium.&amp;lt;br/&amp;gt;1 [[Mitral valve]]&amp;lt;br/&amp;gt;2 [[Left Ventricle]]&amp;lt;br/&amp;gt;3 [[Left Atrium]]&amp;lt;br/&amp;gt;4 [[Aorta]]]]&lt;br /&gt;
&lt;br /&gt;
==Anatomy==&lt;br /&gt;
The mitral valve is typically 4–6 cm² in area. It has two cusps, or leaflets (the anteromedial leaflet and the posterolateral leaflet).&lt;br /&gt;
&lt;br /&gt;
==Pathophysiology==&lt;br /&gt;
Mitral regurgitation is due to either perforation or prolapse of the leaflets, dilation of the mitral annulus or rupture of the papillary muscles or chordae tendineae.  There are several phases of mitral regurgitation (acute, chronic compensated, and chronic decompensated). In the acute phase, the volume and pressure overload in the left atrium is transmitted backward into the pulmonary vasculature to cause an elevation of the [[pulomanry capillary wedge pressure]] which causes [[dyspnea]], [[PND]], [[orthopnea]] and [[rales]].  During the chronic compensated phase of mitral regurgitation, the left ventricle maintains forward [[cardiac output]] by filling with a larger volume of blood than usual to accomodate the fact that a portion of the blood will go backwards into the left atrium.  In the decompensated phase, the left ventricle begins to dilate and fail. The markers of decompensation are as follows:&lt;br /&gt;
&lt;br /&gt;
# &#039;&#039;&#039;Left ventricular end-diastolic dimension greater than 70 mm&#039;&#039;&#039;&lt;br /&gt;
# &#039;&#039;&#039;Left ventricular end-systolic dimension greater than 45 to 47 mm&#039;&#039;&#039;&lt;br /&gt;
# &#039;&#039;&#039;Left ventricular [[ejection fraction]] (LVEF) less than 50 to 55 percent&#039;&#039;&#039;&lt;br /&gt;
&lt;br /&gt;
==Epidemiology and Demographics==&lt;br /&gt;
The incidence of mitral regurgitation is approximately 2% in a modern Western population. In the past, rheumatic heart disease was the leading cause of mitral regurgitation in Western countries, but now [[mitral valve prolapse]] is the leading cause and accounts for 45% of cases in Western countries.  In Asia, North Africa, and the Middle East, and among some immagrant populations in the US, rheumatic heart disease remains the leading cause of mitral regurgitation.&lt;br /&gt;
&lt;br /&gt;
Overall, mitral regurgitation affects both males and females equally &amp;lt;ref&amp;gt;[http://www.clevelandclinicmeded.com/medicalpubs/diseasemanagement/cardiology/mitral-valve-disease/ The Cleveland Clinic Center for Continuing Education &amp;gt; Mitral Valve Disease: Stenosis and Regurgitation] Authors:  Ronan J. Curtin and Brian P. Griffin. Retrieved September 2010&amp;lt;/ref&amp;gt;. However, there are some minor imbalances when age is considered. In patients younger than 20 years, there is a male preponderance, and the severity of involvement is greater in males over the age of 50.&lt;br /&gt;
&lt;br /&gt;
==Complications==&lt;br /&gt;
Mild mitral regurgitation regurgitation is associated with few if any complications. However, when severe, mitral regurgitation may lead to development of (in alphabetical order):&lt;br /&gt;
*[[Atrial Fibrillation]]&lt;br /&gt;
*[[Cardiogenic Shock]]&lt;br /&gt;
*[[Endocarditis]]&lt;br /&gt;
*[[Pulmonary Edema]]&lt;br /&gt;
*[[Pulmonary Hypertension]]&lt;br /&gt;
*[[Right Heart Failure]]&lt;br /&gt;
*[[Thromboembolism]]-[[Stroke]]&lt;br /&gt;
&lt;br /&gt;
==Prognosis==&lt;br /&gt;
*Acute mitral regurgitation with [[cardiogenic shock]] is associated with an operative mortality of 80%.&lt;br /&gt;
*Patients with asymptomatic chronic severe [[mitral regurgitation]] have a high likelihood of developing symptoms or LV dysfunction over the course of 6 to 10 years &amp;lt;ref name=&amp;quot;pmid8875918&amp;quot;&amp;gt;{{cite journal |author=Ling LH, Enriquez-Sarano M, Seward JB, Tajik AJ, Schaff HV, Bailey KR, Frye RL |title=Clinical outcome of mitral regurgitation due to flail leaflet |journal=[[The New England Journal of Medicine]] |volume=335 |issue=19 |pages=1417–23 |year=1996 |month=November |pmid=8875918 |doi=10.1056/NEJM199611073351902|url=http://dx.doi.org/10.1056/NEJM199611073351902 |accessdate=2011-03-06}}&amp;lt;/ref&amp;gt; &amp;lt;ref name=&amp;quot;pmid15745978&amp;quot;&amp;gt;{{cite journal |author=Enriquez-Sarano M, Avierinos JF, Messika-Zeitoun D, Detaint D, Capps M, Nkomo V, Scott C, Schaff HV, Tajik AJ |title=Quantitative determinants of the outcome of asymptomatic mitral regurgitation |journal=[[The New England Journal of Medicine]] |volume=352 |issue=9 |pages=875–83 |year=2005 |month=March |pmid=15745978 |doi=10.1056/NEJMoa041451 |url=http://dx.doi.org/10.1056/NEJMoa041451|accessdate=2011-03-06}}&amp;lt;/ref&amp;gt; &amp;lt;ref name=&amp;quot;pmid16651470&amp;quot;&amp;gt;{{cite journal |author=Rosenhek R, Rader F, Klaar U, Gabriel H, Krejc M, Kalbeck D, Schemper M, Maurer G, Baumgartner H|title=Outcome of watchful waiting in asymptomatic severe mitral regurgitation |journal=[[Circulation]] |volume=113 |issue=18 |pages=2238–44 |year=2006 |month=May |pmid=16651470|doi=10.1161/CIRCULATIONAHA.105.599175 |url=http://circ.ahajournals.org/cgi/pmidlookup?view=long&amp;amp;pmid=16651470 |accessdate=2011-03-06}}&amp;lt;/ref&amp;gt;. However, the incidence of [[sudden death]] in asymptomatic patients with normal LV function varies widely among these studies.&lt;br /&gt;
&lt;br /&gt;
*The prognosis is poor in patients with severe symptomatic [[mitral regurgitation]] with an eight year survival rate of only 33% in the absence of surgical intervention. [[Heart failure]] being the common cause with [[sudden death]] attributing to ventricular arrhythmia &amp;lt;ref name=&amp;quot;pmid1936025&amp;quot;&amp;gt;{{cite journal |author=Delahaye JP, Gare JP, Viguier E, Delahaye F, De Gevigney G, Milon H |title=Natural history of severe mitral regurgitation |journal=[[European Heart Journal]] |volume=12 Suppl B |issue= |pages=5–9 |year=1991 |month=July |pmid=1936025 |doi=|url=http://eurheartj.oxfordjournals.org/cgi/pmidlookup?view=long&amp;amp;pmid=1936025 |accessdate=2011-03-06}}&amp;lt;/ref&amp;gt;.&lt;br /&gt;
&lt;br /&gt;
*In patients with severe mitral regurgitation due to a ﬂail [[posterior mitral leaﬂet]], 90% of patients are either dead or require mitral valve surgery by 10 years with the mortality rate in patients with severe mitral regurgitation being 6% to 7% per year. However, the risk of death is higher in those patients with a [[left ventricular ejection fraction]] &amp;lt;60% or with [[NYHA]] functional class III–IV symptoms &amp;lt;ref name=&amp;quot;pmid8875918&amp;quot;&amp;gt;{{cite journal |author=Ling LH, Enriquez-Sarano M, Seward JB, Tajik AJ, Schaff HV, Bailey KR, Frye RL |title=Clinical outcome of mitral regurgitation due to flail leaflet |journal=[[The New England Journal of Medicine]] |volume=335 |issue=19 |pages=1417–23 |year=1996 |month=November |pmid=8875918|doi=10.1056/NEJM199611073351902 |url=http://dx.doi.org/10.1056/NEJM199611073351902 |accessdate=2011-03-06}}&amp;lt;/ref&amp;gt; &amp;lt;ref name=&amp;quot;pmid9918527&amp;quot;&amp;gt;{{cite journal |author=Tribouilloy CM, Enriquez-Sarano M, Schaff HV, Orszulak TA, Bailey KR, Tajik AJ, Frye RL |title=Impact of preoperative symptoms on survival after surgical correction of organic mitral regurgitation: rationale for optimizing surgical indications |journal=[[Circulation]] |volume=99 |issue=3 |pages=400–5 |year=1999 |month=January |pmid=9918527 |doi=|url=http://circ.ahajournals.org/cgi/pmidlookup?view=long&amp;amp;pmid=9918527 |accessdate=2011-03-06}}&amp;lt;/ref&amp;gt;. &lt;br /&gt;
&lt;br /&gt;
*Severe symptoms also predict a poor outcome after mitral valve repair or replacement. Postoperative survival rates in patients with NYHA functional class III–IV symptoms at 5 and 10 years are 73 ± 3% and 48 ± 4%, respectively. While in patients with NYHA functional class I/II symptoms before surgery survival rates at 5 and 10 years are 90 ± 2% and 76 ± 5%, respectively &amp;lt;ref name=&amp;quot;pmid9918527&amp;quot;&amp;gt;{{cite journal |author=Tribouilloy CM, Enriquez-Sarano M, Schaff HV, Orszulak TA, Bailey KR, Tajik AJ, Frye RL |title=Impact of preoperative symptoms on survival after surgical correction of organic mitral regurgitation: rationale for optimizing surgical indications |journal=[[Circulation]] |volume=99 |issue=3|pages=400–5 |year=1999 |month=January |pmid=9918527 |doi= |url=http://circ.ahajournals.org/cgi/pmidlookup?view=long&amp;amp;pmid=9918527 |accessdate=2011-03-06}}&amp;lt;/ref&amp;gt;. &lt;br /&gt;
&lt;br /&gt;
==Causes==&lt;br /&gt;
Mitral regurgitation is due to either perforation or prolapse of the leaflets, dilation of the mitral annulus or rupture of the [[papillary muscle rupture|papillary muscles]] or chordae tendineae.  There are several phases of mitral regurgitation (acute, chronic compensated, and chronic decompensated).&lt;br /&gt;
===Acute Mitral Regurgitation===&lt;br /&gt;
*[[Heart attack]] or [[acute MI]]: Dysfunction or injury to the mitral valve following a heart attack. [[Papillary muscle rupture]] or dysfunction that is associated with [[ST elevation myocardial infarction]].&lt;br /&gt;
*[[Endocarditis]]: The infaction may cause perforation of the leaflet, erosion of the surrounding structures, or a vagetation may not permit the leaflets to coapt.&lt;br /&gt;
*Trauma&lt;br /&gt;
&lt;br /&gt;
===Chronic Mitral Regurgitation===&lt;br /&gt;
*[[Mitral valve prolapse]]:  This disorder now accounts for 45% of cases of mitral regurgitation in the Western world.&lt;br /&gt;
*[[Ischemic heart disease]] / [[Coronary artery disease]]:  This can be due to either papillary muscle dysfunction or left ventricular dilation and functional mitral regurgitation.  Ischemia is responsible for 3% to 25% of MR cases.&lt;br /&gt;
*[[Rheumatic heart disease]]:  In the past, this was the most common cause of MR in the Western world. In developing countries, [[rheumatic heart disease]] remains the most common cause.&lt;br /&gt;
&lt;br /&gt;
==Differentiating Mitral Regurgitation From Other Diseases==&lt;br /&gt;
The blowing [[holosystolic murmur]] of mitral regurgitation must be distinguished from [[tricuspid regurgitation]] and a [[ventricular septal defect]].&lt;br /&gt;
&lt;br /&gt;
==Diagnosis==&lt;br /&gt;
===History and Symptoms===&lt;br /&gt;
Acute and decompensated mitral insufficiency is associated with symptoms of congestive heart failure including [[dyspnea]], [[PND]], [[orthopnea]], and [[exercise intolerance]].  In chronic compensated mitral regurgitation there may be few symptoms.&lt;br /&gt;
&lt;br /&gt;
===Physical Examination===&lt;br /&gt;
Chronic compensated mitral regurgitation causes a blowing [[holosystolic]] murmur which radiates to the axilla.  The severity of the murmur is not associated with the volume of regurgitation.  A [[third heart sound]] ([[S3]]) may be present.  In patients with mitral regurgitation due to [[mitral valve prolapse]], a click may be present.&lt;br /&gt;
&lt;br /&gt;
===Chest X-Ray===&lt;br /&gt;
The chest [[x-ray]] in individuals with chronic [[mitral regurgitation]] is characterized by enlargement of the [[left atrium]] and the [[left ventricle]].  In acute mitral regurgitation, [[pulmonary edema]] is present, but the heart is not enlarged.&lt;br /&gt;
&lt;br /&gt;
===Ventriculogram===&lt;br /&gt;
Echocardiography is the primary imaging modality that is used to diagnose and serially evaluate mitral regurgitation, but the ventriculogram can also be used to quantitate the magnitude of mitral regurgitation.&lt;br /&gt;
&lt;br /&gt;
===Electrocardiogram===&lt;br /&gt;
In severe cases of mitral regurgitation, [[left ventricular hypertrophy with strain]]; [[left atrial enlargement]], and signs of [[pulmonary hypertension]] may be observed on the resting EKG. Chronic mitral regurgitation is associated with an increased risk for [[atrial fibrillation]].&lt;br /&gt;
&lt;br /&gt;
===Echocardiography===&lt;br /&gt;
Transthoracic echocardiography should be performed in a patient with suspected mitral regurgitation to confirm the diagnosis and to establish the baseline severity of disease. It should then be performed to monitor the course of disease over time. Color doppler flow on the transthoracic echocardiogram (TTE) will reveal a jet of blood flowing from the left ventricle into the left atrium during [[ventricular systole]]. Echocardiographic features that suggest severe mitral regurgitation include systolic reversal of flow in the pulmonary veins and filling of the entire left atrial cavity by the regurgitant jet of MR.&lt;br /&gt;
&lt;br /&gt;
===Cardiac Catheterization===&lt;br /&gt;
In patients with mitral regurgitation who have risk factors for Coronary artery disease, such as advanced age, hypercholesterolemia, and hypertension, or when there is a suspicion that mitral regurgitation is ischemic in origin, coronary angiography should be performed before surgery.&lt;br /&gt;
&lt;br /&gt;
===Assessment of Severity===&lt;br /&gt;
The severity of MR can be assessed by both clinical and echocardiographic criteria. Careful history is important to establish an estimate of baseline exercise tolerance of the patient.&lt;br /&gt;
&lt;br /&gt;
The 2006 [[ACC]]/[[AHA]] guidelines included recommendations for echocardiographic monitoring in asymptomatic patients with chronic MR &amp;lt;ref name=&amp;quot;pmid18820172&amp;quot;&amp;gt;{{cite journal| author=Bonow RO, Carabello BA, Chatterjee K, de Leon AC, Faxon DP, Freed MD et al.| title=2008 Focused update incorporated into the ACC/AHA 2006 guidelines for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 1998 Guidelines for the Management of Patients With Valvular Heart Disease): endorsed by the Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons. | journal=Circulation | year= 2008 | volume= 118 | issue= 15 | pages= e523-661 | pmid=18820172| doi=10.1161/CIRCULATIONAHA.108.190748 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;amp;tool=sumsearch.org/cite&amp;amp;retmode=ref&amp;amp;cmd=prlinks&amp;amp;id=18820172  }} &amp;lt;/ref&amp;gt;. Echocardiography is performed to assess the left ventricular ejection fraction and end-systolic dimension.&lt;br /&gt;
&lt;br /&gt;
&amp;lt;table border=&amp;quot;1&amp;quot; cellpadding=&amp;quot;5&amp;quot; cellspacing=&amp;quot;0&amp;quot; align=&amp;quot;left&amp;quot;&amp;gt;&lt;br /&gt;
&amp;lt;caption&amp;gt;&#039;&#039;&#039;Determination of the degree of mitral regurgitation&#039;&#039;&#039;&amp;lt;/caption&amp;gt;&lt;br /&gt;
&amp;lt;tr&amp;gt;&lt;br /&gt;
&amp;lt;th style=&amp;quot;background:#efefef;&amp;quot;&amp;gt;Degree of mitral regurgitation&amp;lt;/th&amp;gt;&lt;br /&gt;
&amp;lt;th style=&amp;quot;background:#efefef;&amp;quot;&amp;gt;Regurgitant fraction&amp;lt;/th&amp;gt;&lt;br /&gt;
&amp;lt;th style=&amp;quot;background:#efefef;&amp;quot; width=&amp;quot;100px&amp;quot;&amp;gt;Regurgitant Orifice area&amp;lt;/th&amp;gt;&lt;br /&gt;
&amp;lt;/tr&amp;gt;&lt;br /&gt;
&amp;lt;tr&amp;gt;&amp;lt;td&amp;gt;Mild mitral regurgitation&amp;lt;/td&amp;gt;&amp;lt;td&amp;gt;&amp;lt; 20 percent&amp;lt;/td&amp;gt;&amp;lt;/tr&amp;gt;&lt;br /&gt;
&amp;lt;tr&amp;gt;&amp;lt;td&amp;gt;Moderate mitral regurgitation&amp;lt;/td&amp;gt;&amp;lt;td&amp;gt;20 - 40 percent&amp;lt;/td&amp;gt;&amp;lt;/tr&amp;gt;&lt;br /&gt;
&amp;lt;tr&amp;gt;&amp;lt;td&amp;gt;Moderate to severe mitral regurgitation&amp;lt;/td&amp;gt;&amp;lt;td&amp;gt;40 - 60 percent&amp;lt;/td&amp;gt;&amp;lt;/tr&amp;gt;&lt;br /&gt;
&amp;lt;tr&amp;gt;&amp;lt;td&amp;gt;Severe mitral regurgitation&amp;lt;/td&amp;gt;&amp;lt;td&amp;gt;&amp;gt; 60 percent&amp;lt;/td&amp;gt;&amp;lt;td&amp;gt;&amp;gt; 0.3 cm&amp;lt;sup&amp;gt;2&amp;lt;/sup&amp;gt;&amp;lt;/td&amp;gt;&amp;lt;/tr&amp;gt;&lt;br /&gt;
&amp;lt;/table&amp;gt;&lt;br /&gt;
&amp;lt;br clear=&amp;quot;left&amp;quot;/&amp;gt;&lt;br /&gt;
==Treatment==&lt;br /&gt;
Vasodilator therapy with [[ACE inhibitors]] and [[hydralazine]] is the foundation of medical therapy and once the patient becomes symptomatic, mitral valve surgery is the definitive therapy.  This chapter reviews general treatment measures for the patient with mitral regurgitation.&lt;br /&gt;
&lt;br /&gt;
===Afterload Reduction===&lt;br /&gt;
* Afterload reduction should be instituted with the use of [[vasodilators]] such as [[ACE inhibitors]] and [[hydralazine]].&lt;br /&gt;
&lt;br /&gt;
===Diuretics===&lt;br /&gt;
*Diuretics are useful in reducing left ventricular volumes to improve functional mitral regurgitation and to improve [[pulmonary edema]].&lt;br /&gt;
&lt;br /&gt;
===Digitalis===&lt;br /&gt;
*[[Digitalis]] may be used to strengthen contractility, and potentially reduce hospitalization in patients with congestive heart failure.&lt;br /&gt;
&lt;br /&gt;
===Diet===&lt;br /&gt;
*A low-sodium diet may be helpful.&lt;br /&gt;
&lt;br /&gt;
===Activity===&lt;br /&gt;
*Most patients with chronic compensated mitral regurgitation have no symptoms; but if a person develops symptoms, activity should be restricted.&lt;br /&gt;
&lt;br /&gt;
===Beta Blockers===&lt;br /&gt;
[[Beta blockers]] are generally not recommended as they would slow the compensatory tachycardia and would allow greater time over which the regurgitation could occur and increase the regurgitant volume.&lt;br /&gt;
&lt;br /&gt;
===Calcium Channel Blockers===&lt;br /&gt;
* In the presence of [[atrial fibrillation]], a [[calcium channel blocker]] or [[digoxin]] can be administered to slow the heart rate down and improve left ventricular filling.&lt;br /&gt;
&lt;br /&gt;
===Cardioversion===&lt;br /&gt;
Cardioversion should be considered in the patient with atrial fibrillation or flutter who is hemodynamically unstable.&lt;br /&gt;
&lt;br /&gt;
===Anticoagulation===&lt;br /&gt;
* Anti-coagulation therapy should be considered in patients with [[atrial fibrillation]] and in patients with prosthetic [[mitral valve replacement]] surgery.&lt;br /&gt;
&lt;br /&gt;
===Antibiotic Prophylaxis===&lt;br /&gt;
* Prophylactic antibiotics prior to a periodontal procedure which involves manipulation of gingival tissue, the periapical region of a tooth, or perforation of oral mucosa is recommended in patients with previous [[infective endocarditis]], patients who have a prosthetic mitral valve implanted and in those with congentital heart disease.&amp;lt;ref name=&amp;quot;pmid17446442&amp;quot;&amp;gt;{{cite journal |author=Wilson W, Taubert KA, Gewitz M, Lockhart PB, Baddour LM, Levison M, Bolger A, Cabell CH, Takahashi M, Baltimore RS, Newburger JW, Strom BL, Tani LY, Gerber M, Bonow RO, Pallasch T, Shulman ST, Rowley AH, Burns JC, Ferrieri P, Gardner T, Goff D, Durack DT |title=Prevention of infective endocarditis: guidelines from the American Heart Association: a guideline from the American Heart Association Rheumatic Fever, Endocarditis, and Kawasaki Disease Committee, Council on Cardiovascular Disease in the Young, and the Council on Clinical Cardiology, Council on Cardiovascular Surgery and Anesthesia, and the Quality of Care and Outcomes Research Interdisciplinary Working Group |journal=[[Circulation]] |volume=116 |issue=15 |pages=1736–54 |year=2007 |month=October |pmid=17446442 |doi=10.1161/CIRCULATIONAHA.106.183095 |url=http://circ.ahajournals.org/cgi/pmidlookup?view=long&amp;amp;pmid=17446442 |accessdate=2011-03-16}}&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
===Surgery===&lt;br /&gt;
Vasodilator theray with [[ACE inhibitor]]s and [[hydralazine]] is the mainstay of therapy in patient with chronic compensated mitral regurgitation. Acute mitral regurgitation requires urgent [[mitral valve repair]] or [[mitral valve replacement]].  MV surgery is beneficial for patients with chronic severe MR and NYHA functional class II, III, or IV symptoms in the absence of severe LV dysfunction (severe LV dysfunction is defined as ejection fraction less than 0.30) and/or end-systolic dimension greater than 55 mm.  MV surgery is beneficial for asymptomatic patients with chronic severe MR and mild to moderate LV dysfunction, ejection fraction 0.30 to 0.60, and/or end-systolic dimension greater than or equal to 40 mm. MV repair is recommended over MV replacement in the majority of patients with severe chronic MR who require surgery, and patients should be referred to surgical centers experienced in MV repair.&lt;br /&gt;
==References==&lt;br /&gt;
{{Reflist|2}}&lt;br /&gt;
{{WikiDoc Help Menu}}&lt;br /&gt;
{{WikiDoc Sources}}&lt;br /&gt;
&lt;br /&gt;
[[Category:Valvular heart disease]]&lt;br /&gt;
[[Category:Cardiology]]&lt;br /&gt;
[[Category:Cardiac surgery]]&lt;br /&gt;
[[Category:Surgery]]&lt;br /&gt;
[[Category:Overview complete]]&lt;br /&gt;
[[Category:Template complete]]&lt;br /&gt;
[[Category:Disease]]&lt;/div&gt;</summary>
		<author><name>Varun Kumar</name></author>
	</entry>
	<entry>
		<id>https://www.wikidoc.org/index.php?title=Mitral_regurgitation_overview&amp;diff=642356</id>
		<title>Mitral regurgitation overview</title>
		<link rel="alternate" type="text/html" href="https://www.wikidoc.org/index.php?title=Mitral_regurgitation_overview&amp;diff=642356"/>
		<updated>2012-04-16T01:20:15Z</updated>

		<summary type="html">&lt;p&gt;Varun Kumar: &lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;{{Mitral regurgitation}}&lt;br /&gt;
{{CMG}}; &#039;&#039;&#039;Associate Editor-In-Chief:&#039;&#039;&#039; {{CZ}}; [[Varun Kumar]], M.B.B.S.; [[Lakshmi Gopalakrishnan]], M.B.B.S; [[User:Mohammed Sbeih|Mohammed A. Sbeih, M.D.]] [mailto:msbeih@perfuse.org].&lt;br /&gt;
==Overview==&lt;br /&gt;
&#039;&#039;&#039;Mitral regurgitation&#039;&#039;&#039; (&#039;&#039;&#039;MR&#039;&#039;&#039;), &#039;&#039;&#039;mitral insufficiency&#039;&#039;&#039; or &#039;&#039;&#039;mitral incompetence&#039;&#039;&#039; is  a disorder of the [[heart]] in which  the [[mitral valve]] does not close properly when the heart pumps out [[blood]].  It is the abnormal leaking of blood from the [[left ventricle]],  through the mitral valve,  and into the [[left atrium]], when the left ventricle contracts, i.e. there is [[Regurgitation (circulation)|regurgitation]] of blood back into the left atrium &amp;lt;ref&amp;gt;[http://www.mountsinai.org/Other/Diseases/Mitral%20valve%20regurgitation Mitral valve regurgitation] at [[Mount Sinai Hospital, New York|Mount Sinai Hospital]]&amp;lt;/ref&amp;gt;. MR is the most common form of [[valvular heart disease]] &amp;lt;ref name=&#039;MedlineMitChron2008&#039;&amp;gt;{{cite encyclopedia |last=Weinrauch |first=LA |author= |authorlink= |coauthors= |editor=|encyclopedia=Medline Plus Encyclopedia |title=Mitral regurgitation - chronic |url=http://www.nlm.nih.gov/medlineplus/ency/article/000176.htm |accessdate=2009-12-04 |edition=|date=2008-05-12 |year= |publisher=U.S. National Library of Medicine and National Institutes of Health |volume= |location= |id= |doi= |pages= |quote= }}&amp;lt;/ref&amp;gt;.&lt;br /&gt;
Diseases that weaken or damage the valve or the heart tissue around the valve cause mitral regurgitation.&lt;br /&gt;
After age 55, some degree of mitral regurgitation is found in almost 20% of men and women who have an echocardiogram.&lt;br /&gt;
[[Image:Mitral Regurgitation.png|thumb|left|200px|&#039;&#039;&#039;Mitral regurgitation (schematic drawing)&#039;&#039;&#039;&amp;lt;br/&amp;gt;During systole, contraction of the left ventricle causes abnormal backflow (arrow) into the left atrium.&amp;lt;br/&amp;gt;1 [[Mitral valve]]&amp;lt;br/&amp;gt;2 [[Left Ventricle]]&amp;lt;br/&amp;gt;3 [[Left Atrium]]&amp;lt;br/&amp;gt;4 [[Aorta]]]]&lt;br /&gt;
&lt;br /&gt;
==Anatomy==&lt;br /&gt;
The mitral valve is typically 4–6 cm² in area. It has two cusps, or leaflets (the anteromedial leaflet and the posterolateral leaflet).&lt;br /&gt;
&lt;br /&gt;
==Pathophysiology==&lt;br /&gt;
Mitral regurgitation is due to either perforation or prolapse of the leaflets, dilation of the mitral annulus or rupture of the papillary muscles or chordae tendineae.  There are several phases of mitral regurgitation (acute, chronic compensated, and chronic decompensated). In the acute phase, the volume and pressure overload in the left atrium is transmitted backward into the pulmonary vasculature to cause an elevation of the [[pulomanry capillary wedge pressure]] which causes [[dyspnea]], [[PND]], [[orthopnea]] and [[rales]].  During the chronic compensated phase of mitral regurgitation, the left ventricle maintains forward [[cardiac output]] by filling with a larger volume of blood than usual to accomodate the fact that a portion of the blood will go backwards into the left atrium.  In the decompensated phase, the left ventricle begins to dilate and fail. The markers of decompensation are as follows:&lt;br /&gt;
&lt;br /&gt;
# &#039;&#039;&#039;Left ventricular end-diastolic dimension greater than 70 mm&#039;&#039;&#039;&lt;br /&gt;
# &#039;&#039;&#039;Left ventricular end-systolic dimension greater than 45 to 47 mm&#039;&#039;&#039;&lt;br /&gt;
# &#039;&#039;&#039;Left ventricular [[ejection fraction]] (LVEF) less than 50 to 55 percent&#039;&#039;&#039;&lt;br /&gt;
&lt;br /&gt;
==References==&lt;br /&gt;
{{Reflist|2}}&lt;br /&gt;
{{WikiDoc Help Menu}}&lt;br /&gt;
{{WikiDoc Sources}}&lt;br /&gt;
&lt;br /&gt;
[[Category:Valvular heart disease]]&lt;br /&gt;
[[Category:Cardiology]]&lt;br /&gt;
[[Category:Cardiac surgery]]&lt;br /&gt;
[[Category:Surgery]]&lt;br /&gt;
[[Category:Overview complete]]&lt;br /&gt;
[[Category:Template complete]]&lt;br /&gt;
[[Category:Disease]]&lt;/div&gt;</summary>
		<author><name>Varun Kumar</name></author>
	</entry>
	<entry>
		<id>https://www.wikidoc.org/index.php?title=Monocytosis&amp;diff=642230</id>
		<title>Monocytosis</title>
		<link rel="alternate" type="text/html" href="https://www.wikidoc.org/index.php?title=Monocytosis&amp;diff=642230"/>
		<updated>2012-04-15T18:31:56Z</updated>

		<summary type="html">&lt;p&gt;Varun Kumar: &lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;{{DiseaseDisorder infobox |&lt;br /&gt;
  Name           = {{PAGENAME}} |&lt;br /&gt;
  Image          = Monocytosis.jpg |&lt;br /&gt;
  Caption        = Bone marrow smear from a patient with a 23-month history of CML who developed a slight monocytosis, increased blasts in the blood and marrow, and an increase in marrow eosinophils with abnormal basophilic-staining granules. Cytogenetic studies showed cells with both a t(9;22) and an inv (16) abnormality. (Wright-Giemsa stain). &amp;lt;br&amp;gt; &amp;lt;small&amp;gt; [http://www.peir.net Image courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology] &amp;lt;/small&amp;gt; | &lt;br /&gt;
  ICD10          = {{ICD10|D|72|8|d|70}} |&lt;br /&gt;
  ICD9           = {{ICD9|288.8}} |&lt;br /&gt;
  ICDO           = |&lt;br /&gt;
  OMIM           = |&lt;br /&gt;
  DiseasesDB     = 22713 |&lt;br /&gt;
  MedlinePlus    = |&lt;br /&gt;
  eMedicineSubj  = |&lt;br /&gt;
  eMedicineTopic = |&lt;br /&gt;
}}&lt;br /&gt;
{{SI}}&lt;br /&gt;
{{CMG}}&lt;br /&gt;
&lt;br /&gt;
==Overview==&lt;br /&gt;
&#039;&#039;&#039;Monocytosis&#039;&#039;&#039; is an increase in the number of circulating [[monocyte]]s. In humans, 950/μL is regarded as at the upper limit of normal; monocyte counts above this level are regarded as monocytosis.&lt;br /&gt;
&lt;br /&gt;
== Differential Diagnosis of Causes of {{PAGENAME}} ==&lt;br /&gt;
&#039;&#039;&#039;(By organ system)&#039;&#039;&#039;&lt;br /&gt;
{|height:100px&amp;quot; border=&amp;quot;1&amp;quot;&lt;br /&gt;
|style=&amp;quot;height:100px&amp;quot;; style=&amp;quot;width:25%&amp;quot; border=&amp;quot;1&amp;quot; bgcolor=&amp;quot;LightSteelBlue&amp;quot; | &#039;&#039;&#039;Cardiovascular&#039;&#039;&#039;&lt;br /&gt;
|style=&amp;quot;height:100px&amp;quot;; style=&amp;quot;width:75%&amp;quot; border=&amp;quot;1&amp;quot; bgcolor=&amp;quot;Beige&amp;quot; | [[Bacterial Endocarditis]]&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Chemical / poisoning&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Dermatologic&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Drug Side Effect&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Ear Nose Throat&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes&lt;br /&gt;
|- &lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Endocrine&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| [[Sarcoidosis]]&lt;br /&gt;
|- &lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Environmental&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| [[Brucellosis]], [[Kala-azar]], [[Listeriosis]], [[Rocky Mountain spotted fever]]&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Gastroenterologic&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| [[Cirrhosis]], [[Crohn&#039;s disease]], Infectious [[hepatitis]], [[Inflammatory bowel disease]], [[Irritable Bowel Syndrome]], [[Sarcoidosis]], [[Ulcerative colitis]]&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Genetic&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| [[Gaucher&#039;s Disease]], [[Kostmann syndrome]], [[Sarcoidosis]]&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Hematologic&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| [[Acute lymphocytic leukemia]], Benign familial [[neutropenia]], [[Chronic myeloid leukaemia]], Chronic [[neutropenia]], [[Cyclical neutropenia]], [[Granulocyte-macrophage colony stimulating factor]], [[Hodgkin lymphoma]], [[Kostmann syndrome]], [[Lymphoproliferative disease]], [[Myelodysplastic syndrome]], [[Myeloma]], [[Myeloproliferative disease]], [[Polyarteritis nodosa]], Recovery from [[neutropenia]], [[Visceral leishmaniasis]]&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Iatrogenic&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Infectious Disease&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| [[Bacterial Endocarditis]], [[Brucellosis]], [[Cytomegalovirus]], [[Herpes Zoster Virus]], [[Infectious Endocarditis]], Infectious [[hepatitis]], [[Kala-azar]], [[Listeriosis]], [[Malaria]], [[Mononeucleosis]], [[Mycobacterium tuberculosis]], [[Relapsing fever]], [[Rocky Mountain spotted fever]], [[Syphillis]], [[Trypanosomiasis]], [[Whooping cough]]&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Musculoskeletal / Ortho&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| [[Rheumatoid arthritis]]&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Neurologic&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Nutritional / Metabolic&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| [[Gaucher&#039;s Disease]], [[Lipid storage disease]]&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Obstetric/Gynecologic&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Oncologic&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| [[Acute lymphocytic leukemia]], [[Chronic myeloid leukaemia]], [[Hodgkin lymphoma]], [[Myeloproliferative disease]], [[Non-Hodgkin lymphoma]], Other malignant [[lymphoma]]s&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Opthalmologic&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Overdose / Toxicity&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Psychiatric&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Pulmonary&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| [[Mycobacterium tuberculosis]], [[Whooping cough]]&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Renal / Electrolyte&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Rheum / Immune / Allergy&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| [[Crohn&#039;s disease]], [[Inflammatory bowel disease]], [[Irritable Bowel Syndrome]], [[Polyarteritis nodosa]], [[Rheumatoid arthritis]], [[Sarcoidosis]], [[Systemic lupus erythematosus]], [[Ulcerative colitis]]&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Sexual&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| [[Syphillis]]&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Trauma&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Urologic&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| No underlying causes&lt;br /&gt;
|-&lt;br /&gt;
|-bgcolor=&amp;quot;LightSteelBlue&amp;quot;&lt;br /&gt;
| &#039;&#039;&#039;Miscellaneous&#039;&#039;&#039;&lt;br /&gt;
|bgcolor=&amp;quot;Beige&amp;quot;| [[Kala-azar]]&lt;br /&gt;
|-&lt;br /&gt;
|} &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;(In alphabetical order)&#039;&#039;&#039;&lt;br /&gt;
*[[Acute lymphocytic leukemia]]&lt;br /&gt;
*[[Bacterial Endocarditis]]&lt;br /&gt;
*Benign familial [[neutropenia]] &lt;br /&gt;
*[[Brucellosis]]&lt;br /&gt;
*[[Carcinoma]]&lt;br /&gt;
* [[Chronic myeloid leukaemia]]&lt;br /&gt;
*Chronic [[neutropenia]]&lt;br /&gt;
*[[Cirrhosis]]&lt;br /&gt;
* [[Crohn&#039;s disease]]&lt;br /&gt;
* [[Cyclical neutropenia]]&lt;br /&gt;
*[[Cytomegalovirus]]&lt;br /&gt;
*[[Drugs]]&lt;br /&gt;
*[[Gaucher&#039;s Disease]]&lt;br /&gt;
* [[Granulocyte-macrophage colony stimulating factor]]&lt;br /&gt;
*[[Herpes Zoster Virus]]&lt;br /&gt;
* [[Hodgkin lymphoma]]&lt;br /&gt;
*[[Infectious Endocarditis]]&lt;br /&gt;
*Infectious [[hepatitis]]&lt;br /&gt;
*[[Inflammatory bowel disease]]&lt;br /&gt;
*[[Irritable Bowel Syndrome]]&lt;br /&gt;
*[[Kala-azar]]&lt;br /&gt;
* [[Kostmann syndrome]]&lt;br /&gt;
*[[Lipid storage disease]]&lt;br /&gt;
*[[listeriosis]]&lt;br /&gt;
*[[Lymphoproliferative disease]]&lt;br /&gt;
*[[Malaria]]&lt;br /&gt;
*[[Mononeucleosis]]&lt;br /&gt;
*[[Mycobacterium tuberculosis]]&lt;br /&gt;
*[[Myelodysplastic syndrome]]&lt;br /&gt;
*[[Myeloma]]&lt;br /&gt;
*[[Myeloproliferative disease]]&lt;br /&gt;
*[[Non-Hodgkin lymphoma]]&lt;br /&gt;
*Other malignant [[lymphoma]]s&lt;br /&gt;
* [[Polyarteritis nodosa]]&lt;br /&gt;
*Recovery from [[neutropenia]]&lt;br /&gt;
*[[Relapsing fever]]&lt;br /&gt;
*[[Rheumatoid arthritis]]&lt;br /&gt;
*[[Rocky Mountain spotted fever]]&lt;br /&gt;
*[[Sarcoidosis]]&lt;br /&gt;
*[[Syphillis]]&lt;br /&gt;
* [[Systemic lupus erythematosus]]&lt;br /&gt;
*[[Trypanosomiasis]]&lt;br /&gt;
*[[Tuberculosis]]&lt;br /&gt;
* [[Ulcerative colitis]]&lt;br /&gt;
* [[Visceral leishmaniasis]]&lt;br /&gt;
*[[Whooping cough]]&lt;br /&gt;
&lt;br /&gt;
==References==&lt;br /&gt;
{{reflist|2}}&lt;br /&gt;
{{Hematology}}&lt;br /&gt;
&lt;br /&gt;
[[Category:Hematology]]&lt;br /&gt;
[[Category:Mature chapter]]&lt;br /&gt;
&lt;br /&gt;
[[de:Monozytose]]&lt;br /&gt;
[[sq:Monocitoza]]&lt;br /&gt;
{{WikiDoc Help Menu}}&lt;br /&gt;
{{WikiDoc Sources}}&lt;/div&gt;</summary>
		<author><name>Varun Kumar</name></author>
	</entry>
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