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Sick sinus syndrome revolves around an improperly propagated signal from the [[sinoatrial]](SA) node. Some of the causes for this propagation abnormality include degenerative fibrosis of the SA node, abnormalities in ion-channel conduction, and and a remodeling of the node itself. As a disease of the elderly, it is most commonly thought to be secondary to the age-related idiopathic fibrosis of the nodal tissue.<ref name="pmid23939447">{{cite journal| author=Semelka M, Gera J, Usman S| title=Sick sinus syndrome: a review. | journal=Am Fam Physician | year= 2013 | volume= 87 | issue= 10 | pages= 691-6 | pmid=23939447 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23939447  }} </ref> Studies on familial and congenital presentations of sick sinus syndrome have also revealed genetic contributions to dysfunctional ion channels.<ref name="pmid14523039">{{cite journal| author=Benson DW, Wang DW, Dyment M, Knilans TK, Fish FA, Strieper MJ et al.| title=Congenital sick sinus syndrome caused by recessive mutations in the cardiac sodium channel gene (SCN5A). | journal=J Clin Invest | year= 2003 | volume= 112 | issue= 7 | pages= 1019-28 | pmid=14523039 | doi=10.1172/JCI18062 | pmc=198523 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=14523039  }} </ref> Recent research has revealed a higher incidence of SSS in carriers of a rare variant of the [[MYH6]] gene, which encodes the alpha heavy chain subunit of cardiac [[myosin]], further delineating a possible genetic basis to the disease. <ref name="pmid21378987">{{cite journal| author=Holm H, Gudbjartsson DF, Sulem P, Masson G, Helgadottir HT, Zanon C et al.| title=A rare variant in MYH6 is associated with high risk of sick sinus syndrome. | journal=Nat Genet | year= 2011 | volume= 43 | issue= 4 | pages= 316-20 | pmid=21378987 | doi=10.1038/ng.781 | pmc=3066272 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21378987  }} </ref>
{{Sick sinus syndrome}}
 
==Overview==
In some patients, heart failure and atrial fibrillation can also be causes of remodeling of the SA node leading to increased sinus node recovery time, abnormal propagation of the action potential from the node and changes in nodal sensitivity. <ref name="pmid8941126">{{cite journal| author=Elvan A, Wylie K, Zipes DP| title=Pacing-induced chronic atrial fibrillation impairs sinus node function in dogs. Electrophysiological remodeling. | journal=Circulation | year= 1996 | volume= 94 | issue= 11 | pages= 2953-60 | pmid=8941126 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8941126  }} </ref> <ref name="pmid17420362">{{cite journal| author=Dobrzynski H, Boyett MR, Anderson RH| title=New insights into pacemaker activity: promoting understanding of sick sinus syndrome. | journal=Circulation | year= 2007 | volume= 115 | issue= 14 | pages= 1921-32 | pmid=17420362 | doi=10.1161/CIRCULATIONAHA.106.616011 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17420362  }} </ref> [[Hemochromatosis]], [[sarcoidosis]], [[amyloidosis]] and other infiltrative disease process may contribute to intrinsic dysfunction of the [[sinoatrial]] node, as can chronic ischemia secondary to atherosclerotic changes of arteries supplying the SA node.<ref name="pmid23939447">{{cite journal| author=Semelka M, Gera J, Usman S| title=Sick sinus syndrome: a review. | journal=Am Fam Physician | year= 2013 | volume= 87 | issue= 10 | pages= 691-6 | pmid=23939447 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23939447  }} </ref> <ref name="pmid2035437">{{cite journal| author=Alboni P, Baggioni GF, Scarfò S, Cappato R, Percoco GF, Paparella N et al.| title=Role of sinus node artery disease in sick sinus syndrome in inferior wall acute myocardial infarction. | journal=Am J Cardiol | year= 1991 | volume= 67 | issue= 15 | pages= 1180-4 | pmid=2035437 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2035437  }} </ref>  
Sick sinus syndrome occurs as an improperly propagated signal from the [[sinoatrial]](SA) node. Age-dependent progressive fibrosis of the sinus nodal tissue and Remodeling of sinuatrial node are the potential mechanisms of this abnormally formed signal propagation.  
 
==Pathophysiology==
*Sick sinus syndrome occurs as the result of age-dependent progressive fibrosis of the sinus nodal tissue and atrial myocardium. This leads to abnormal formation and propagation of atrial impulse and the resultant bradycardic or pause-related syndromes.<ref name="Lev1954">{{cite journal|last1=Lev|first1=M.|title=Aging Changes in the Human Sinoatrial Node|journal=Journal of Gerontology|volume=9|issue=1|year=1954|pages=1–9|issn=0022-1422|doi=10.1093/geronj/9.1.1}}</ref><ref name="pmid23939447">{{cite journal| author=Semelka M, Gera J, Usman S| title=Sick sinus syndrome: a review. | journal=Am Fam Physician | year= 2013 | volume= 87 | issue= 10 | pages= 691-6 | pmid=23939447 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23939447  }} </ref> Studies on familial and congenital presentations of sick sinus syndrome have also revealed genetic contributions to dysfunctional ion channels.<ref name="pmid14523039">{{cite journal| author=Benson DW, Wang DW, Dyment M, Knilans TK, Fish FA, Strieper MJ et al.| title=Congenital sick sinus syndrome caused by recessive mutations in the cardiac sodium channel gene (SCN5A). | journal=J Clin Invest | year= 2003 | volume= 112 | issue= 7 | pages= 1019-28 | pmid=14523039 | doi=10.1172/JCI18062 | pmc=198523 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=14523039  }} </ref> Recent research has revealed a higher incidence of SSS in carriers of a rare variant of the [[MYH6]] gene, which encodes the alpha heavy chain subunit of cardiac [[myosin]], further delineating a possible genetic basis to the disease. <ref name="pmid21378987">{{cite journal| author=Holm H, Gudbjartsson DF, Sulem P, Masson G, Helgadottir HT, Zanon C et al.| title=A rare variant in MYH6 is associated with high risk of sick sinus syndrome. | journal=Nat Genet | year= 2011 | volume= 43 | issue= 4 | pages= 316-20 | pmid=21378987 | doi=10.1038/ng.781 | pmc=3066272 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21378987  }} </ref>
*Remodeling of sinuatrial node as a result of  heart failure and atrial fibrillation can also be causes of increased sinus node recovery time, abnormal propagation of the action potential from the node and changes in nodal sensitivity.<ref name="pmid8941126">{{cite journal| author=Elvan A, Wylie K, Zipes DP| title=Pacing-induced chronic atrial fibrillation impairs sinus node function in dogs. Electrophysiological remodeling. | journal=Circulation | year= 1996 | volume= 94 | issue= 11 | pages= 2953-60 | pmid=8941126 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8941126  }} </ref> <ref name="pmid17420362">{{cite journal| author=Dobrzynski H, Boyett MR, Anderson RH| title=New insights into pacemaker activity: promoting understanding of sick sinus syndrome. | journal=Circulation | year= 2007 | volume= 115 | issue= 14 | pages= 1921-32 | pmid=17420362 | doi=10.1161/CIRCULATIONAHA.106.616011 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17420362  }} </ref> [[Hemochromatosis]], [[sarcoidosis]], [[amyloidosis]] and other infiltrative disease process may contribute to intrinsic dysfunction of the [[sinoatrial]] node, as can chronic ischemia secondary to atherosclerotic changes of arteries supplying the SA node.<ref name="pmid23939447">{{cite journal| author=Semelka M, Gera J, Usman S| title=Sick sinus syndrome: a review. | journal=Am Fam Physician | year= 2013 | volume= 87 | issue= 10 | pages= 691-6 | pmid=23939447 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23939447  }} </ref> <ref name="pmid2035437">{{cite journal| author=Alboni P, Baggioni GF, Scarfò S, Cappato R, Percoco GF, Paparella N et al.| title=Role of sinus node artery disease in sick sinus syndrome in inferior wall acute myocardial infarction. | journal=Am J Cardiol | year= 1991 | volume= 67 | issue= 15 | pages= 1180-4 | pmid=2035437 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2035437  }} </ref>  
== References ==
== References ==
{{Reflist|2}}
{{Reflist|2}}
 
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Revision as of 14:23, 26 March 2020

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Overview

Sick sinus syndrome occurs as an improperly propagated signal from the sinoatrial(SA) node. Age-dependent progressive fibrosis of the sinus nodal tissue and Remodeling of sinuatrial node are the potential mechanisms of this abnormally formed signal propagation.

Pathophysiology

  • Sick sinus syndrome occurs as the result of age-dependent progressive fibrosis of the sinus nodal tissue and atrial myocardium. This leads to abnormal formation and propagation of atrial impulse and the resultant bradycardic or pause-related syndromes.[1][2] Studies on familial and congenital presentations of sick sinus syndrome have also revealed genetic contributions to dysfunctional ion channels.[3] Recent research has revealed a higher incidence of SSS in carriers of a rare variant of the MYH6 gene, which encodes the alpha heavy chain subunit of cardiac myosin, further delineating a possible genetic basis to the disease. [4]
  • Remodeling of sinuatrial node as a result of heart failure and atrial fibrillation can also be causes of increased sinus node recovery time, abnormal propagation of the action potential from the node and changes in nodal sensitivity.[5] [6] Hemochromatosis, sarcoidosis, amyloidosis and other infiltrative disease process may contribute to intrinsic dysfunction of the sinoatrial node, as can chronic ischemia secondary to atherosclerotic changes of arteries supplying the SA node.[2] [7]

References

  1. Lev, M. (1954). "Aging Changes in the Human Sinoatrial Node". Journal of Gerontology. 9 (1): 1–9. doi:10.1093/geronj/9.1.1. ISSN 0022-1422.
  2. 2.0 2.1 Semelka M, Gera J, Usman S (2013). "Sick sinus syndrome: a review". Am Fam Physician. 87 (10): 691–6. PMID 23939447.
  3. Benson DW, Wang DW, Dyment M, Knilans TK, Fish FA, Strieper MJ; et al. (2003). "Congenital sick sinus syndrome caused by recessive mutations in the cardiac sodium channel gene (SCN5A)". J Clin Invest. 112 (7): 1019–28. doi:10.1172/JCI18062. PMC 198523. PMID 14523039.
  4. Holm H, Gudbjartsson DF, Sulem P, Masson G, Helgadottir HT, Zanon C; et al. (2011). "A rare variant in MYH6 is associated with high risk of sick sinus syndrome". Nat Genet. 43 (4): 316–20. doi:10.1038/ng.781. PMC 3066272. PMID 21378987.
  5. Elvan A, Wylie K, Zipes DP (1996). "Pacing-induced chronic atrial fibrillation impairs sinus node function in dogs. Electrophysiological remodeling". Circulation. 94 (11): 2953–60. PMID 8941126.
  6. Dobrzynski H, Boyett MR, Anderson RH (2007). "New insights into pacemaker activity: promoting understanding of sick sinus syndrome". Circulation. 115 (14): 1921–32. doi:10.1161/CIRCULATIONAHA.106.616011. PMID 17420362.
  7. Alboni P, Baggioni GF, Scarfò S, Cappato R, Percoco GF, Paparella N; et al. (1991). "Role of sinus node artery disease in sick sinus syndrome in inferior wall acute myocardial infarction". Am J Cardiol. 67 (15): 1180–4. PMID 2035437.