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Atrial septal defect

2011-08-17T16:11:03Z

C. Michael Gibson: /* References */

{{Infobox_Disease |
Name = {{PAGENAME}} |
DiseasesDB = 1089 |
ICD10 = {{ICD10|Q|21|1|q|20}} |
ICD9 = {{ICD9|745.5}}-{{ICD9|745.6}} |
ICDO = |
OMIM = 108800 |
MedlinePlus = |
eMedicineSubj = |
eMedicineTopic = |
MeshName = Atrial+Septal+Defects |
MeshNumber = C14.240.400.560.375 |
}}
{{Atrial septal defect}}
{{CMG}}; '''Associate Editors-In-Chief:''' [[Priyamvada Singh|Priyamvada Singh, MBBS]] [[mailto:psingh@perfuse.org]]; {{CZ}}; '''Assistant Editor-In-Chief:''' [[Kristin Feeney|Kristin Feeney, B.S.]] [[mailto:kfeeney@perfuse.org]]

==[[Atrial septal defect overview | Overview]]==

==[[Atrial septal defect pathophysiology | Pathophysiology]]==

==[[Atrial septal defect epidemiology|Epidemiology]]==

==[[Atrial septal defect natural history|Natural history, complications, and prognosis]]==

==[[Atrial septal defect causes | Causes]]==
[[Atrial septal defect genetics|Genetics]] | [[Atrial septal defect embryology|Embryology]]

==[[Atrial septal defect classifications | Classifications of atrial septal defects]] ==
[[Atrial septal defect ostium primum | Ostium primum atrial septal defect]] | [[Atrial septal defect ostium secundum | Ostum secundum atrial septal defect]] | [[Atrial septal defect patent foramen ovale | Patent foramen ovale]] | [[Atrial septal defect sinus venosus | Sinus venosus atrial septal defect]] | [[Atrial septal defect common or single atrium | Common or single atrium]]

==[[Atrial septal defect diagnosis | Diagnosis]]==
[[Atrial septal defect history and symptoms|History & Symptoms]]|[[Atrial septal defect diagnosis physical examination | Physical examination]]|[[Atrial septal defect chest x-ray | Chest X-ray]] | [[Atrial septal defect electrocardiogram | Electrocardiogram]] | [[Atrial septal defect echocardiography | Echocardiography]] | [[Atrial septal defect trans-cranial doppler ultrasound | Trans-cranial doppler ultrasound]] | [[Atrial septal defect MRI | MRI]] |[[Atrial septal defect CT | CT]]|[[ACC/AHA recommendations for evaluation of the unoperated patient in atrial septal defect|ACC/AHA recommendations for evaluation of the unoperated patient]]

==Treatment==
'''[[Atrial septal defect medical therapy|Medical therapy]]'''

'''[[Atrial septal defect surgical therapy|Surgical therapy]]'''

[[Atrial septal defect preoperative evaluation | Pre-operative evaluation]] | [[Atrial septal defect surgical closure | Surgical closure]] | [[Atrial septal defect percutaneous closure | Percutaneous closure]]

'''[[ACC/AHA guidelines for reproduction in patients with atrial septal defect|ACC/AHA guidelines for reproduction]]

==[[Atrial septal defect associated conditions|Associated conditions]]==
[[Atrial septal defect decompression sickness | Decompression sickness]] | [[Atrial septal defect paradoxical emboli | Paradoxical emboli]] | [[Atrial septal defect migraine | Migraine]]

==See also==
*[[Atrioventricular septal defect]]
*[[Congenital heart disease]]
*[[Ventricular septal defect]]

==External links==
* [http://www.pediatricheartsurgery.com Pediatric Heart Surgery]
* [http://www.youtube.com/watch?v=PbQhiv6OB0E Pediatric Cardiac Surgery: Atrial Septal Defect Repair]

[[Category:Cardiology]]
[[Category:Congenital heart disease]]
[[Category:Pediatrics]]
[[Category:Disease state]]

[[tr:Atriyal septal defekt]]

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Bowel obstruction

2011-08-15T13:28:05Z

C. Michael Gibson: /* External links */

{{DiseaseDisorder infobox |
Name = Bowel obstruction |
ICD10 = {{ICD10|K|56||k|55}} |
ICD9 = {{ICD9|560}} |
ICDO = |
Image = Bowel obstruction.jpg |
Caption = Bowel obstruction |
OMIM = |
MedlinePlus = 000260 |
eMedicineSubj = |
eMedicineTopic = |
DiseasesDB = 15838 |
}}
'''For patient information click [[{{PAGENAME}} (patient information)|here]]'''

{{SI}}
{{CMG}}

==Overview==
'''Bowel obstruction''' is a mechanical or functional obstruction of the intestines, preventing the normal transit of the products of digestion. It can occur at any level distal to the [[duodenum]] of the [[small intestine]] and is a [[medical emergency]]. Although many cases are not treated surgically, it is a [[surgery|surgical]] problem.
==Differential Diagnosis of Causes of Bowel Obstruction==

===By Localization===

====Small bowel obstruction====

* [[Adhesion (medicine)|Adhesions]] from previous abdominal surgery
* [[Carcinoid]] rare, preferred location: ileum
* [[Crohn's disease]] causing adhesions or inflammatory strictures
* [[Foreign body|Foreign bodies]] (e.g. [[gallstone]]s in [[Ileus|gallstone ileus]], swallowed objects)
* [[Hernia]]s containing bowel
* [[Intestinal atresia]]
* [[Intussusception (medical disorder)|Intussusception]] in children
* [[Ischaemia|Ischaemic]] strictures
* [[Neoplasia|Neoplasms]], benign or malignant
* [[Volvulus]]

<div align="left">
<gallery heights="175" widths="175">
Image:Bowel Obstrution2008.jpg|Upright abdominal X-ray demonstrating a small bowel obstruction. Note multiple air fluid levels.
</gallery>
</div>

====Large bowel obstruction====
Causes of [[large bowel]] obstruction include:
* [[neoplasia|Neoplasm]]s
* [[Hernia]]s
* [[Inflammatory bowel disease]]
* Colonic [[volvulus]] (sigmoid, caecal, transverse colon)
* [[Constipation|Faecal impaction]]
* [[Intestinal atresia|Colon atresia]]
* Benign strictures (Diverticular Disease)

<div align="left">
<gallery heights="175" widths="175">
Image:LargeBowelObsUp2008.jpg|Upright abdominal X-ray of a patient with a large bowel obstruction showing multiple air fluid levels and dilated loops of bowel.
</gallery>
</div>

===By organ system===

*Miscellaneous syndromes
:* [[Intestinal pseudoobstruction|Pseudo-obstruction]] or [[Ogilvie's syndrome]]
:* Paralytic [[Ileus]]

*Chromosomal abnormalities
:* [[Down syndrome]]

*Autosomal dominant conditions
:* [[Neurofibromatosis]] type 1

*Malignant neoplastic conditions
:* [[Carcinoid tumours]] and [[carcinoid syndrome]]
:* [[Colorectal cancer]]
:* [[Ovarian cancer]]
:* [[Pseudomyxoma peritonei]]
:* [[Small bowel lymphoma]]
:* [[Stomach cancer]]

*Trauma, mechanical and physical conditions

:* Bowel strangulation
:* Femoral [[hernia]]
:* [[Ileus]]
:* Inguinal [[hernia]]
:* Intestinal stricture
:* Intestinal [[volvulus]]
:* [[Intussusception]] of intestine
:* Large bowel obstruction
:* Obturator [[hernia]]
:* Peritoneal [[adhesions]]
:* Small bowel obstruction

*Infectious disorders

:* Intra-abdominal [[sepsis]]
:* [[Pneumonia]] or other systemic illness
:* [[Ascariasis]]

===By mechanism===

==== Mechanical Obstruction ====
* Adenomatous polyps
* Adhesions
* Adhesive bands
* Annular [[pancreas]]
* Ascariades
* [[Atresia]]
* Biliary calculus
* Bowel duplication
* [[Carcinomatosis]]
* [[Colon Cancer]]
* Congenital [[megacolon]]
* [[Crohn's Disease]]
* Cysts
* Diverticular stricture
* [[Diverticulitis]]
* [[Endometriosis]]
* Foreign body
* [[Gallstone]] ileus
* Hematoma of the bowel wall
* [[Hernia]]
* Hirschprung's disease
* Iatrogenic
* Imperforate anus
* Incarcerated hernia
* Inflammatory
* Intrabdominal abscess
* Intrabdominal hematoma
* Invagination, intussisception
* [[Ischemia]]
* Malrotation
* [[Meckel's Diverticulum]]
* Megacolon
* Multiple polyposis syndromes
* Neoplasm
* [[Ovarian Cancer]]
* Pneumatosis intestinalis
* Postoperative
* [[Pregnancy]]
* [[Radiation]] induced stenosis
* [[Sarcoma]]
* [[Scleroderma]]
* Surgical anastomosis
* Therapy with dietary fiber
* [[Trauma]]
* [[Tuberculosis]]
* [[Ulcerative colitis]]
* [[Volvulus]]

==== Non-Mechanical Obstruction ====
* Acid-base imbalance
* Acute [[pancreatitis]]
* Anticholinergics
* Antihistamines
* Apoplexy
* [[Brain tumor]]
* [[Cancer]]
* [[Catecholamines]]
* [[Cholecystolithiasis]]
* Connective tissue disease
* Diabetic [[coma]]
* [[Empyema]]
* [[Hyperparathyroidism]]
* [[Hypokalemia]]
* [[Lead poisoning]]
* [[Lymphoma]]
* [[Mechanical ventilation]]
* [[Mesenteric infarction]]
* [[Morphine]]
* Narcotics
* [[Osteomyelitis]] of the spine
* [[Ovarian torsion]]
* [[Pancreatitis]]
* Penetrating wounds
* Perinephric [[abscess]]
* Peritoneal [[carcinomatosis]]
* [[Peritonitis]]
* [[Pneumonia]]
* [[Porphyria]]
* Postoperative
* Psoas [[abscess]]
* [[Pyelonephritis]]
* [[Renal colic]]
* [[Retroperitoneal hematoma]]
* Spinal cord inflammation
* Spinal cord injury
* Spinal cord trauma
* Systemic [[infection]]
* [[Testicular torsion]]
* Ulcer perforation
* [[Uremia]]
* Uro[[sepsis]]
* Vitamin deficiency

==== Pseudo-Obstruction ====
* Aerophagia
* Functional bowel disease

==Signs, symptoms and causes==
Depending on the level of obstruction, bowel obstruction can present with [[abdominal pain]], [[abdominal distension]], [[vomiting]], [[fecal vomiting]], and [[constipation]].

Obstruction may be due to causes within the bowel lumen, within the wall of the bowel, or external to the bowel (such as compression, entrapment or [[volvulus]]).

Bowel obstruction may be complicated by [[dehydration]] and [[Electrolyte disturbance|electrolyte abnormalities]] due to vomiting; respiratory compromise from pressure on the [[diaphragm (anatomy)|diaphragm]] by a distended abdomen, or [[aspiration]] of vomitus; bowel [[ischaemia]] or perforation from prolonged distension or pressure from a foreign body.

In small bowel obstruction the pain tends to be colicky (cramping and intermittent) in nature, with spasms lasting a few minutes. The pain tends to be central and mid-abdominal. Vomiting occurs before constipation.

In large bowel obstruction the pain is felt lower in the abdomen and the spasms last longer. Constipation occurs earlier and vomiting may be less prominent. Proximal obstruction of the large bowel may present as small bowel obstruction.

==Diagnosis==
The main diagnostic tools are [[blood test]]s, [[X-ray]]s of the abdomen, [[Computed axial tomography|CT scanning]] and/or [[medical ultrasonography|ultrasound]]. If a mass is identified, [[biopsy]] may determine the nature of the mass.

[[Radiology|Radiological]] signs of bowel obstruction include bowel distension and the presence of multiple (more than six) gas-fluid levels on supine and erect abdominal [[Radiography|radiographs]].

Contrast enema or small bowel series or [[CT scan]] can be used to define the level of obstruction, whether the obstruction is partial or complete, and to help define the cause of the obstruction.

According to a [[meta-analysis]] of prospective studies by the [[Cochrane Collaboration]], the appearance of water-soluble contrast in the cecum on an abdominal radiograph within 24 hours of oral administration predicts resolution of an adhesive small bowel obstruction with a pooled [[sensitivity (tests)|sensitivity]] of 96% and [[specificity (tests)|specificity]] of 96%. PMID 15674958

[[Colonoscopy]], small bowel investigation with ingested camera or push [[endoscopy]], and [[laparoscopy]] are other diagnostic options.

==Treatment==
Some causes of bowel obstruction may resolve spontaneously; many require operative treatment.

In adults, frequently the surgical intervention and the treatment of the causative lesion are required. In malignant large bowel obstruction, endoscopically placed self-expanding metal [[stents]] may be used to temporarily relieve the obstruction as a bridge to surgery, or as palliation.

===Small bowel obstruction===
In the management of small bowel obstructions it is often said that "[n]ever let the sun rise or set on small-bowel obstruction"<ref>{{cite journal |author=Maglinte DD, Kelvin FM, Rowe MG, Bender GN, Rouch DM |title=Small-bowel obstruction: optimizing radiologic investigation and nonsurgical management |journal=Radiology |volume=218 |issue=1 |pages=39-46 |year=2001 |pmid=11152777 |doi=}}[radiology.rsnajnls.org/cgi/reprint/218/1/39.pdf Free Full Text]. Accessed on: July 19, 2007.</ref> because they are sometimes fatal if treatment is delayed.

Treatment for a small bowel obstruction is both non-surgical (conservative) and surgical.

Conservative treatment involves insertion of a [[Nasogastric intubation|nasogastric tube]], correction of dehydration and [[electrolyte]] abnormalities. [[Opioid]] pain relievers may be used for patients with severe pain. [[Antiemetic]]s may be administered if the patient is vomiting. Adhesive obstructions often settle without surgery. If obstruction is complete a surgery is required.

Small bowel obstruction caused by [[Crohn's disease]], peritoneal [[carcinomatosis]], sclerosing [[peritonitis]], [[Radiation enteropathy|radiation enteritis]] and postpartum bowel obstruction are typically treated conservatively, i.e. without surgery. Conversely, a small bowel obstruction in a "virgin abdomen" (an abdomen that has not seen an operation) is almost never treated conservatively.

===Bowel obstruction in children===
Fetal and neonatal bowel obstructions are often caused by an [[intestinal atresia]] where there is a narrowing or absence of a part of the intestine. These atresias are often discovered before birth via a [[sonogram]] and treated with using [[laparotomy]] after birth. If the area affected is small then the surgeon may be able to remove the damaged portion and join the intestine back together. In instantances where the narrowing is longer, or the area is damaged and cannot be used for a period of time, a temporary [[stoma (medicine)|stoma]] may be placed.

==Pathological Findings==

[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]

<div align="left">
<gallery heights="175" widths="175">
Image:Bowel obstruction 1.jpg|Intestine: Ileus Newborn Cause Unknown: Gross natural color opened body with protruding grossly dilated loops of bowel there was no evidence of necrotizing enteritis
Image:Bowel obstruction 2.jpg|Intestine: Ileus Newborn Cause Unknown: Gross natural color close-up view of distended gut loops
</gallery>
</div>

==References==
<references/>

==See also==
*[[Ileus]]
*[[Colorectal cancer]]

{{Gastroenterology}}

[[Category:General surgery]]
[[Category:Medical emergencies]]
[[Category:Gastroenterology]]
[[Category:Emergency medicine]]
[[Category:Signs and symptoms]]
[[Category:Intensive care medicine]]

[[de:Darmverschluss]]
[[it:Ileo (intestinale)]]
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Pulsus bisferiens

2011-08-15T03:50:57Z

C. Michael Gibson:

''''{{Infobox Disease
| Name = Pulsus bisferiens
| Image =
| Caption =
| DiseasesDB = 32530
| ICD10 =
| ICD9 =
| ICDO =
| OMIM =
| MedlinePlus =
| eMedicineSubj =
| eMedicineTopic =
| MeshID =
}}

{{SI}}

{{CMG}}

'''''Synonyms and keywords:''''' Bisferious pulse, biphasic pulse, spike and dome pattern

==Overview==
'''Pulsus bisferiens''' is a [[sign (medicine)|sign]] where, on [[palpation]] of the [[pulse]], a double peak in the aortic waveform is observed with each [[cardiac cycle]]. ''Bisferious'' means striking twice.

==Pathophysiology==
===Hypertrophic Cardiomyopathy===
Pulsus bisferiens is due to [[systolic anterior motion]] (SAM) of the mitral valve. Because the mitral valve leaflet doesn't get pulled into the left ventricular outflow tract (LVOT) until after the[[aortic valve]] opens, the initial upstroke of the arterial pulse pressure will be normal. When the mitral valve leaflet gets pushed into the LVOT, the arterial pulse will momentarily collapse and will later be followed by a second rise in the pulse pressure, as the left ventricular pressure overcomes the increased obstruction caused by the SAM of the mitral valve. This can be seen on the physical examination as a double tap upon palpation of the apical impulse and as a double pulsation upon palpation of the carotid pulse, known as ''[[pulsus bisferiens]]''or a "[[spike and dome pattern]]" to the carotid pulse.

==Differential Diagnosis Of Causes Of Pulsus Bisferiens==
Classically, it is detected when [[aortic insufficiency]] exists in association with [[aortic stenosis]], but may also be found in isolated but severe [[aortic insufficiency]], and [[hypertrophic obstructive cardiomyopathy]].

==See also==
*[[Hypertrophic cardiomyopathy]]
*[[Aortic regurgitation]]

{{Circulatory system pathology}}

[[Category:Cardiology]]
[[Category:Signs and symptoms]]
[[Category:Physical examination]]

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Pulsus bisferiens

2011-08-15T03:50:19Z

C. Michael Gibson:

''''{{Infobox Disease
| Name = Pulsus bisferiens
| Image =
| Caption =
| DiseasesDB = 32530
| ICD10 =
| ICD9 =
| ICDO =
| OMIM =
| MedlinePlus =
| eMedicineSubj =
| eMedicineTopic =
| MeshID =
}}

{{SI}}

{{CMG}}

'''''Synonyms and keywords:''''' Bisferious pulse, biphasic pulse, spike and dome pattern

==Overview==
'''Pulsus bisferiens''' is a [[sign (medicine)|sign]] where, on [[palpation]] of the [[pulse]], a double peak in the aortic waveform is observed with each [[cardiac cycle]]. ''Bisferious'' means striking twice.

==Pathophysiology==
===Hypertrophic Cardiomyopathy===
Pulsus bisferiens is due to [[systolic anterior motion]] (SAM) of the mitral valve. Because the mitral valve leaflet doesn't get pulled into the left ventricular outflow tract (LVOT) until after the[[aortic valve]] opens, the initial upstroke of the arterial pulse pressure will be normal. When the mitral valve leaflet gets pushed into the LVOT, the arterial pulse will momentarily collapse and will later be followed by a second rise in the pulse pressure, as the left ventricular pressure overcomes the increased obstruction caused by the SAM of the mitral valve. This can be seen on the physical examination as a double tap upon palpation of the apical impulse and as a double pulsation upon palpation of the carotid pulse, known as ''[[pulsus bisferiens]]''or a "[[spike and dome pattern]]" to the carotid pulse.

==Differential Diagnosis Of Causes Of Pulsus Bisferiens==
Classically, it is detected when [[aortic insufficiency]] exists in association with [[aortic stenosis]], but may also be found in isolated but severe [[aortic insufficiency]], and [[hypertrophic obstructive cardiomyopathy]].

==See also==
*[[Hypertrophic cardiomyopathy]]

{{Circulatory system pathology}}

[[Category:Cardiology]]
[[Category:Signs and symptoms]]
[[Category:Physical examination]]

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Pulsus bisferiens

2011-08-15T03:46:19Z

C. Michael Gibson:

Spike and dome pattern

2011-08-15T03:45:37Z

C. Michael Gibson: ←Redirected page to Pulsus bisferiens

#redirect:[[Pulsus bisferiens]]

File:Bifid pulse.gif

2011-08-15T03:37:13Z

C. Michael Gibson:

Pulsus bisferiens

2011-08-15T03:33:05Z

C. Michael Gibson:

Pulsus bisferiens

2011-08-15T03:30:38Z

C. Michael Gibson:

{{Infobox Disease
| Name = Pulsus bisferiens
| Image =
| Caption =
| DiseasesDB = 32530
| ICD10 =
| ICD9 =
| ICDO =
| OMIM =
| MedlinePlus =
| eMedicineSubj =
| eMedicineTopic =
| MeshID =
}}

{{SI}}

{{CMG}}

'''''Synonyms and keywords:''''' Bisferious pulse, biphasic pulse

==Overview==
'''Pulsus bisferiens''', also '''bisferious pulse''' or '''biphasic pulse''', is a [[sign (medicine)|sign]] where, on [[palpation]] of the [[pulse]], a double peak per [[cardiac cycle]] can be appreciated. ''Bisferious'' means striking twice.

==Differential diagnosis of causes of pulsus bisferiens==
Classically, it is detected when [[aortic insufficiency]] exists in association with [[aortic stenosis]], but may also be found in isolated but severe [[aortic insufficiency]], and [[hypertrophic obstructive cardiomyopathy]].

==See also==
*[[Hypertrophic cardiomyopathy]]

{{Circulatory system pathology}}

[[Category:Cardiology]]
[[Category:Signs and symptoms]]
[[Category:Physical examination]]

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Pulsus bisferiens

2011-08-15T03:29:09Z

C. Michael Gibson: /* Differential diagnosis of causes of pulsus bisferiens */

{{Infobox_Disease |
Name = {{PAGENAME}} |
Image = |
Caption = |
DiseasesDB = |
ICD10 = |
ICD9 = |
ICDO = |
OMIM = |
MedlinePlus = |
eMedicineSubj = |
eMedicineTopic = |
MeshID = |
}}
{{SI}}

{{CMG}}

'''''Synonyms and keywords:''''' Bisferious pulse, biphasic pulse

==Overview==
'''Pulsus bisferiens''', also '''bisferious pulse''' or '''biphasic pulse''', is a [[sign (medicine)|sign]] where, on [[palpation]] of the [[pulse]], a double peak per [[cardiac cycle]] can be appreciated. ''Bisferious'' means striking twice.

==Differential diagnosis of causes of pulsus bisferiens==
Classically, it is detected when [[aortic insufficiency]] exists in association with [[aortic stenosis]], but may also be found in isolated but severe [[aortic insufficiency]], and [[hypertrophic obstructive cardiomyopathy]].

==See also==
*[[Hypertrophic cardiomyopathy]]

{{Circulatory system pathology}}

[[Category:Cardiology]]
[[Category:Signs and symptoms]]
[[Category:Physical examination]]

{{WikiDoc Help Menu}}
{{WikiDoc Sources}}

Pulsus bisferiens

2011-08-15T03:28:44Z

C. Michael Gibson:

{{Infobox_Disease |
Name = {{PAGENAME}} |
Image = |
Caption = |
DiseasesDB = |
ICD10 = |
ICD9 = |
ICDO = |
OMIM = |
MedlinePlus = |
eMedicineSubj = |
eMedicineTopic = |
MeshID = |
}}
{{SI}}

{{CMG}}

'''''Synonyms and keywords:''''' Bisferious pulse, biphasic pulse

==Overview==
'''Pulsus bisferiens''', also '''bisferious pulse''' or '''biphasic pulse''', is a [[sign (medicine)|sign]] where, on [[palpation]] of the [[pulse]], a double peak per [[cardiac cycle]] can be appreciated. ''Bisferious'' means striking twice.

==Differential diagnosis of causes of pulsus bisferiens==
Classically, it is detected when [[aortic insufficiency]] exists in association with [[aortic stenosis]], but may also be found in isolated but severe [[aortic insufficiency]], and [[hypertrophic obstructive cardiomyopathy]].

The first lift is due to "percussion wave"(P) and the second lift is due to tidal wave (T).
*If P>T - AR>AS
*If T>P - AS>AR

==See also==
*[[Hypertrophic cardiomyopathy]]

{{Circulatory system pathology}}

[[Category:Cardiology]]
[[Category:Signs and symptoms]]
[[Category:Physical examination]]

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Hypertrophic cardiomyopathy outflow obstruction

2011-08-15T03:27:37Z

C. Michael Gibson: /* Systolic Anterior Motion of the Mitral Valve (SAM) */

Hypertrophic cardiomyopathy outflow obstruction

2011-08-15T03:14:53Z

C. Michael Gibson: /* Systolic Anterior Motion of the Mitral Valve (SAM) */

{{Hypertrophic cardiomyopathy}}

'''Editors-In-Chief:''' [[C. Michael Gibson, M.S., M.D.]] [mailto:mgibson@perfuse.org]

==Overview==
Depending on the degree of obstruction of the outflow of [[blood]] from the [[left ventricle]] of the heart, HCM can be defined as obstructive or non-obstructive. About 25% of individuals with HCM demonstrate an obstruction to the outflow of blood from the left ventricle during rest. In other individuals obstruction only occurs under certain conditions. This is known as dynamic outflow obstruction, because the degree of obstruction is variable and is dependent on the amount of blood in the ventricle immediately before ventricle [[systole (medicine)|systole]] (contraction).

==Location Of The Left Ventricular Outflow Obstruction==
The left ventricular obstruction can be either
*'''Mid-cavitary:''' the middle of the ventricle or
*'''Sub-aortic:''' just below the [[aortic valve]]

==Systolic Anterior Motion of the Mitral Valve (SAM)==
If dynamic outflow obstruction is present in a patient with HCM, it is usually due to systolic anterior motion (SAM) of the anterior leaflet of the [[mitral valve]]. Systolic anterior motion of the mitral valve (SAM) may be due a subaortic bulge of the septum along with narrowing the left ventricular outflow tract, which taken together cause high velocity flow. This in turn is associated with the Venturi effect which is a local low pressure zone in the left ventricular outflow tract. This low pressure zone was thought to suck the [[mitral valve]] anteriorly into the septum. More recently, however, SAM onset has been observed to be instead a low velocity phenomenon. <ref name="Jiang, Levine et al 1987">Jiang L, Levine RA, King ME, Weyman AE. An integrated mechanism for systolic anterior motion of the mitral valve in hypertrophic cardiomyopathy based on echocardiographic observations. ''Am Heart J'' 1987; '''113''':633–44</ref> <ref name="Sherrid, Gunsburg et al 2000">Sherrid MV, Gunsburg DZ, Moldenhauer S, Pearle G. Systolic anterior motion begins at low left ventricular outflow tract velocity in obstructive hypertrophic cardiomyopathy. ''[[Journal of the American College of Cardiology|J Am Coll Cardiol]]'' 2000; '''36''':1344–54</ref>. The role of Venturi forces in the left ventricular outflow tract may be less important than previously thought.

<youtube v=Y7JUVTXHBs0/>

<youtube v=6TWb-wIL0H0/>

While the Venturi effect was thought to cause the abnormality in prior studies, more recent echocardiographic studies indicates that drag, which is more of a pushing force rather than a sucking force like the Venturi effect, may be the dominant hydrodynamic force acting on the mitral leaflets
<ref name="Jiang, Levine et al 1987"/><ref name="Sherrid, Gunsburg et al 2000"/><ref name="Sherrid, Chu et al 1993">Sherrid MV, Chu Ck, DeLia E, Mogtader A, Dwyer Jr. EM, An echocardiographic study of the fluid mechanics of obstruction in hypertrophic cardiomyopathy. ''[[Journal of the American College of Cardiology|J Am Coll Cardiol]]'' 1993; '''22''':816–25</ref><ref name="Levine, Vlahakes et al 1995">Levine RA, Vlahakes GJ, Lefebvre X, et al. Papillary muscle displacement causes systolic anterior motion of the mitral valve. ''[[Circulation (journal)|Circulation]]'' 1995; '''91''':1189–95</ref><ref name="Messmer 1994">Messmer BJ. Extended myectomy for hypertrophic obstructive cardiomyopathy. ''Ann Thorac Surg'' 1994; '''58''':575–7</ref>
<ref name="Schoendube, Klues et al 1995">Schoendube FA, Klues HG, Reith S, Flachskampf FA, Hanrath P, Messmer BJ. Long-term clinical and echocardiographic follow-up after surgical correction of hypertrophic obstructive cardiomyopathy with extended myectomy and reconstruction of the subvalvular mitral apparatus. ''[[Circulation (journal)|Circulation]]'' 1995; '''92''':II-122–7</ref>.
In obstructive HCM the mitral leaflets are often large
<ref name="Klues, Maron et al 1992">Klues HG, Maron BJ, Dollar AL, Roberts WC. Diverstiy of structural mitral valve alterations in hypertrophic cardiomyopathy. ''[[Circulation (journal)|Circulation]]'' 1992; '''85''':1651–60</ref>
and are anteriorly positioned in the LV cavity
<ref name="Jiang, Levine et al 1987"/>
<ref name="Henry, Clark et al 1975">Henry WL, Clark CE, Griffith JM, Epstein SE. Mechanism of left ventricular outflow obstruction in patients with obstructive asymmetric septal hypertrophy (idiopathic hypertrophic subaortic stenosis). ''Am J Cardiol'' 1975; '''35''':337–45</ref>
due to anteriorly positioned papillary muscles<ref name="Jiang, Levine et al 1987"/> that at surgery are often "agglutinated" onto the LV anterior wall by abnormal attachments
<ref name="Messmer 1994"/>
<ref name="Schoendube, Klues et al 1995"/>.

The mid-septal bulge aggravates the malposition of the valve and redirects outflow so that it comes from a lateral and posterior direction<ref name="Sherrid, Chu et al 1993"/>. The abnormally directed outflow may be visualized behind and lateral to the enlarged mitral valve, where it catches it, and pushes it into the septum <ref name="Jiang, Levine et al 1987"/>
<ref name="Sherrid, Gunsburg et al 2000"/>
<ref name="Sherrid, Chu et al 1993"/>
<ref name="Levine, Vlahakes et al 1995"/>.
There is a crucial overlap between the inflow and outflow portions of the left ventricle
<ref name="Schwammenthal and Levine 1996">Schwammenthal E, Levine RA. Dynamic subaortic obstruction: a disease of the mitral valve suitable for surgical repair? ''[[Journal of the American College of Cardiology|J Am Coll Cardiol]]'' 1996; '''28''':203–6</ref>.
As SAM progresses in early systole the angle between outflow and the protruding mitral leaflet increases. A greater surface area of the leaflets is now exposed to drag which amplifies the force on the leaflets – drag increases with increasing angle relative to flow<ref name="Sherrid, Chu et al 1993"/>. An analogy is an open door in a drafty corridor: the door starts by moving slowly and then accelerates as it presents a greater surface area to the wind and finally it slams shut. The necessary conditions that predispose to SAM are: anterior position of the mitral valve in the LV, altered LV geometry that allows flow to strike the mitral valve from behind, and chordal slack
<ref name="Jiang, Levine et al 1987"/>
<ref name="Sherrid, Gunsburg et al 2000"/>
<ref name="Sherrid, Chu et al 1993"/>
<ref name="Levine, Vlahakes et al 1995"/>.
SAM may considered anteriorly directed mitral prolapse
<ref name="Sherrid, Gunsburg et al 2000"/>
<ref name="Sherrid, Chu et al 1993"/>
<ref name="Levine, Vlahakes et al 1995"/>.
In both conditions the mitral valve is enlarged and is displaced in systole by the pushing force of flow resulting in mitral regurgitation.

Because the mitral valve leaflet doesn't get pulled into the LVOT until after the aortic valve opens, the initial upstroke of the arterial pulse will be normal. When the mitral valve leaflet gets pushed into the LVOT, the arterial pulse will momentarily collapse and be followed by a second rise, as the left ventricular pressure overcomes the increased obstruction that SAM of the mitral valve causes. This can be seen on the physical examination as a double tap upon palpation of the apical impulse and as a double pulsation upon palpation of the carotid pulse, known as ''[[pulsus bisferiens]]''.

==References==
{{Reflist|2}}

[[Category: Cardiology]]
[[Category: Cardiomyopathy]]
[[Category: Overview complete]]
[[Category: Template complete]]
[[Category: Genetic disorders]]

Hypertrophic cardiomyopathy outflow obstruction

2011-08-15T03:06:46Z

C. Michael Gibson: /* Systolic Anterior Motion of the Mitral Valve (SAM) */

{{Hypertrophic cardiomyopathy}}

'''Editors-In-Chief:''' [[C. Michael Gibson, M.S., M.D.]] [mailto:mgibson@perfuse.org]

==Overview==
Depending on the degree of obstruction of the outflow of [[blood]] from the [[left ventricle]] of the heart, HCM can be defined as obstructive or non-obstructive. About 25% of individuals with HCM demonstrate an obstruction to the outflow of blood from the left ventricle during rest. In other individuals obstruction only occurs under certain conditions. This is known as dynamic outflow obstruction, because the degree of obstruction is variable and is dependent on the amount of blood in the ventricle immediately before ventricle [[systole (medicine)|systole]] (contraction).

==Location Of The Left Ventricular Outflow Obstruction==
The left ventricular obstruction can be either
*'''Mid-cavitary:''' the middle of the ventricle or
*'''Sub-aortic:''' just below the [[aortic valve]]

==Systolic Anterior Motion of the Mitral Valve (SAM)==
Dynamic outflow obstruction (when present in HCM) is usually due to systolic anterior motion (SAM) of the anterior leaflet of the [[mitral valve]]. Systolic anterior motion of the mitral valve (SAM) may be due to the septal subaortic bulge, narrowing the outflow tract, which in turn causes a high velocity flow and a Venturi effect — a local low pressure zone in the left ventricular outflow tract. This low pressure zone was thought to suck the [[mitral valve]] anteriorly into the septum. But SAM onset is observed to be a low velocity phenomenon: SAM begins at velocities no different from those measured in normals
<ref name="Jiang, Levine et al 1987">Jiang L, Levine RA, King ME, Weyman AE. An integrated mechanism for systolic anterior motion of the mitral valve in hypertrophic cardiomyopathy based on echocardiographic observations. ''Am Heart J'' 1987; '''113''':633–44</ref>
<ref name="Sherrid, Gunsburg et al 2000">Sherrid MV, Gunsburg DZ, Moldenhauer S, Pearle G. Systolic anterior motion begins at low left ventricular outflow tract velocity in obstructive hypertrophic cardiomyopathy. ''[[Journal of the American College of Cardiology|J Am Coll Cardiol]]'' 2000; '''36''':1344–54</ref>.
Hence, the magnitude and importance of Venturi forces in the outflow tract are may be less than previously thought, and Venturi forces may not be the main forces that initiates SAM.

<youtube v=Y7JUVTXHBs0/>

<youtube v=6TWb-wIL0H0/>

While the Venturi effect was thought to cause the abnormality in prior studies, more recent echocardiographic studies indicates that drag, which is more of a pushing force rather than a sucking force like the Venturieffect is the dominant hydrodynamic force acting on the mitral leaflets
<ref name="Jiang, Levine et al 1987"/>
<ref name="Sherrid, Gunsburg et al 2000"/>
<ref name="Sherrid, Chu et al 1993">Sherrid MV, Chu Ck, DeLia E, Mogtader A, Dwyer Jr. EM, An echocardiographic study of the fluid mechanics of obstruction in hypertrophic cardiomyopathy. ''[[Journal of the American College of Cardiology|J Am Coll Cardiol]]'' 1993; '''22''':816–25</ref>
<ref name="Levine, Vlahakes et al 1995">Levine RA, Vlahakes GJ, Lefebvre X, et al. Papillary muscle displacement causes systolic anterior motion of the mitral valve. ''[[Circulation (journal)|Circulation]]'' 1995; '''91''':1189–95</ref>
<ref name="Messmer 1994">Messmer BJ. Extended myectomy for hypertrophic obstructive cardiomyopathy. ''Ann Thorac Surg'' 1994; '''58''':575–7</ref>
<ref name="Schoendube, Klues et al 1995">Schoendube FA, Klues HG, Reith S, Flachskampf FA, Hanrath P, Messmer BJ. Long-term clinical and echocardiographic follow-up after surgical correction of hypertrophic obstructive cardiomyopathy with extended myectomy and reconstruction of the subvalvular mitral apparatus. ''[[Circulation (journal)|Circulation]]'' 1995; '''92''':II-122–7</ref>.
In obstructive HCM the mitral leaflets are often large
<ref name="Klues, Maron et al 1992">Klues HG, Maron BJ, Dollar AL, Roberts WC. Diverstiy of structural mitral valve alterations in hypertrophic cardiomyopathy. ''[[Circulation (journal)|Circulation]]'' 1992; '''85''':1651–60</ref>
and are anteriorly positioned in the LV cavity
<ref name="Jiang, Levine et al 1987"/>
<ref name="Henry, Clark et al 1975">Henry WL, Clark CE, Griffith JM, Epstein SE. Mechanism of left ventricular outflow obstruction in patients with obstructive asymmetric septal hypertrophy (idiopathic hypertrophic subaortic stenosis). ''Am J Cardiol'' 1975; '''35''':337–45</ref>
due to anteriorly positioned papillary muscles<ref name="Jiang, Levine et al 1987"/> that at surgery are often "agglutinated" onto the LV anterior wall by abnormal attachments
<ref name="Messmer 1994"/>
<ref name="Schoendube, Klues et al 1995"/>.

The mid-septal bulge aggravates the malposition of the valve and redirects outflow so that it comes from a lateral and posterior direction<ref name="Sherrid, Chu et al 1993"/>. The abnormally directed outflow may be visualized behind and lateral to the enlarged mitral valve, where it catches it, and pushes it into the septum <ref name="Jiang, Levine et al 1987"/>
<ref name="Sherrid, Gunsburg et al 2000"/>
<ref name="Sherrid, Chu et al 1993"/>
<ref name="Levine, Vlahakes et al 1995"/>.
There is a crucial overlap between the inflow and outflow portions of the left ventricle
<ref name="Schwammenthal and Levine 1996">Schwammenthal E, Levine RA. Dynamic subaortic obstruction: a disease of the mitral valve suitable for surgical repair? ''[[Journal of the American College of Cardiology|J Am Coll Cardiol]]'' 1996; '''28''':203–6</ref>.
As SAM progresses in early systole the angle between outflow and the protruding mitral leaflet increases. A greater surface area of the leaflets is now exposed to drag which amplifies the force on the leaflets – drag increases with increasing angle relative to flow<ref name="Sherrid, Chu et al 1993"/>. An analogy is an open door in a drafty corridor: the door starts by moving slowly and then accelerates as it presents a greater surface area to the wind and finally it slams shut. The necessary conditions that predispose to SAM are: anterior position of the mitral valve in the LV, altered LV geometry that allows flow to strike the mitral valve from behind, and chordal slack
<ref name="Jiang, Levine et al 1987"/>
<ref name="Sherrid, Gunsburg et al 2000"/>
<ref name="Sherrid, Chu et al 1993"/>
<ref name="Levine, Vlahakes et al 1995"/>.
SAM may considered anteriorly directed mitral prolapse
<ref name="Sherrid, Gunsburg et al 2000"/>
<ref name="Sherrid, Chu et al 1993"/>
<ref name="Levine, Vlahakes et al 1995"/>.
In both conditions the mitral valve is enlarged and is displaced in systole by the pushing force of flow resulting in mitral regurgitation.

Because the mitral valve leaflet doesn't get pulled into the LVOT until after the aortic valve opens, the initial upstroke of the arterial pulse will be normal. When the mitral valve leaflet gets pushed into the LVOT, the arterial pulse will momentarily collapse and be followed by a second rise, as the left ventricular pressure overcomes the increased obstruction that SAM of the mitral valve causes. This can be seen on the physical examination as a double tap upon palpation of the apical impulse and as a double pulsation upon palpation of the carotid pulse, known as ''[[pulsus bisferiens]]''.

==References==
{{Reflist|2}}

[[Category: Cardiology]]
[[Category: Cardiomyopathy]]
[[Category: Overview complete]]
[[Category: Template complete]]
[[Category: Genetic disorders]]

SAM

2011-08-14T20:15:34Z

C. Michael Gibson: ←Redirected page to Hypertrophic cardiomyopathy outflow obstruction#Systolic Anterior Motion of the Mitral Valve (SAM)

#redirect:[[Hypertrophic cardiomyopathy outflow obstruction#Systolic Anterior Motion of the Mitral Valve (SAM)]]

Hypertrophic cardiomyopathy outflow obstruction

2011-08-14T20:14:15Z

C. Michael Gibson: /* Systolic Anterior Motion of the Mitral Valve (SAM) */

{{Hypertrophic cardiomyopathy}}

'''Editors-In-Chief:''' [[C. Michael Gibson, M.S., M.D.]] [mailto:mgibson@perfuse.org]

==Overview==
Depending on the degree of obstruction of the outflow of [[blood]] from the [[left ventricle]] of the heart, HCM can be defined as obstructive or non-obstructive. About 25% of individuals with HCM demonstrate an obstruction to the outflow of blood from the left ventricle during rest. In other individuals obstruction only occurs under certain conditions. This is known as dynamic outflow obstruction, because the degree of obstruction is variable and is dependent on the amount of blood in the ventricle immediately before ventricle [[systole (medicine)|systole]] (contraction).

==Location Of The Left Ventricular Outflow Obstruction==
The left ventricular obstruction can be either
*'''Mid-cavitary:''' the middle of the ventricle or
*'''Sub-aortic:''' just below the [[aortic valve]]

==Systolic Anterior Motion of the Mitral Valve (SAM)==
Dynamic outflow obstruction (when present in HCM) is usually due to systolic anterior motion (SAM) of the anterior leaflet of the [[mitral valve]]. Systolic anterior motion of the mitral valve (SAM) may be due to the septal subaortic bulge, narrowing the outflow tract, which in turn causes a high velocity flow and a Venturi effect — a local low pressure zone in the left ventricular outflow tract. This low pressure zone was thought to suck the [[mitral valve]] anteriorly into the septum. But SAM onset is observed to be a low velocity phenomenon: SAM begins at velocities no different from those measured in normals
<ref name="Jiang, Levine et al 1987">Jiang L, Levine RA, King ME, Weyman AE. An integrated mechanism for systolic anterior motion of the mitral valve in hypertrophic cardiomyopathy based on echocardiographic observations. ''Am Heart J'' 1987; '''113''':633–44</ref>
<ref name="Sherrid, Gunsburg et al 2000">Sherrid MV, Gunsburg DZ, Moldenhauer S, Pearle G. Systolic anterior motion begins at low left ventricular outflow tract velocity in obstructive hypertrophic cardiomyopathy. ''[[Journal of the American College of Cardiology|J Am Coll Cardiol]]'' 2000; '''36''':1344–54</ref>.
Hence, the magnitude and importance of Venturi forces in the outflow tract are may be less than previously thought, and Venturi forces may not be the main forces that initiates SAM.

<youtube v=Y7JUVTXHBs0/>

<youtube v=6TWb-wIL0H0/>

Recent echocardiographic evidence indicates that drag, the pushing force of flow is the dominant hydrodynamic force on the mitral leaflets
<ref name="Jiang, Levine et al 1987"/>
<ref name="Sherrid, Gunsburg et al 2000"/>
<ref name="Sherrid, Chu et al 1993">Sherrid MV, Chu Ck, DeLia E, Mogtader A, Dwyer Jr. EM, An echocardiographic study of the fluid mechanics of obstruction in hypertrophic cardiomyopathy. ''[[Journal of the American College of Cardiology|J Am Coll Cardiol]]'' 1993; '''22''':816–25</ref>
<ref name="Levine, Vlahakes et al 1995">Levine RA, Vlahakes GJ, Lefebvre X, et al. Papillary muscle displacement causes systolic anterior motion of the mitral valve. ''[[Circulation (journal)|Circulation]]'' 1995; '''91''':1189–95</ref>
<ref name="Messmer 1994">Messmer BJ. Extended myectomy for hypertrophic obstructive cardiomyopathy. ''Ann Thorac Surg'' 1994; '''58''':575–7</ref>
<ref name="Schoendube, Klues et al 1995">Schoendube FA, Klues HG, Reith S, Flachskampf FA, Hanrath P, Messmer BJ. Long-term clinical and echocardiographic follow-up after surgical correction of hypertrophic obstructive cardiomyopathy with extended myectomy and reconstruction of the subvalvular mitral apparatus. ''[[Circulation (journal)|Circulation]]'' 1995; '''92''':II-122–7</ref>.
In obstructive HCM the mitral leaflets are often large
<ref name="Klues, Maron et al 1992">Klues HG, Maron BJ, Dollar AL, Roberts WC. Diverstiy of structural mitral valve alterations in hypertrophic cardiomyopathy. ''[[Circulation (journal)|Circulation]]'' 1992; '''85''':1651–60</ref>
and are anteriorly positioned in the LV cavity
<ref name="Jiang, Levine et al 1987"/>
<ref name="Henry, Clark et al 1975">Henry WL, Clark CE, Griffith JM, Epstein SE. Mechanism of left ventricular outflow obstruction in patients with obstructive asymmetric septal hypertrophy (idiopathic hypertrophic subaortic stenosis). ''Am J Cardiol'' 1975; '''35''':337–45</ref>
due to anteriorly positioned papillary muscles<ref name="Jiang, Levine et al 1987"/> that at surgery are often "agglutinated" onto the LV anterior wall by abnormal attachments
<ref name="Messmer 1994"/>
<ref name="Schoendube, Klues et al 1995"/>.

The mid-septal bulge aggravates the malposition of the valve and redirects outflow so that it comes from a lateral and posterior direction<ref name="Sherrid, Chu et al 1993"/>. The abnormally directed outflow may be visualized behind and lateral to the enlarged mitral valve, where it catches it, and pushes it into the septum <ref name="Jiang, Levine et al 1987"/>
<ref name="Sherrid, Gunsburg et al 2000"/>
<ref name="Sherrid, Chu et al 1993"/>
<ref name="Levine, Vlahakes et al 1995"/>.
There is a crucial overlap between the inflow and outflow portions of the left ventricle
<ref name="Schwammenthal and Levine 1996">Schwammenthal E, Levine RA. Dynamic subaortic obstruction: a disease of the mitral valve suitable for surgical repair? ''[[Journal of the American College of Cardiology|J Am Coll Cardiol]]'' 1996; '''28''':203–6</ref>.
As SAM progresses in early systole the angle between outflow and the protruding mitral leaflet increases. A greater surface area of the leaflets is now exposed to drag which amplifies the force on the leaflets – drag increases with increasing angle relative to flow<ref name="Sherrid, Chu et al 1993"/>. An analogy is an open door in a drafty corridor: the door starts by moving slowly and then accelerates as it presents a greater surface area to the wind and finally it slams shut. The necessary conditions that predispose to SAM are: anterior position of the mitral valve in the LV, altered LV geometry that allows flow to strike the mitral valve from behind, and chordal slack
<ref name="Jiang, Levine et al 1987"/>
<ref name="Sherrid, Gunsburg et al 2000"/>
<ref name="Sherrid, Chu et al 1993"/>
<ref name="Levine, Vlahakes et al 1995"/>.
SAM may considered anteriorly directed mitral prolapse
<ref name="Sherrid, Gunsburg et al 2000"/>
<ref name="Sherrid, Chu et al 1993"/>
<ref name="Levine, Vlahakes et al 1995"/>.
In both conditions the mitral valve is enlarged and is displaced in systole by the pushing force of flow resulting in mitral regurgitation.

Because the mitral valve leaflet doesn't get pulled into the LVOT until after the aortic valve opens, the initial upstroke of the arterial pulse will be normal. When the mitral valve leaflet gets pushed into the LVOT, the arterial pulse will momentarily collapse and be followed by a second rise, as the left ventricular pressure overcomes the increased obstruction that SAM of the mitral valve causes. This can be seen on the physical examination as a double tap upon palpation of the apical impulse and as a double pulsation upon palpation of the carotid pulse, known as ''[[pulsus bisferiens]]''.

==References==
{{Reflist|2}}

[[Category: Cardiology]]
[[Category: Cardiomyopathy]]
[[Category: Overview complete]]
[[Category: Template complete]]
[[Category: Genetic disorders]]

Hypertrophic cardiomyopathy outflow obstruction

2011-08-14T20:11:48Z

C. Michael Gibson: /* Pathophysiology */

{{Hypertrophic cardiomyopathy}}

'''Editors-In-Chief:''' [[C. Michael Gibson, M.S., M.D.]] [mailto:mgibson@perfuse.org]

==Overview==
Depending on the degree of obstruction of the outflow of [[blood]] from the [[left ventricle]] of the heart, HCM can be defined as obstructive or non-obstructive. About 25% of individuals with HCM demonstrate an obstruction to the outflow of blood from the left ventricle during rest. In other individuals obstruction only occurs under certain conditions. This is known as dynamic outflow obstruction, because the degree of obstruction is variable and is dependent on the amount of blood in the ventricle immediately before ventricle [[systole (medicine)|systole]] (contraction).

==Location Of The Left Ventricular Outflow Obstruction==
The left ventricular obstruction can be either
*'''Mid-cavitary:''' the middle of the ventricle or
*'''Sub-aortic:''' just below the [[aortic valve]]

==Systolic Anterior Motion of the Mitral Valve (SAM)==
Dynamic outflow obstruction (when present in HCM) is usually due to systolic anterior motion (SAM) of the anterior leaflet of the [[mitral valve]]. Systolic anterior motion of the mitral valve (SAM) may be due to the septal subaortic bulge, narrowing the outflow tract, which in turn causes a high velocity flow and a Venturi effect — a local low pressure zone in the left ventricular outflow tract. This low pressure zone was thought to suck the [[mitral valve]] anteriorly into the septum. But SAM onset is observed to be a low velocity phenomenon: SAM begins at velocities no different from those measured in normals
<ref name="Jiang, Levine et al 1987">Jiang L, Levine RA, King ME, Weyman AE. An integrated mechanism for systolic anterior motion of the mitral valve in hypertrophic cardiomyopathy based on echocardiographic observations. ''Am Heart J'' 1987; '''113''':633–44</ref>
<ref name="Sherrid, Gunsburg et al 2000">Sherrid MV, Gunsburg DZ, Moldenhauer S, Pearle G. Systolic anterior motion begins at low left ventricular outflow tract velocity in obstructive hypertrophic cardiomyopathy. ''[[Journal of the American College of Cardiology|J Am Coll Cardiol]]'' 2000; '''36''':1344–54</ref>.
Hence, the magnitude and importance of Venturi forces in the outflow tract are may be less than previously thought, and Venturi forces may not be the main forces that initiates SAM.

<youtube v=Y7JUVTXHBs0/>

Recent echocardiographic evidence indicates that drag, the pushing force of flow is the dominant hydrodynamic force on the mitral leaflets
<ref name="Jiang, Levine et al 1987"/>
<ref name="Sherrid, Gunsburg et al 2000"/>
<ref name="Sherrid, Chu et al 1993">Sherrid MV, Chu Ck, DeLia E, Mogtader A, Dwyer Jr. EM, An echocardiographic study of the fluid mechanics of obstruction in hypertrophic cardiomyopathy. ''[[Journal of the American College of Cardiology|J Am Coll Cardiol]]'' 1993; '''22''':816–25</ref>
<ref name="Levine, Vlahakes et al 1995">Levine RA, Vlahakes GJ, Lefebvre X, et al. Papillary muscle displacement causes systolic anterior motion of the mitral valve. ''[[Circulation (journal)|Circulation]]'' 1995; '''91''':1189–95</ref>
<ref name="Messmer 1994">Messmer BJ. Extended myectomy for hypertrophic obstructive cardiomyopathy. ''Ann Thorac Surg'' 1994; '''58''':575–7</ref>
<ref name="Schoendube, Klues et al 1995">Schoendube FA, Klues HG, Reith S, Flachskampf FA, Hanrath P, Messmer BJ. Long-term clinical and echocardiographic follow-up after surgical correction of hypertrophic obstructive cardiomyopathy with extended myectomy and reconstruction of the subvalvular mitral apparatus. ''[[Circulation (journal)|Circulation]]'' 1995; '''92''':II-122–7</ref>.
In obstructive HCM the mitral leaflets are often large
<ref name="Klues, Maron et al 1992">Klues HG, Maron BJ, Dollar AL, Roberts WC. Diverstiy of structural mitral valve alterations in hypertrophic cardiomyopathy. ''[[Circulation (journal)|Circulation]]'' 1992; '''85''':1651–60</ref>
and are anteriorly positioned in the LV cavity
<ref name="Jiang, Levine et al 1987"/>
<ref name="Henry, Clark et al 1975">Henry WL, Clark CE, Griffith JM, Epstein SE. Mechanism of left ventricular outflow obstruction in patients with obstructive asymmetric septal hypertrophy (idiopathic hypertrophic subaortic stenosis). ''Am J Cardiol'' 1975; '''35''':337–45</ref>
due to anteriorly positioned papillary muscles<ref name="Jiang, Levine et al 1987"/> that at surgery are often "agglutinated" onto the LV anterior wall by abnormal attachments
<ref name="Messmer 1994"/>
<ref name="Schoendube, Klues et al 1995"/>.

The mid-septal bulge aggravates the malposition of the valve and redirects outflow so that it comes from a lateral and posterior direction<ref name="Sherrid, Chu et al 1993"/>. The abnormally directed outflow may be visualized behind and lateral to the enlarged mitral valve, where it catches it, and pushes it into the septum <ref name="Jiang, Levine et al 1987"/>
<ref name="Sherrid, Gunsburg et al 2000"/>
<ref name="Sherrid, Chu et al 1993"/>
<ref name="Levine, Vlahakes et al 1995"/>.
There is a crucial overlap between the inflow and outflow portions of the left ventricle
<ref name="Schwammenthal and Levine 1996">Schwammenthal E, Levine RA. Dynamic subaortic obstruction: a disease of the mitral valve suitable for surgical repair? ''[[Journal of the American College of Cardiology|J Am Coll Cardiol]]'' 1996; '''28''':203–6</ref>.
As SAM progresses in early systole the angle between outflow and the protruding mitral leaflet increases. A greater surface area of the leaflets is now exposed to drag which amplifies the force on the leaflets – drag increases with increasing angle relative to flow<ref name="Sherrid, Chu et al 1993"/>. An analogy is an open door in a drafty corridor: the door starts by moving slowly and then accelerates as it presents a greater surface area to the wind and finally it slams shut. The necessary conditions that predispose to SAM are: anterior position of the mitral valve in the LV, altered LV geometry that allows flow to strike the mitral valve from behind, and chordal slack
<ref name="Jiang, Levine et al 1987"/>
<ref name="Sherrid, Gunsburg et al 2000"/>
<ref name="Sherrid, Chu et al 1993"/>
<ref name="Levine, Vlahakes et al 1995"/>.
SAM may considered anteriorly directed mitral prolapse
<ref name="Sherrid, Gunsburg et al 2000"/>
<ref name="Sherrid, Chu et al 1993"/>
<ref name="Levine, Vlahakes et al 1995"/>.
In both conditions the mitral valve is enlarged and is displaced in systole by the pushing force of flow resulting in mitral regurgitation.

Because the mitral valve leaflet doesn't get pulled into the LVOT until after the aortic valve opens, the initial upstroke of the arterial pulse will be normal. When the mitral valve leaflet gets pushed into the LVOT, the arterial pulse will momentarily collapse and be followed by a second rise, as the left ventricular pressure overcomes the increased obstruction that SAM of the mitral valve causes. This can be seen on the physical examination as a double tap upon palpation of the apical impulse and as a double pulsation upon palpation of the carotid pulse, known as ''[[pulsus bisferiens]]''.

==References==
{{Reflist|2}}

[[Category: Cardiology]]
[[Category: Cardiomyopathy]]
[[Category: Overview complete]]
[[Category: Template complete]]
[[Category: Genetic disorders]]

Hypertrophic cardiomyopathy outflow obstruction

2011-08-14T20:11:04Z

C. Michael Gibson: /* Pathophysiology */

{{Hypertrophic cardiomyopathy}}

'''Editors-In-Chief:''' [[C. Michael Gibson, M.S., M.D.]] [mailto:mgibson@perfuse.org]

==Overview==
Depending on the degree of obstruction of the outflow of [[blood]] from the [[left ventricle]] of the heart, HCM can be defined as obstructive or non-obstructive. About 25% of individuals with HCM demonstrate an obstruction to the outflow of blood from the left ventricle during rest. In other individuals obstruction only occurs under certain conditions. This is known as dynamic outflow obstruction, because the degree of obstruction is variable and is dependent on the amount of blood in the ventricle immediately before ventricle [[systole (medicine)|systole]] (contraction).

==Location Of The Left Ventricular Outflow Obstruction==
The left ventricular obstruction can be either
*'''Mid-cavitary:''' the middle of the ventricle or
*'''Sub-aortic:''' just below the [[aortic valve]]

==Pathophysiology==
Dynamic outflow obstruction (when present in HCM) is usually due to systolic anterior motion (SAM) of the anterior leaflet of the [[mitral valve]]. Systolic anterior motion of the mitral valve (SAM) may be due to the septal subaortic bulge, narrowing the outflow tract, which in turn causes a high velocity flow and a Venturi effect — a local low pressure zone in the left ventricular outflow tract. This low pressure zone was thought to suck the [[mitral valve]] anteriorly into the septum. But SAM onset is observed to be a low velocity phenomenon: SAM begins at velocities no different from those measured in normals
<ref name="Jiang, Levine et al 1987">Jiang L, Levine RA, King ME, Weyman AE. An integrated mechanism for systolic anterior motion of the mitral valve in hypertrophic cardiomyopathy based on echocardiographic observations. ''Am Heart J'' 1987; '''113''':633–44</ref>
<ref name="Sherrid, Gunsburg et al 2000">Sherrid MV, Gunsburg DZ, Moldenhauer S, Pearle G. Systolic anterior motion begins at low left ventricular outflow tract velocity in obstructive hypertrophic cardiomyopathy. ''[[Journal of the American College of Cardiology|J Am Coll Cardiol]]'' 2000; '''36''':1344–54</ref>.
Hence, the magnitude and importance of Venturi forces in the outflow tract are may be less than previously thought, and Venturi forces may not be the main forces that initiates SAM.

<youtube v=Y7JUVTXHBs0/>

Recent echocardiographic evidence indicates that drag, the pushing force of flow is the dominant hydrodynamic force on the mitral leaflets
<ref name="Jiang, Levine et al 1987"/>
<ref name="Sherrid, Gunsburg et al 2000"/>
<ref name="Sherrid, Chu et al 1993">Sherrid MV, Chu Ck, DeLia E, Mogtader A, Dwyer Jr. EM, An echocardiographic study of the fluid mechanics of obstruction in hypertrophic cardiomyopathy. ''[[Journal of the American College of Cardiology|J Am Coll Cardiol]]'' 1993; '''22''':816–25</ref>
<ref name="Levine, Vlahakes et al 1995">Levine RA, Vlahakes GJ, Lefebvre X, et al. Papillary muscle displacement causes systolic anterior motion of the mitral valve. ''[[Circulation (journal)|Circulation]]'' 1995; '''91''':1189–95</ref>
<ref name="Messmer 1994">Messmer BJ. Extended myectomy for hypertrophic obstructive cardiomyopathy. ''Ann Thorac Surg'' 1994; '''58''':575–7</ref>
<ref name="Schoendube, Klues et al 1995">Schoendube FA, Klues HG, Reith S, Flachskampf FA, Hanrath P, Messmer BJ. Long-term clinical and echocardiographic follow-up after surgical correction of hypertrophic obstructive cardiomyopathy with extended myectomy and reconstruction of the subvalvular mitral apparatus. ''[[Circulation (journal)|Circulation]]'' 1995; '''92''':II-122–7</ref>.
In obstructive HCM the mitral leaflets are often large
<ref name="Klues, Maron et al 1992">Klues HG, Maron BJ, Dollar AL, Roberts WC. Diverstiy of structural mitral valve alterations in hypertrophic cardiomyopathy. ''[[Circulation (journal)|Circulation]]'' 1992; '''85''':1651–60</ref>
and are anteriorly positioned in the LV cavity
<ref name="Jiang, Levine et al 1987"/>
<ref name="Henry, Clark et al 1975">Henry WL, Clark CE, Griffith JM, Epstein SE. Mechanism of left ventricular outflow obstruction in patients with obstructive asymmetric septal hypertrophy (idiopathic hypertrophic subaortic stenosis). ''Am J Cardiol'' 1975; '''35''':337–45</ref>
due to anteriorly positioned papillary muscles<ref name="Jiang, Levine et al 1987"/> that at surgery are often "agglutinated" onto the LV anterior wall by abnormal attachments
<ref name="Messmer 1994"/>
<ref name="Schoendube, Klues et al 1995"/>.

The mid-septal bulge aggravates the malposition of the valve and redirects outflow so that it comes from a lateral and posterior direction<ref name="Sherrid, Chu et al 1993"/>. The abnormally directed outflow may be visualized behind and lateral to the enlarged mitral valve, where it catches it, and pushes it into the septum <ref name="Jiang, Levine et al 1987"/>
<ref name="Sherrid, Gunsburg et al 2000"/>
<ref name="Sherrid, Chu et al 1993"/>
<ref name="Levine, Vlahakes et al 1995"/>.
There is a crucial overlap between the inflow and outflow portions of the left ventricle
<ref name="Schwammenthal and Levine 1996">Schwammenthal E, Levine RA. Dynamic subaortic obstruction: a disease of the mitral valve suitable for surgical repair? ''[[Journal of the American College of Cardiology|J Am Coll Cardiol]]'' 1996; '''28''':203–6</ref>.
As SAM progresses in early systole the angle between outflow and the protruding mitral leaflet increases. A greater surface area of the leaflets is now exposed to drag which amplifies the force on the leaflets – drag increases with increasing angle relative to flow<ref name="Sherrid, Chu et al 1993"/>. An analogy is an open door in a drafty corridor: the door starts by moving slowly and then accelerates as it presents a greater surface area to the wind and finally it slams shut. The necessary conditions that predispose to SAM are: anterior position of the mitral valve in the LV, altered LV geometry that allows flow to strike the mitral valve from behind, and chordal slack
<ref name="Jiang, Levine et al 1987"/>
<ref name="Sherrid, Gunsburg et al 2000"/>
<ref name="Sherrid, Chu et al 1993"/>
<ref name="Levine, Vlahakes et al 1995"/>.
SAM may considered anteriorly directed mitral prolapse
<ref name="Sherrid, Gunsburg et al 2000"/>
<ref name="Sherrid, Chu et al 1993"/>
<ref name="Levine, Vlahakes et al 1995"/>.
In both conditions the mitral valve is enlarged and is displaced in systole by the pushing force of flow resulting in mitral regurgitation.

Because the mitral valve leaflet doesn't get pulled into the LVOT until after the aortic valve opens, the initial upstroke of the arterial pulse will be normal. When the mitral valve leaflet gets pushed into the LVOT, the arterial pulse will momentarily collapse and be followed by a second rise, as the left ventricular pressure overcomes the increased obstruction that SAM of the mitral valve causes. This can be seen on the physical examination as a double tap upon palpation of the apical impulse and as a double pulsation upon palpation of the carotid pulse, known as ''[[pulsus bisferiens]]''.

==References==
{{Reflist|2}}

[[Category: Cardiology]]
[[Category: Cardiomyopathy]]
[[Category: Overview complete]]
[[Category: Template complete]]
[[Category: Genetic disorders]]

Hypertrophic cardiomyopathy outflow obstruction

2011-08-14T20:01:02Z

C. Michael Gibson: /* Location Of The Left Ventricular Outflow Obstruction */

{{Hypertrophic cardiomyopathy}}

'''Editors-In-Chief:''' [[C. Michael Gibson, M.S., M.D.]] [mailto:mgibson@perfuse.org]

==Overview==
Depending on the degree of obstruction of the outflow of [[blood]] from the [[left ventricle]] of the heart, HCM can be defined as obstructive or non-obstructive. About 25% of individuals with HCM demonstrate an obstruction to the outflow of blood from the left ventricle during rest. In other individuals obstruction only occurs under certain conditions. This is known as dynamic outflow obstruction, because the degree of obstruction is variable and is dependent on the amount of blood in the ventricle immediately before ventricle [[systole (medicine)|systole]] (contraction).

==Location Of The Left Ventricular Outflow Obstruction==
The left ventricular obstruction can be either
*'''Mid-cavitary:''' the middle of the ventricle or
*'''Sub-aortic:''' just below the [[aortic valve]]

==Pathophysiology==
Dynamic outflow obstruction (when present in HCM) is usually due to systolic anterior motion (SAM) of the anterior leaflet of the [[mitral valve]]. Systolic anterior motion of the mitral valve (SAM) was initially thought to be due to the septal subaortic bulge, narrowing the outflow tract, causing high velocity flow and a Venturi effect — a local underpressure in the outflow tract. Low pressure was thought to suck the mitral valve anteriorly into the septum. But SAM onset is observed to be a low velocity phenomenon: SAM begins at velocities no different from those measured in normals
<ref name="Jiang, Levine et al 1987">Jiang L, Levine RA, King ME, Weyman AE. An integrated mechanism for systolic anterior motion of the mitral valve in hypertrophic cardiomyopathy based on echocardiographic observations. ''Am Heart J'' 1987; '''113''':633–44</ref>
<ref name="Sherrid, Gunsburg et al 2000">Sherrid MV, Gunsburg DZ, Moldenhauer S, Pearle G. Systolic anterior motion begins at low left ventricular outflow tract velocity in obstructive hypertrophic cardiomyopathy. ''[[Journal of the American College of Cardiology|J Am Coll Cardiol]]'' 2000; '''36''':1344–54</ref>.
Hence, the magnitude and importance of Venturi forces in the outflow tract are much less than previously thought, and Venturi forces cannot be the main force that initiates SAM.

Recent echocardiographic evidence indicates that drag, the pushing force of flow is the dominant hydrodynamic force on the mitral leaflets
<ref name="Jiang, Levine et al 1987"/>
<ref name="Sherrid, Gunsburg et al 2000"/>
<ref name="Sherrid, Chu et al 1993">Sherrid MV, Chu Ck, DeLia E, Mogtader A, Dwyer Jr. EM, An echocardiographic study of the fluid mechanics of obstruction in hypertrophic cardiomyopathy. ''[[Journal of the American College of Cardiology|J Am Coll Cardiol]]'' 1993; '''22''':816–25</ref>
<ref name="Levine, Vlahakes et al 1995">Levine RA, Vlahakes GJ, Lefebvre X, et al. Papillary muscle displacement causes systolic anterior motion of the mitral valve. ''[[Circulation (journal)|Circulation]]'' 1995; '''91''':1189–95</ref>
<ref name="Messmer 1994">Messmer BJ. Extended myectomy for hypertrophic obstructive cardiomyopathy. ''Ann Thorac Surg'' 1994; '''58''':575–7</ref>
<ref name="Schoendube, Klues et al 1995">Schoendube FA, Klues HG, Reith S, Flachskampf FA, Hanrath P, Messmer BJ. Long-term clinical and echocardiographic follow-up after surgical correction of hypertrophic obstructive cardiomyopathy with extended myectomy and reconstruction of the subvalvular mitral apparatus. ''[[Circulation (journal)|Circulation]]'' 1995; '''92''':II-122–7</ref>.
In obstructive HCM the mitral leaflets are often large
<ref name="Klues, Maron et al 1992">Klues HG, Maron BJ, Dollar AL, Roberts WC. Diverstiy of structural mitral valve alterations in hypertrophic cardiomyopathy. ''[[Circulation (journal)|Circulation]]'' 1992; '''85''':1651–60</ref>
and are anteriorly positioned in the LV cavity
<ref name="Jiang, Levine et al 1987"/>
<ref name="Henry, Clark et al 1975">Henry WL, Clark CE, Griffith JM, Epstein SE. Mechanism of left ventricular outflow obstruction in patients with obstructive asymmetric septal hypertrophy (idiopathic hypertrophic subaortic stenosis). ''Am J Cardiol'' 1975; '''35''':337–45</ref>
due to anteriorly positioned papillary muscles<ref name="Jiang, Levine et al 1987"/> that at surgery are often "agglutinated" onto the LV anterior wall by abnormal attachments
<ref name="Messmer 1994"/>
<ref name="Schoendube, Klues et al 1995"/>.

The mid-septal bulge aggravates the malposition of the valve and redirects outflow so that it comes from a lateral and posterior direction<ref name="Sherrid, Chu et al 1993"/>. The abnormally directed outflow may be visualized behind and lateral to the enlarged mitral valve, where it catches it, and pushes it into the septum <ref name="Jiang, Levine et al 1987"/>
<ref name="Sherrid, Gunsburg et al 2000"/>
<ref name="Sherrid, Chu et al 1993"/>
<ref name="Levine, Vlahakes et al 1995"/>.
There is a crucial overlap between the inflow and outflow portions of the left ventricle
<ref name="Schwammenthal and Levine 1996">Schwammenthal E, Levine RA. Dynamic subaortic obstruction: a disease of the mitral valve suitable for surgical repair? ''[[Journal of the American College of Cardiology|J Am Coll Cardiol]]'' 1996; '''28''':203–6</ref>.
As SAM progresses in early systole the angle between outflow and the protruding mitral leaflet increases. A greater surface area of the leaflets is now exposed to drag which amplifies the force on the leaflets – drag increases with increasing angle relative to flow<ref name="Sherrid, Chu et al 1993"/>. An analogy is an open door in a drafty corridor: the door starts by moving slowly and then accelerates as it presents a greater surface area to the wind and finally it slams shut. The necessary conditions that predispose to SAM are: anterior position of the mitral valve in the LV, altered LV geometry that allows flow to strike the mitral valve from behind, and chordal slack
<ref name="Jiang, Levine et al 1987"/>
<ref name="Sherrid, Gunsburg et al 2000"/>
<ref name="Sherrid, Chu et al 1993"/>
<ref name="Levine, Vlahakes et al 1995"/>.
SAM may considered anteriorly directed mitral prolapse
<ref name="Sherrid, Gunsburg et al 2000"/>
<ref name="Sherrid, Chu et al 1993"/>
<ref name="Levine, Vlahakes et al 1995"/>.
In both conditions the mitral valve is enlarged and is displaced in systole by the pushing force of flow resulting in mitral regurgitation.

Because the mitral valve leaflet doesn't get pulled into the LVOT until after the aortic valve opens, the initial upstroke of the arterial pulse will be normal. When the mitral valve leaflet gets pushed into the LVOT, the arterial pulse will momentarily collapse and be followed by a second rise, as the left ventricular pressure overcomes the increased obstruction that SAM of the mitral valve causes. This can be seen on the physical examination as a double tap upon palpation of the apical impulse and as a double pulsation upon palpation of the carotid pulse, known as ''[[pulsus bisferiens]]''.

==References==
{{Reflist|2}}

[[Category: Cardiology]]
[[Category: Cardiomyopathy]]
[[Category: Overview complete]]
[[Category: Template complete]]
[[Category: Genetic disorders]]

Hypertrophic cardiomyopathy outflow obstruction

2011-08-14T19:58:47Z

C. Michael Gibson: /* Overview */

{{Hypertrophic cardiomyopathy}}

'''Editors-In-Chief:''' [[C. Michael Gibson, M.S., M.D.]] [mailto:mgibson@perfuse.org]

==Overview==
Depending on the degree of obstruction of the outflow of [[blood]] from the [[left ventricle]] of the heart, HCM can be defined as obstructive or non-obstructive. About 25% of individuals with HCM demonstrate an obstruction to the outflow of blood from the left ventricle during rest. In other individuals obstruction only occurs under certain conditions. This is known as dynamic outflow obstruction, because the degree of obstruction is variable and is dependent on the amount of blood in the ventricle immediately before ventricle [[systole (medicine)|systole]] (contraction).

==Location Of The Left Ventricular Outflow Obstruction==
The obstruction can be located in the middle of the ventricle (mid-cavitary) or just below the aortic valve (sub-aortic).

==Pathophysiology==
Dynamic outflow obstruction (when present in HCM) is usually due to systolic anterior motion (SAM) of the anterior leaflet of the [[mitral valve]]. Systolic anterior motion of the mitral valve (SAM) was initially thought to be due to the septal subaortic bulge, narrowing the outflow tract, causing high velocity flow and a Venturi effect — a local underpressure in the outflow tract. Low pressure was thought to suck the mitral valve anteriorly into the septum. But SAM onset is observed to be a low velocity phenomenon: SAM begins at velocities no different from those measured in normals
<ref name="Jiang, Levine et al 1987">Jiang L, Levine RA, King ME, Weyman AE. An integrated mechanism for systolic anterior motion of the mitral valve in hypertrophic cardiomyopathy based on echocardiographic observations. ''Am Heart J'' 1987; '''113''':633–44</ref>
<ref name="Sherrid, Gunsburg et al 2000">Sherrid MV, Gunsburg DZ, Moldenhauer S, Pearle G. Systolic anterior motion begins at low left ventricular outflow tract velocity in obstructive hypertrophic cardiomyopathy. ''[[Journal of the American College of Cardiology|J Am Coll Cardiol]]'' 2000; '''36''':1344–54</ref>.
Hence, the magnitude and importance of Venturi forces in the outflow tract are much less than previously thought, and Venturi forces cannot be the main force that initiates SAM.

Recent echocardiographic evidence indicates that drag, the pushing force of flow is the dominant hydrodynamic force on the mitral leaflets
<ref name="Jiang, Levine et al 1987"/>
<ref name="Sherrid, Gunsburg et al 2000"/>
<ref name="Sherrid, Chu et al 1993">Sherrid MV, Chu Ck, DeLia E, Mogtader A, Dwyer Jr. EM, An echocardiographic study of the fluid mechanics of obstruction in hypertrophic cardiomyopathy. ''[[Journal of the American College of Cardiology|J Am Coll Cardiol]]'' 1993; '''22''':816–25</ref>
<ref name="Levine, Vlahakes et al 1995">Levine RA, Vlahakes GJ, Lefebvre X, et al. Papillary muscle displacement causes systolic anterior motion of the mitral valve. ''[[Circulation (journal)|Circulation]]'' 1995; '''91''':1189–95</ref>
<ref name="Messmer 1994">Messmer BJ. Extended myectomy for hypertrophic obstructive cardiomyopathy. ''Ann Thorac Surg'' 1994; '''58''':575–7</ref>
<ref name="Schoendube, Klues et al 1995">Schoendube FA, Klues HG, Reith S, Flachskampf FA, Hanrath P, Messmer BJ. Long-term clinical and echocardiographic follow-up after surgical correction of hypertrophic obstructive cardiomyopathy with extended myectomy and reconstruction of the subvalvular mitral apparatus. ''[[Circulation (journal)|Circulation]]'' 1995; '''92''':II-122–7</ref>.
In obstructive HCM the mitral leaflets are often large
<ref name="Klues, Maron et al 1992">Klues HG, Maron BJ, Dollar AL, Roberts WC. Diverstiy of structural mitral valve alterations in hypertrophic cardiomyopathy. ''[[Circulation (journal)|Circulation]]'' 1992; '''85''':1651–60</ref>
and are anteriorly positioned in the LV cavity
<ref name="Jiang, Levine et al 1987"/>
<ref name="Henry, Clark et al 1975">Henry WL, Clark CE, Griffith JM, Epstein SE. Mechanism of left ventricular outflow obstruction in patients with obstructive asymmetric septal hypertrophy (idiopathic hypertrophic subaortic stenosis). ''Am J Cardiol'' 1975; '''35''':337–45</ref>
due to anteriorly positioned papillary muscles<ref name="Jiang, Levine et al 1987"/> that at surgery are often "agglutinated" onto the LV anterior wall by abnormal attachments
<ref name="Messmer 1994"/>
<ref name="Schoendube, Klues et al 1995"/>.

The mid-septal bulge aggravates the malposition of the valve and redirects outflow so that it comes from a lateral and posterior direction<ref name="Sherrid, Chu et al 1993"/>. The abnormally directed outflow may be visualized behind and lateral to the enlarged mitral valve, where it catches it, and pushes it into the septum <ref name="Jiang, Levine et al 1987"/>
<ref name="Sherrid, Gunsburg et al 2000"/>
<ref name="Sherrid, Chu et al 1993"/>
<ref name="Levine, Vlahakes et al 1995"/>.
There is a crucial overlap between the inflow and outflow portions of the left ventricle
<ref name="Schwammenthal and Levine 1996">Schwammenthal E, Levine RA. Dynamic subaortic obstruction: a disease of the mitral valve suitable for surgical repair? ''[[Journal of the American College of Cardiology|J Am Coll Cardiol]]'' 1996; '''28''':203–6</ref>.
As SAM progresses in early systole the angle between outflow and the protruding mitral leaflet increases. A greater surface area of the leaflets is now exposed to drag which amplifies the force on the leaflets – drag increases with increasing angle relative to flow<ref name="Sherrid, Chu et al 1993"/>. An analogy is an open door in a drafty corridor: the door starts by moving slowly and then accelerates as it presents a greater surface area to the wind and finally it slams shut. The necessary conditions that predispose to SAM are: anterior position of the mitral valve in the LV, altered LV geometry that allows flow to strike the mitral valve from behind, and chordal slack
<ref name="Jiang, Levine et al 1987"/>
<ref name="Sherrid, Gunsburg et al 2000"/>
<ref name="Sherrid, Chu et al 1993"/>
<ref name="Levine, Vlahakes et al 1995"/>.
SAM may considered anteriorly directed mitral prolapse
<ref name="Sherrid, Gunsburg et al 2000"/>
<ref name="Sherrid, Chu et al 1993"/>
<ref name="Levine, Vlahakes et al 1995"/>.
In both conditions the mitral valve is enlarged and is displaced in systole by the pushing force of flow resulting in mitral regurgitation.

Because the mitral valve leaflet doesn't get pulled into the LVOT until after the aortic valve opens, the initial upstroke of the arterial pulse will be normal. When the mitral valve leaflet gets pushed into the LVOT, the arterial pulse will momentarily collapse and be followed by a second rise, as the left ventricular pressure overcomes the increased obstruction that SAM of the mitral valve causes. This can be seen on the physical examination as a double tap upon palpation of the apical impulse and as a double pulsation upon palpation of the carotid pulse, known as ''[[pulsus bisferiens]]''.

==References==
{{Reflist|2}}

[[Category: Cardiology]]
[[Category: Cardiomyopathy]]
[[Category: Overview complete]]
[[Category: Template complete]]
[[Category: Genetic disorders]]

Hypertrophic cardiomyopathy anatomic abnormalities

2011-08-14T19:50:13Z

C. Michael Gibson: /* Left Ventricular Hypertrophy */

{{Hypertrophic cardiomyopathy}}

'''Editors-In-Chief:''' [[C. Michael Gibson, M.S., M.D.]] [mailto:mgibson@perfuse.org]

==Overview==
Individuals with HCM have some degree of [[left ventricular hypertrophy]]. In approximately 2/3rds of cases this is an asymmetric hypertrophy, involving the inter-ventricular septum, and is known as [[asymmetric septal hypertrophy]] ([http://www.cardiomyopathy.org/html/which_card_hcm.htm ASH]). This is in contrast to the symmetric and concentric hypertrophy seen in [[aortic stenosis]] or [[hypertension]].

==Left Ventricle==
The degree of ventricular hypertrophy is variable ranging from diffuse involvement of both ventricles to isolated involvement of a portion of one segment of the [[LV]].

Data from two large registries indicates that;
*55% of cases involve the septum and anterolateral free wall,
*20% involve the entire septum alone,
*10% are limited to the basal septum and 15% are limited to the apical or distal LV (Yamaguchi variant).

Some genetic variants may manifest very little overt [[LVH]] but are still associated with an increased risk of [[sudden cardiac death]] (SCD).

==Outflow Tract==
The [[left ventricular outflow tract]] is often small.

==Mitral Valve==
The [[mitral valve]] maybe elongated and enlarged.

==References==
{{Reflist|2}}

[[Category: Cardiology]]
[[Category: Cardiomyopathy]]
[[Category: Overview complete]]
[[Category: Template complete]]
[[Category: Genetic disorders]]

Hypertrophic cardiomyopathy anatomic abnormalities

2011-08-14T19:49:40Z

C. Michael Gibson: /* Outflow Tract */

{{Hypertrophic cardiomyopathy}}

'''Editors-In-Chief:''' [[C. Michael Gibson, M.S., M.D.]] [mailto:mgibson@perfuse.org]

==Overview==
Individuals with HCM have some degree of [[left ventricular hypertrophy]]. In approximately 2/3rds of cases this is an asymmetric hypertrophy, involving the inter-ventricular septum, and is known as [[asymmetric septal hypertrophy]] ([http://www.cardiomyopathy.org/html/which_card_hcm.htm ASH]). This is in contrast to the symmetric and concentric hypertrophy seen in [[aortic stenosis]] or [[hypertension]].

==Left Ventricular Hypertrophy==
The degree of ventricular hypertrophy is variable ranging from diffuse involvement of both ventricles to isolated involvement of a portion of one segment of the [[LV]].

Data from two large registries indicates that;
*55% of cases involve the septum and anterolateral free wall,
*20% involve the entire septum alone,
*10% are limited to the basal septum and 15% are limited to the apical or distal LV (Yamaguchi variant).

Some genetic variants may manifest very little overt [[LVH]] but are still associated with an increased risk of [[sudden cardiac death]] (SCD).

==Outflow Tract==
The [[left ventricular outflow tract]] is often small.

==Mitral Valve==
The [[mitral valve]] maybe elongated and enlarged.

==References==
{{Reflist|2}}

[[Category: Cardiology]]
[[Category: Cardiomyopathy]]
[[Category: Overview complete]]
[[Category: Template complete]]
[[Category: Genetic disorders]]

Hypertrophic cardiomyopathy anatomic abnormalities

2011-08-14T19:47:47Z

C. Michael Gibson: /* Hypertrophy */

{{Hypertrophic cardiomyopathy}}

'''Editors-In-Chief:''' [[C. Michael Gibson, M.S., M.D.]] [mailto:mgibson@perfuse.org]

==Overview==
Individuals with HCM have some degree of [[left ventricular hypertrophy]]. In approximately 2/3rds of cases this is an asymmetric hypertrophy, involving the inter-ventricular septum, and is known as [[asymmetric septal hypertrophy]] ([http://www.cardiomyopathy.org/html/which_card_hcm.htm ASH]). This is in contrast to the symmetric and concentric hypertrophy seen in [[aortic stenosis]] or [[hypertension]].

==Left Ventricular Hypertrophy==
The degree of ventricular hypertrophy is variable ranging from diffuse involvement of both ventricles to isolated involvement of a portion of one segment of the [[LV]].

Data from two large registries indicates that;
*55% of cases involve the septum and anterolateral free wall,
*20% involve the entire septum alone,
*10% are limited to the basal septum and 15% are limited to the apical or distal LV (Yamaguchi variant).

Some genetic variants may manifest very little overt [[LVH]] but are still associated with an increased risk of [[sudden cardiac death]] (SCD).

==Outflow Tract==
The left ventricular outflow tract is often small.

==References==
{{Reflist|2}}

[[Category: Cardiology]]
[[Category: Cardiomyopathy]]
[[Category: Overview complete]]
[[Category: Template complete]]
[[Category: Genetic disorders]]

Hypertrophic cardiomyopathy anatomic abnormalities

2011-08-14T19:46:50Z

C. Michael Gibson: /* Hypertrophy */

{{Hypertrophic cardiomyopathy}}

'''Editors-In-Chief:''' [[C. Michael Gibson, M.S., M.D.]] [mailto:mgibson@perfuse.org]

==Overview==
Individuals with HCM have some degree of [[left ventricular hypertrophy]]. In approximately 2/3rds of cases this is an asymmetric hypertrophy, involving the inter-ventricular septum, and is known as [[asymmetric septal hypertrophy]] ([http://www.cardiomyopathy.org/html/which_card_hcm.htm ASH]). This is in contrast to the symmetric and concentric hypertrophy seen in [[aortic stenosis]] or [[hypertension]].

==Hypertrophy==
The degree of ventricular hypertrophy is variable ranging from diffuse involvement of both ventricles to isolated involvement of a portion of one segment of the [[LV]].

Data from two large registries indicates that;
*55% of cases involve the septum and anterolateral free wall,
*20% involve the entire septum alone,
*10% are limited to the basal septum and 15% are limited to the apical or distal LV (Yamaguchi variant).

Some genetic variants may manifest very little overt [[LVH]] but are still associated with an increased risk of [[sudden cardiac death]] (SCD).

==Outflow Tract==
The left ventricular outflow tract is often small.

==References==
{{Reflist|2}}

[[Category: Cardiology]]
[[Category: Cardiomyopathy]]
[[Category: Overview complete]]
[[Category: Template complete]]
[[Category: Genetic disorders]]

Hypertrophic cardiomyopathy anatomic abnormalities

2011-08-14T19:45:31Z

C. Michael Gibson: /* Overview */

{{Hypertrophic cardiomyopathy}}

'''Editors-In-Chief:''' [[C. Michael Gibson, M.S., M.D.]] [mailto:mgibson@perfuse.org]

==Overview==
Individuals with HCM have some degree of [[left ventricular hypertrophy]]. In approximately 2/3rds of cases this is an asymmetric hypertrophy, involving the inter-ventricular septum, and is known as [[asymmetric septal hypertrophy]] ([http://www.cardiomyopathy.org/html/which_card_hcm.htm ASH]). This is in contrast to the symmetric and concentric hypertrophy seen in [[aortic stenosis]] or [[hypertension]].

==Hypertrophy==
The degree of ventricular hypertrophy is variable ranging from diffuse involvement of both ventricles to isolated involvement of a portion of one segment of the [[LV]].

Data from two large registries indicates that;
*55% of cases involve the septum and anterolateral free wall,
*20% involve the entire septum alone,
*10% are limited to the basal septum and 15% are limited to the apical or distal LV (Yamaguchi variant).

Some genetic variants may manifest very little overt [[LVH]] but are still associated with an increased risk of [[sudden cardiac death]] (SCD).

==References==
{{Reflist|2}}

[[Category: Cardiology]]
[[Category: Cardiomyopathy]]
[[Category: Overview complete]]
[[Category: Template complete]]
[[Category: Genetic disorders]]

Hypertrophic cardiomyopathy outflow obstruction

2011-08-14T19:42:07Z

C. Michael Gibson: /* Overview */

{{Hypertrophic cardiomyopathy}}

'''Editors-In-Chief:''' [[C. Michael Gibson, M.S., M.D.]] [mailto:mgibson@perfuse.org]

==Overview==
Depending on the degree of obstruction of the outflow of [[blood]] from the [[left ventricle]] of the heart, HCM can be defined as obstructive or non-obstructive. About 25% of individuals with HCM demonstrate an obstruction to the outflow of blood from the left ventricle during rest. In other individuals obstruction only occurs under certain conditions. This is known as dynamic outflow obstruction, because the degree of obstruction is variable and is dependent on the amount of blood in the ventricle immediately before ventricle [[systole (medicine)|systole]] (contraction).

==Pathophysiology==
Dynamic outflow obstruction (when present in HCM) is usually due to systolic anterior motion (SAM) of the anterior leaflet of the [[mitral valve]]. Systolic anterior motion of the mitral valve (SAM) was initially thought to be due to the septal subaortic bulge, narrowing the outflow tract, causing high velocity flow and a Venturi effect — a local underpressure in the outflow tract. Low pressure was thought to suck the mitral valve anteriorly into the septum. But SAM onset is observed to be a low velocity phenomenon: SAM begins at velocities no different from those measured in normals
<ref name="Jiang, Levine et al 1987">Jiang L, Levine RA, King ME, Weyman AE. An integrated mechanism for systolic anterior motion of the mitral valve in hypertrophic cardiomyopathy based on echocardiographic observations. ''Am Heart J'' 1987; '''113''':633–44</ref>
<ref name="Sherrid, Gunsburg et al 2000">Sherrid MV, Gunsburg DZ, Moldenhauer S, Pearle G. Systolic anterior motion begins at low left ventricular outflow tract velocity in obstructive hypertrophic cardiomyopathy. ''[[Journal of the American College of Cardiology|J Am Coll Cardiol]]'' 2000; '''36''':1344–54</ref>.
Hence, the magnitude and importance of Venturi forces in the outflow tract are much less than previously thought, and Venturi forces cannot be the main force that initiates SAM.

Recent echocardiographic evidence indicates that drag, the pushing force of flow is the dominant hydrodynamic force on the mitral leaflets
<ref name="Jiang, Levine et al 1987"/>
<ref name="Sherrid, Gunsburg et al 2000"/>
<ref name="Sherrid, Chu et al 1993">Sherrid MV, Chu Ck, DeLia E, Mogtader A, Dwyer Jr. EM, An echocardiographic study of the fluid mechanics of obstruction in hypertrophic cardiomyopathy. ''[[Journal of the American College of Cardiology|J Am Coll Cardiol]]'' 1993; '''22''':816–25</ref>
<ref name="Levine, Vlahakes et al 1995">Levine RA, Vlahakes GJ, Lefebvre X, et al. Papillary muscle displacement causes systolic anterior motion of the mitral valve. ''[[Circulation (journal)|Circulation]]'' 1995; '''91''':1189–95</ref>
<ref name="Messmer 1994">Messmer BJ. Extended myectomy for hypertrophic obstructive cardiomyopathy. ''Ann Thorac Surg'' 1994; '''58''':575–7</ref>
<ref name="Schoendube, Klues et al 1995">Schoendube FA, Klues HG, Reith S, Flachskampf FA, Hanrath P, Messmer BJ. Long-term clinical and echocardiographic follow-up after surgical correction of hypertrophic obstructive cardiomyopathy with extended myectomy and reconstruction of the subvalvular mitral apparatus. ''[[Circulation (journal)|Circulation]]'' 1995; '''92''':II-122–7</ref>.
In obstructive HCM the mitral leaflets are often large
<ref name="Klues, Maron et al 1992">Klues HG, Maron BJ, Dollar AL, Roberts WC. Diverstiy of structural mitral valve alterations in hypertrophic cardiomyopathy. ''[[Circulation (journal)|Circulation]]'' 1992; '''85''':1651–60</ref>
and are anteriorly positioned in the LV cavity
<ref name="Jiang, Levine et al 1987"/>
<ref name="Henry, Clark et al 1975">Henry WL, Clark CE, Griffith JM, Epstein SE. Mechanism of left ventricular outflow obstruction in patients with obstructive asymmetric septal hypertrophy (idiopathic hypertrophic subaortic stenosis). ''Am J Cardiol'' 1975; '''35''':337–45</ref>
due to anteriorly positioned papillary muscles<ref name="Jiang, Levine et al 1987"/> that at surgery are often "agglutinated" onto the LV anterior wall by abnormal attachments
<ref name="Messmer 1994"/>
<ref name="Schoendube, Klues et al 1995"/>.

The mid-septal bulge aggravates the malposition of the valve and redirects outflow so that it comes from a lateral and posterior direction<ref name="Sherrid, Chu et al 1993"/>. The abnormally directed outflow may be visualized behind and lateral to the enlarged mitral valve, where it catches it, and pushes it into the septum <ref name="Jiang, Levine et al 1987"/>
<ref name="Sherrid, Gunsburg et al 2000"/>
<ref name="Sherrid, Chu et al 1993"/>
<ref name="Levine, Vlahakes et al 1995"/>.
There is a crucial overlap between the inflow and outflow portions of the left ventricle
<ref name="Schwammenthal and Levine 1996">Schwammenthal E, Levine RA. Dynamic subaortic obstruction: a disease of the mitral valve suitable for surgical repair? ''[[Journal of the American College of Cardiology|J Am Coll Cardiol]]'' 1996; '''28''':203–6</ref>.
As SAM progresses in early systole the angle between outflow and the protruding mitral leaflet increases. A greater surface area of the leaflets is now exposed to drag which amplifies the force on the leaflets – drag increases with increasing angle relative to flow<ref name="Sherrid, Chu et al 1993"/>. An analogy is an open door in a drafty corridor: the door starts by moving slowly and then accelerates as it presents a greater surface area to the wind and finally it slams shut. The necessary conditions that predispose to SAM are: anterior position of the mitral valve in the LV, altered LV geometry that allows flow to strike the mitral valve from behind, and chordal slack
<ref name="Jiang, Levine et al 1987"/>
<ref name="Sherrid, Gunsburg et al 2000"/>
<ref name="Sherrid, Chu et al 1993"/>
<ref name="Levine, Vlahakes et al 1995"/>.
SAM may considered anteriorly directed mitral prolapse
<ref name="Sherrid, Gunsburg et al 2000"/>
<ref name="Sherrid, Chu et al 1993"/>
<ref name="Levine, Vlahakes et al 1995"/>.
In both conditions the mitral valve is enlarged and is displaced in systole by the pushing force of flow resulting in mitral regurgitation.

Because the mitral valve leaflet doesn't get pulled into the LVOT until after the aortic valve opens, the initial upstroke of the arterial pulse will be normal. When the mitral valve leaflet gets pushed into the LVOT, the arterial pulse will momentarily collapse and be followed by a second rise, as the left ventricular pressure overcomes the increased obstruction that SAM of the mitral valve causes. This can be seen on the physical examination as a double tap upon palpation of the apical impulse and as a double pulsation upon palpation of the carotid pulse, known as ''[[pulsus bisferiens]]''.

==References==
{{Reflist|2}}

[[Category: Cardiology]]
[[Category: Cardiomyopathy]]
[[Category: Overview complete]]
[[Category: Template complete]]
[[Category: Genetic disorders]]

Athlete's heart changes

2011-08-14T19:35:22Z

C. Michael Gibson:

{{SI}}

{{CMG}}

==Overview==
Athlete's heart is a term that refers to concentric and symmetric hypertrophy of the left ventricle that occurs in some athletes. It is important to distinguish Athlete's heart, which is not a true [[cardiomyopathy]] from [[hypertrophic obstructive cardiomyopathy]] ([[HOCM)]], which is a true [[cardiomyopathy]] and places the athlete at risk of [[sudden death]].

==Traditional Criteria for Distinguishing Athlete's Heart from HOCM==
Several criteria can be used to distinguish these two entities:
===The degree of left ventricular wall thickness===
*In athlete's heart the LVH is symmetric and less than or = to 12 mm
*Rarely the LV thickness can be 14-16 mm and this makes it difficult to distinguish from HOCM. Athletes who engage in strength training may develop this pattern, ahtletes who engage in endurance training do not.
*If the degree of thickening is out of proportion to the type and intensity of exercise, this suggests HOCM

===The pattern of left ventricular wall thickness===
*Athleste's heart is symmetric
*HOCM is more often asymmetric, but may in some cases be symmetric
===The left ventricular cavity size===
*HOCM has smaller LV cavitary dimensions in general

==Sophisticated Criteria and Testing to Distinguish Athlete's Heart from HOCM==
*Doppler mitral valve inflow patterns are diagnostic of [[HOCM]] 9prolonged isovolumic relaxation time, reduced peak E velocity, prolonged deceleration time, increased peak A velocity, and decreased E/A ratio as compared to normal controls or athletes)
*Tissue doppler echocardiography
* Electrocardiogram: HOCM is favored if there are prominent q waves, large increases in voltages, and deep T wave inversions
*The presence of an LV outflow tract gradient favors the diagnosis of [[HOCM]]
*A speckled pattern on MRI favors the diagnosis of [[HOCM]]

[[Category:Cardiology]]

{{Circulatory system pathology}}

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{{WikiDoc Sources}}

Hypertrophic cardiomyopathy echocardiography

2011-08-14T19:34:39Z

C. Michael Gibson: /* Diagnostic Fefatures */

{{Hypertrophic cardiomyopathy}}

'''Editors-In-Chief:''' [[C. Michael Gibson, M.S., M.D.]] [mailto:mgibson@perfuse.org]

==Overview==
Echocardiography is the imaging modality of choice in the diagnosis of hypertrophic cardiomyopathy.

==Diagnostic Fefatures==
*Left ventricular hypertrophy (LVH) most often in an asymmetric distribution,
*Thickening of the left ventricular wall in the absence of cavitary dilation and the presence of hyperdynamic activity (in fact there may be systolic cavity obliteration or near obliteration)
*Absnece of any other cause of left ventricular hypertrophy such as [[aortic stenosis]] or [[hypertension]]

==Left Ventricular Wall Thickness==
*The traditional definition requires a wall thickness > 15 mm.
*Borderline wall thicknesses of 13-14 mm must be distinguished from extreme variants of [[athletes heart]]
*There are some genetic variants that yield a normal wall thickness.

==References==
{{Reflist|2}}

[[Category: Cardiology]]
[[Category: Cardiomyopathy]]
[[Category: Overview complete]]
[[Category: Template complete]]
[[Category: Genetic disorders]]

Hypertrophic cardiomyopathy genetics

2011-08-14T19:31:54Z

C. Michael Gibson: /* Genetics */

{{Hypertrophic cardiomyopathy}}
{{CMG}}

==Overview==
Hypertrophic cardiomyopathy is inherited as an [[autosomal dominant]] trait and is attributed to mutations in one of a number of genes that encode for one of the [[sarcomere]] [[protein]]s. Children of a patient with HCM have a 50% chance of inheriting the trait.

==Mutations==
Specific gene mutations that have been identified include the following:

{| class="wikitable" class="sortable wikitable"
|-
! Gene
! Locus
! Type
|-
| [[MYH7]]
| 14q12
| CMH1
|-
| [[TNNT2]]
| 1q32
| CMH2
|-
| [[TPM1]]
| 15q22.1
| CMH3 ({{OMIM2|115196}})
|-
| [[MYBPC3]]
| 11p11.2
| CMH4 ({{OMIM2|115197}})
|-
| ?
| ?
| CMH5
|-
| [[PRKAG2]]
| 7q36
| CMH6 ({{OMIM2|600858}})
|-
| [[TNNI3]]
| 19q13.4
| CMH7
|-
| [[MYL3]]
| 3p
| CMH8 ({{OMIM2|608751}})
|-
| [[Titin|TTN]]
| 2q24.3
| CMH9
|-
| [[MYL2]]
| 12q23-q24
| CMH10
|-
| [[ACTC1]]
| 15q14
| CMH11 ({{OMIM2|612098}})
|-
| [[CSRP3]]
| 11p15.1
| CMH12 ({{OMIM2|612124}})
|}

While most literature so far focuses on European, American, and Japanese populations, HCM appears in all racial groups. The incidence of HCM is about 0.2% to 0.5% of the general population.

==Genetics==

HCM is the most common genetically transmitted cardiovascular disease. Penetrance of HCM is incomplete and age-related. The disease may be sporadic but affected family members are discovered in 13% of cases. More than 70 mutations involving at least 7 chromosomes encoding structural proteins of the myocyte have been discovered. These mutations have varying degrees of penetrance and even the same mutation may have variable expression, implying superimposed effects of other genes or environmental influences.

Hypertrophic cardiomyopathy is inherited as an [[autosomal dominant]] trait and is attributed to mutations in one of a number of genes that encode for one of the [[sarcomere]] [[protein]]s including beta-cardiac myosin heavy chain (the first gene identified), cardiac actin, [[troponin T|cardiac troponin T]], alpha-tropomyosin, [[troponin I|cardiac troponin I]], cardiac myosin-binding protein C, and the myosin light chains. Currently there are more than 400 mutations in these genes. The prognosis is variable, based on the gene mutation. In individuals without a family history of HCM, the most common cause of the disease is a [[mutation|de novo mutation]] of the gene that produces the β-myosin heavy chain.

An insertion/deletion polymorphism in the [[gene]] encoding for [[angiotensin converting enzyme]] (ACE) alters the clinical [[phenotype]] of the disease. The D/D (deletion/deletion) genotype of ACE is associated with more marked hypertrophy of the left ventricle and may be associated with higher risk of adverse outcomes
<ref name="Doolan, Nguyen et al 2004">Doolan G, Nguyen L, Chung J, Ingles J, Semsarian C. Progression of left ventricular hypertrophy and the angiotensin-converting enzyme gene polymorphism in hypertrophic cardiomyopathy. ''Int J Cardiol''. 2004 Aug; '''96'''(2):157–63. ([http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15314809 Medline abstract])</ref> <ref name="Marian, Yu et al 1993">Marian AJ, Yu QT, Workman R, Greve G, Roberts R. Angiotensin-converting enzyme polymorphism in hypertrophic cardiomyopathy and sudden cardiac death. ''Lancet''. 1993 Oct 30; '''342'''(8879):1085–6. ([http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=8105312 Medline abstract])</ref>.

There are some genetic variants that yield a normal wall thickness.

===Specific Chromosomal Abnormalities===

====β [[Myosin]] Heavy Chain-Chromosome 14 q11.2-3====

Accounts for approximately 35%-45% of cases. Significant [[LVH]] ([[left ventricular hypertrophy]]) is usually noted. The Arg403Gln mutation is associated with an extremely poor prognosis with average age of death at 33 years, while the Val606Met mutation is associated with a better prognosis.

====Cardiac Myosin Binding Protein-C-Chromosome 11====

Accounts for another 15%-35% but has a reduced penetrance so may actually be more. Patients generally present later in life and in general, have a better prognosis than with the prior 2 mutations. Up to 60% at age 50 years have no [[LVH]].

====Cardiac Troponin T-Chromosome 11====

Accounts for approximately 15% of cases. Substantially less hypertrophy is noted but histology demonstrates the characteristic myocyte disarray of HCM. Most mutations of this gene are associated with markedly reduced survival.

====Other Genetic Abnormalities====

Other genes encoding alpha tropomyosin, myosin regulatory light chain, cardiac [[troponin I]] and cardiac [[troponin C]] have been implicated. A mutation on Chromosome 7 is associated with HCM and the [[WPW]] ([[Wolff-Parkinson-White syndrome]]).
About 50-60% of patients with a high index of clinical suspicion for HCM will have a mutation identified in at least 1 of 9 sarcomeric genes. Approximately 45% of these mutations occur in the β [[myosin]] heavy chain gene on [[chromosome]] 14 q11.2-3, while approximately 35% involve the cardiac myosin binding protein C gene. Since HCM is typically an [[autosomal dominant]] trait, children of an HCM parent have 50% chance of inheriting the disease-causing mutation. Whenever a mutation is identified through genetic testing, family-specific genetic testing can be used to identify relatives at-risk for the disease ([http://www.ncbi.nlm.nih.gov/bookshelf/br.fcgi?book=gene&part=hyper-card#hyper-card HCM Genetic Testing Overview]). In individuals without a family history of HCM, the most common cause of the disease is a [[mutation|de novo mutation]] of the gene that produces the β-myosin heavy chain.

An insertion/deletion polymorphism in the [[gene]] encoding for [[angiotensin converting enzyme]] (ACE) alters the clinical [[phenotype]] of the disease. The D/D (deletion/deletion) genotype of ACE is associated with more marked hypertrophy of the left ventricle and may be associated with higher risk of adverse outcomes
<ref name="Doolan, Nguyen et al. 2004">{{cite journal |author=Doolan G, Nguyen L, Chung J, Ingles J, Semsarian C |title=Progression of left ventricular hypertrophy and the angiotensin-converting enzyme gene polymorphism in hypertrophic cardiomyopathy |journal=Int J Cardiol |volume=96 |issue=2 |pages=157–63 |year=2004 |month=Aug |pmid=15314809 |doi=10.1016/j.ijcard.2004.05.003 }}</ref>
.<ref name="Marian, Yu et al. 1993">{{cite journal |author=Marian AJ, Yu QT, Workman R, Greve G, Roberts R |title=Angiotensin-converting enzyme polymorphism in hypertrophic cardiomyopathy and sudden cardiac death |journal=Lancet |volume=342 |issue=8879 |pages=1085–6 |year=1993 |month=Oct |pmid=8105312 |doi= 10.1016/0140-6736(93)92064-Z|url=http://linkinghub.elsevier.com/retrieve/pii/0140-6736(93)92064-Z}}</ref>

==References==
{{Reflist|2}}

[[Category: Cardiology]]
[[Category:Cardiomyopathy]]
[[Category: Overview complete]]
[[Category: Template complete]]
[[Category: Genetic disorders]]

Template:Hypertrophic cardiomyopathy

2011-08-14T19:20:30Z

C. Michael Gibson:

{| class="infobox bordered" style="width: 15em; text-align: left; font-size: 90%; background:AliceBlue"
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'''
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[[Hypertrophic cardiomyopathy|Home]]
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[[Hypertrophic cardiomyopathy (patient information)|Patient Info]]
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[[Hypertrophic cardiomyopathy overview|Overview]]
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[[Hypertrophic cardiomyopathy classification|Classification]]
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Pathophysiology
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:[[Hypertrophic cardiomyopathy genetics|Genetics]]
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:[[Hypertrophic cardiomyopathy histopathology|Histopathology]]
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:[[Hypertrophic cardiomyopathy anatomic abnormalities|Anatomic Abnormalities]]
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:[[Hypertrophic cardiomyopathy outflow obstruction|Outflow Obstruction]]
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:[[Hypertrophic cardiomyopathy diastolic dysfunction|Diastolic Dysfunction]]
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:[[Hypertrophic cardiomyopathy ischemia|Ischemia]]
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:[[Hypertrophic cardiomyopathy arrhythmogenesis|Arrhythmogenesis]]
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[[Hypertrophic cardiomyopathy epidemiology and demographics|Epidemiology & Demographics]]
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[[Hypertrophic cardiomyopathy screening|Screening]]
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[[Hypertrophic cardiomyopathy natural history|Natural History, Complications & Prognosis]]
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:[[Hypertrophic cardiomyopathy risk factors for sudden death|Risk Factors For Sudden Death]]
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[[Hypertrophic cardiomyopathy differential diagnosis|Differentiating Hypertrophic cardiomyopathy from other Diseases]]
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Diagnosis
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[[Hypertrophic cardiomyopathy history and symptoms|History & Symptoms]]
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[[Hypertrophic cardiomyopathy physical examination|Physical Examination]]
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[[Hypertrophic cardiomyopathy genetic testing|Genetic Testing]]
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[[Hypertrophic cardiomyopathy electrocardiogram|Electrocardiogram]]
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[[Hypertrophic cardiomyopathy chest x ray|Chest X Ray]]
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[[Hypertrophic cardiomyopathy MRI|MRI]]
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[[Hypertrophic cardiomyopathy CT|CT]]
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[[Hypertrophic cardiomyopathy echocardiography|Echocardiography]]
|-
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[[Hypertrophic cardiomyopathy other imaging findings|Other Imaging Findings]]
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[[Hypertrophic cardiomyopathy other diagnostic studies|Other Diagnostic Studies]]
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Treatment
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[[Hypertrophic cardiomyopathy medical therapy|Medical Therapy]]
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:[[Hypertrophic cardiomyopathy activities and circumstances to avoid|Activities/Circumstances to Avoid]]
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:[[Hypertrophic cardiomyopathy management during childhood|Management During Childhood]]
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:[[Hypertrophic cardiomyopathy management during pregnancy|Management During Pregnancy]]
|-
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[[Hypertrophic cardiomyopathy surgery|Surgery]]
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[http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?CMD=search&db=pubmed&term={{urlencode:{{#if:{{{1|}}}|{{{1}}}|{{PAGENAME}}}}}} Most recent articles]
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Hypertrophic cardiomyopathy gross pathology

2011-08-14T18:30:29Z

C. Michael Gibson: New page: {{Hypertrophic cardiomyopathy}} ==Overview== ==Gross Pathological Findings== <div align="left"> <gallery heights="175" widths="175"> Image:2367.jpg|Cardiomyopathy: Intermediate between h...

Hypertrophic cardiomyopathy histopathology

2011-08-14T18:27:27Z

C. Michael Gibson:

{{Hypertrophic cardiomyopathy}}

'''Editors-In-Chief:''' [[C. Michael Gibson, M.S., M.D.]] [mailto:mgibson@perfuse.org]

==Overview==
On histopathologic examination, hypertrophic cardiomyopathy is characterized by both myocardial disarray and by periarteriolar fibrosis. Myocardial disarray can be associated with aberrant impulse conduction and [[arrhythmias]], and periarteriolar fibrosis can be associated with [[myocardial ischemia]].

==Histopathologic Abnormalities==
===Myocardial Disarray===
In HCM, the normal alignment of muscle cells is disrupted (there is a swirling pattern to the arrangement of the muscle cells), a phenomenon known as [[myocardial disarray]]. HCM is believed to be due to a mutation in one of many [[gene]]s that results in a mutated myosin heavy chain, one of the components of the [[myocyte]] (the muscle cell of the heart). Histopathologically, the cardiac [[sarcomere]] is abnormal resulting in hypertrophy of the [[left ventricle]] in the absence of other disorders that could produce the condition such as [[hypertension]], [[amyloid]] or [[aortic stenosis]]. The presence of [[myocardial disarray]] may be associated with abnormalities of electrical conduction in the heart (including electrical reentry loops) which thereby contributes to an increased risk of [[sudden cardiac death]].

<div align="left">
<gallery heights="115" widths="115">
Image:438.jpg|Myocardial disarray with swirling pattern of myocytes
Image:HCP diagram.JPG|Variants of hypertrophic cardiomyopathy
Image:427.jpg|White areas of fibrosis or scar in a patient with HCM which may contribute in part to arrhythmias
</gallery>
</div>

===Periarteriolar Fibrosis===
Compared to normal arterioles on the left, the arterioles from a patient with hyertension (middle) show moderate periarteriolar thickening and fibrosis. Shown on the right is a patient with HCM in which there is even more signficant periarteriolar thickening and fibrosis. This thickening of the wall of the intramyocardial arterioles leads to an increased wall/lumen ratio, subendocardial ischemia and impaired [[coronary flow reserve]]<ref name="pmid9842009">{{cite journal| author=Lorenzoni R, Gistri R, Cecchi F, Olivotto I, Chiriatti G, Elliott P et al.| title=Coronary vasodilator reserve is impaired in patients with hypertrophic cardiomyopathy and left ventricular dysfunction. | journal=Am Heart J | year= 1998 | volume= 136 | issue= 6 | pages= 972-81 | pmid=9842009 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9842009 }} </ref><ref name="pmid10097830">{{cite journal| author=Choudhury L, Elliott P, Rimoldi O, Ryan M, Lammertsma AA, Boyd H et al.| title=Transmural myocardial blood flow distribution in hypertrophic cardiomyopathy and effect of treatment. | journal=Basic Res Cardiol | year= 1999 | volume= 94 | issue= 1 | pages= 49-59 | pmid=10097830 | doi= | pmc= | url= }} </ref>. Patients who subsequently died in one series had abnormal coronary flow reserve on PET scanning at baseline indicating that ischemia may play a role, at least in part, in subsequent mortality.

<div align="left">
<gallery heights="115" widths="115">
Image:Arteriole-normal.jpg|Normal arteriole
Image:Arteriole-hypertensive.jpg|Hypertensive arteriole with wall thickening and myocyte hypertrophy
Image:Arteriole-hcm.jpg|Arteriole in HCM patient with periarteriole fibrosis and thicknening
</gallery>
</div>

==Microscopic Pathological Findings==

Histopathologically, small vessels have hypertrophy of the tunica media. Combined with increased wall tension, decreased vasodilator reserve and inadequate capillary density, there is a mismatch between blood supply and demand. Over time, it is thought that there is repeated ischemia followed by fibrosis and eventually, dilation and systolic dysfunction (“burned out hypertrophy”).

<div align="left">
<gallery heights="175" widths="175">
Image:3380.jpg|Micro med mag H&E mid-mural myocardium with hypertrophy and interstitial fibrosis atrophy is present marked increase in interstitial fibroblastic cells
Image:3381.jpg|Micro high mag H&E myofiber hypertrophy and interstitial fibrosis with marked increase in interstitial fibroblastic cells
</gallery>
</div>

<div align="left">
<gallery heights="175" widths="175">
Image:3480.jpg|Micro med mag H&E myofiber hypertrophy some atrophy interstitial fibrosis with many fibroblastic cells
Image:3481.jpg|Micro high mag H&E hypertrophied fibers with some evidence of atrophy and marked interstitial fibrosis with many fibroblastic type cells
</gallery>
</div>

<div align="left">
<gallery heights="175" widths="175">
Image:3482.jpg|Micro low mag H&E shows myofiber hypertrophy and interstitial fibrosis
Image:439.jpg|Cardiomyopathy: Micro H&E low mag interventricular septum at junction of normal myofiber orientation with asymmetrical hypertrophy (an excellent example)
</gallery>
</div>

<div align="left">
<gallery heights="175" widths="175">
Image:440.jpg|Cardiomyopathy: Micro H&E low mag marked myofiber disarray asymmetrical hypertrophy
Image:441.jpg|Cardiomyopathy: Micro trichrome high mag marked myofiber disarray
</gallery>
</div>

<div align="left">
<gallery heights="175" widths="175">
Image:442.jpg|Cardiomyopathy: Micro H&E med mag excellent example myofiber disarray
Image:438.jpg|Cardiomyopathy: Micro H&E high mag excellent example myofiber disarray
</gallery>
</div>
==References==
{{Reflist|2}}

[[Category: Cardiology]]
[[Category: Pathology]]
[[Category:Cardiomyopathy]]
[[Category: Overview complete]]
[[Category: Template complete]]
[[Category: Genetic disorders]]

Hypertrophic cardiomyopathy pathologic abnormalities

2011-08-14T18:26:25Z

C. Michael Gibson: /* Microscopic Pathological Findings */

Hypertrophic cardiomyopathy pathologic abnormalities

2011-08-14T18:25:42Z

{{Hypertrophic cardiomyopathy}}

==Overview==
==Gross Pathological Findings==

<div align="left">
<gallery heights="175" widths="175">
Image:2367.jpg|Cardiomyopathy: Intermediate between hypertrophic and dilated
Image:17412.jpg|Hypertrophic cardiomyopathy, concentric
</gallery>
</div>

<div align="left">
<gallery heights="175" widths="175">
Image:4648.jpg|Hypertrophic Obstructive Cardiomyopathy: Gross natural color opened left ventricular outflow tract with subaortic shelf and marked endocardial thickening matching the contour of the anterior mitral leaflet
Image:416.jpg|Cardiomyopathy: Gross apical slice of left and right ventricles concentric hypertrophy with cavitary obliteration sudden unexpected death obstructive cardiomyopathy
</gallery>
</div>

<div align="left">
<gallery heights="175" widths="175">
Image:2369.jpg|Cardiomyopathy Asymmetrical Septal Hypertrophy
Image:455.jpg|Cardiomyopathy: Gross excellent view of mitral valve atrial surface showing thickening which is fibrous in body of valve and myxoid at area of free margin changes presumed secondary to insufficiency due to anterior motion
</gallery>
</div>

<div align="left">
<gallery heights="175" widths="175">
Image:428.jpg|Cardiomyopathy: Gross close up view of a ventricle slice
Image:427.jpg|Cardiomyopathy: Gross ventricular slices hypertrophy and extensive myocardial fibrosis a unique case of global fiber disarray with atrophy and fibrosis
</gallery>
</div>

==Microscopic Pathological Findings==

Histopathologically, small vessels have hypertrophy of the tunica media. Combined with increased wall tension, decreased vasodilator reserve and inadequate capillary density, there is a mismatch between blood supply and demand. Over time, it is thought that there is repeated ischemia followed by fibrosis and eventually, dilation and systolic dysfunction (“burned out hypertrophy”).

<div align="left">
<gallery heights="175" widths="175">
Image:3380.jpg|Micro med mag H&E mid-mural myocardium with hypertrophy and interstitial fibrosis atrophy is present marked increase in interstitial fibroblastic cells
Image:3381.jpg|Micro high mag H&E myofiber hypertrophy and interstitial fibrosis with marked increase in interstitial fibroblastic cells
</gallery>
</div>

<div align="left">
<gallery heights="175" widths="175">
Image:3480.jpg|Micro med mag H&E myofiber hypertrophy some atrophy interstitial fibrosis with many fibroblastic cells
Image:3481.jpg|Micro high mag H&E hypertrophied fibers with some evidence of atrophy and marked interstitial fibrosis with many fibroblastic type cells
</gallery>
</div>

<div align="left">
<gallery heights="175" widths="175">
Image:3482.jpg|Micro low mag H&E shows myofiber hypertrophy and interstitial fibrosis
Image:439.jpg|Cardiomyopathy: Micro H&E low mag interventricular septum at junction of normal myofiber orientation with asymmetrical hypertrophy (an excellent example)
</gallery>
</div>

<div align="left">
<gallery heights="175" widths="175">
Image:440.jpg|Cardiomyopathy: Micro H&E low mag marked myofiber disarray asymmetrical hypertrophy
Image:441.jpg|Cardiomyopathy: Micro trichrome high mag marked myofiber disarray
</gallery>
</div>

<div align="left">
<gallery heights="175" widths="175">
Image:442.jpg|Cardiomyopathy: Micro H&E med mag excellent example myofiber disarray
Image:438.jpg|Cardiomyopathy: Micro H&E high mag excellent example myofiber disarray
</gallery>
</div>

==References==
{{Reflist|2}}

[[Category:Cardiology]]
[[Category:Template complete]]
[[Category:Overview complete]]
[[Category:Pathology]]

ACC/AHA recommendations for surgical intervention in L-transposition of the great arteries

2011-08-13T14:43:48Z

C. Michael Gibson:

{{L-transposition of the great arteries}}

{{Transposition of the great vessels}}

{{CMG}}; '''Associate Editor(s)-In-Chief:''' [[Priyamvada Singh|Priyamvada Singh, M.B.B.S.]] [mailto:psingh@perfuse.org]; {{CZ}}; '''Assistant Editor(s)-In-Chief:''' [[Kristin Feeney|Kristin Feeney, B.S.]] [mailto:kfeeney@perfuse.org]

==Overview==
ACC/AHA recommends different surgical options for patients with congenitally corrected/Levo-transposition of the great arteries

==(ACC/AHA) recommendations for surgical intervention in patients with congenitally corrected transposition of the great arteries (CCTGA) <ref name="pmid19038677">{{cite journal| author=Warnes CA, Williams RG, Bashore TM, Child JS, Connolly HM, Dearani JA et al.| title=ACC/AHA 2008 guidelines for the management of adults with congenital heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Develop Guidelines on the Management of Adults With Congenital Heart Disease). Developed in Collaboration With the American Society of Echocardiography, Heart Rhythm Society, International Society for Adult Congenital Heart Disease, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons. | journal=J Am Coll Cardiol | year= 2008 | volume= 52 | issue= 23 | pages= e1-121 | pmid=19038677 | doi=10.1016/j.jacc.2008.10.001 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19038677 }} </ref>(DONOT EDIT)==

{{cquote|

'''Class I'''

1. Surgeons with training and expertise in CHD should perform operations for patients with CCTGA for the following indications:
::1. Unrepaired CCTGA and severe atrioventricular (AV) valve regurgitation. (Level of Evidence: B)
::2. Anatomic repair with atrial and arterial level switch/Rastelli repair in cases in which the left ventricle is functioning at systemic pressures. (Level of Evidence: B)
::3. Simple ventricular septal defect (VSD) closure when the VSD is not favorable for left ventricular (LV)-to-aorta baffling or is restrictive. (Level of Evidence: B)
::4. LV–to–pulmonary artery conduit in rare cases with LV dysfunction and severe LV outflow obstruction. (Level of Evidence: B)
::5. Evidence of moderate or progressive systemic AV valve regurgitation. (Level of Evidence: B)
::6. Conduit obstruction with systemic or nearly systemic right ventricular (RV) pressures and/or RV dysfunction after anatomic repair. (Level of Evidence: B)
::7. Conduit obstruction and systemic or suprasystemic LV pressures in a patient with nonanatomic correction. (Level of Evidence: B)
::8. Moderate or severe aortic regurgitation (AR)/neo-AR and onset of ventricular dysfunction or progressive ventricular dilatation. (Level of Evidence: B)
}}
'''For ACC/AHA Level of evidence and classes click''':[[ACC AHA Guidelines Classification Scheme]]
==References==
{{Reflist|2}}

ACC/AHA recommendations for surgical intervention in L-transposition of the great arteries

2011-08-13T14:43:00Z

C. Michael Gibson:

Transposition of the great vessels

2011-08-13T14:17:00Z

C. Michael Gibson:

{{DiseaseDisorder infobox |
Name = Transposition of the great vessels |
ICD10 = {{ICD10|Q|21|3|q|20}} |
ICD9 = {{ICD9|745.2}} |
ICDO = |
Image = Transposition of the great vessels svg.png |
Caption = diagram of a healthy heart and one suffering from Transposition of the great vessels |
OMIM = 187500 |
MedlinePlus = 001567 |
eMedicineSubj = |
eMedicineTopic = |
DiseasesDB = 4660 |
MeshID = D013771 |
}}
{{Transposition of the great vessels}}

'''For patient information click [[{{PAGENAME}} (patient information)|here]]'''

{{CMG}}; '''Associate Editor(s)-In-Chief:''' [[Priyamvada Singh|Priyamvada Singh, M.B.B.S.]] [mailto:psingh@perfuse.org]; {{CZ}}; '''Assistant Editor(s)-In-Chief:''' [[Kristin Feeney|Kristin Feeney, B.S.]] [mailto:kfeeney@perfuse.org]

==[[Transposition of the great vessels diagram | Diagram ]]==

==[[Transposition of the great vessels overview | Overview ]]==

==[[Transposition of the great vessels historical perspective | Historical perspective ]]==

==[[Transposition of the great vessels anatomy | Anatomy ]]==

==[[Transposition of the great vessels pathophysiology | Pathophysiology ]]==

==[[Transposition of the great vessels epidemiology and demographics|Epidemiology and demographics]]==

==[[Transposition of the great vessels risk factors | Risk factors ]]==

==[[Transposition of the great vessels screening| Screening ]]==

==Classification==

*[[Dextro-transposition of the great arteries/complete transposition of the great arteries]]
*[[L-transposition of the great arteries or congenitally corrected transposition of the great arteries]]

==[[Transposition of the great vessels natural History, complications & prognosis | Natural History, complications & prognosis]]==

==[[Transposition of the great vessels causes|Causes ]]==

==[[Transposition of the great arteries differential diagnosis |Differentiating Transposition of the great vessels from other Diseases]]==

==Diagnosis==

==[[Transposition of the great vessels history and symptoms|History & Symptoms]]==

==[[Transposition of the great vessels physical examination|Physical Examination]]==

== Lab tests==

==[[Transposition of the great vessels electrocardiogram|Electrocardiogram]]==

==[[Transposition of the great vessels chest x ray|Chest X Ray]]==

==[[Transposition of the great vessels MRI|MRI]]==

==[[Transposition of the great vessels CT|CT]]==

==[[Transposition of the great vessels echocardiography or ultrasound|Echocardiography or Ultrasound]]==

==[[Transposition of the great vessels other diagnostic studies|Other Diagnostic Studies]]==

==Treatment==

==[[Transposition of the great vessels medical therapy|Medical Therapy]]==

==Surgery==

[[Transposition of the great vessels palliative care]]|[[Transposition of the great vessels corrective surgery]]|[[Transposition of the great vessels post-operative care]]
|[[Transposition of the great vessels follow up]]

==[[Transposition of the great vessels prevention|Prevention]]==

==See also==
*[[levo-Transposition of the great arteries]]
*[[Transposition of the great arteries]]
*[[Dextro-transposition of the great arteries]]

==References==
<div class="references-small"><references/></div>

==External links==
*[http://www.ctsnet.org/doc/5518 Cardiothoracic Surgery Network (CTS''Net'')]
* {{eMedicine|ped|2548}}
*[http://www.cincinnatichildrens.org/health/heart-encyclopedia/anomalies/transposition.htm Heart Center Encyclopedia, Cincinnati Children's Hospital Medical Center]

{{Congenital malformations and deformations of circulatory system}}
{{SIB}}
[[Category:Congenital heart disease]]
[[Category:Cardiology]]

[[de:Transposition der großen Arterien]]
[[fr:Transposition des gros vaisseaux]]

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Diastolic dysfunction

2011-08-13T01:18:47Z

C. Michael Gibson:

{{SI}}
{{WikiDoc Cardiology Network Infobox}}

{{CMG}}

'''Assistant Editor in Chief:''' [[user:Hector Tamez|Hector Tamez]] [[mailto:tamez.hector@gmail.com]]

==Overview==
'''Diastolic dysfunction''' refers to an abnormality in the heart's (i.e. [[left ventricle]]'s) filling during [[diastole]]. Diastole is that phase of the [[cardiac cycle]] when the heart (i.e. [[ventricle]]) is not contracting but is actually relaxed and filling with blood that is being returned to it, either from the body (into [[right ventricle]]) or from the lungs (into [[left ventricle]]).

==Significance of Diastolic Dysfunction==
Normally, with reference to the left side of the heart, blood flows from the lungs, into the [[pulmonary veins]], into the [[left atrium]], through the [[mitral valve]], and finally into the [[left ventricle]]. When the [[left ventricle]] cannot be normally filled during diastole, blood will back up into the [[left atrium]] and, eventually, into the lungs. The result is a higher than normal pressure of blood within the vessels of the lung. As a result of hydrostatic forces, this high pressure leads to leaking of fluid (i.e. [[transudate]]) from the lung's blood vessels into the air-spaces ([[alveoli]]) of the lungs. The result is [[pulmonary edema]], a condition characterized by difficulty breathing, inadequate [[oxygenation]] of blood, and, if severe and untreated, death.

It is worth re-emphasizing that the pulmonary edema that can develop as a result of diastolic dysfunction is ''not'' due to poor pumping function of the left ventricle. Indeed, it has resulted from the left ventricle's inability to readily accept blood trying to enter it from the left atrium.

==Pathophysiology==
The primary reason for the left ventricle's inability to properly fill with blood during diastole (i.e. diastolic dysfunction) is that it has become stiff (i.e. non-compliant). In the setting of a stiff left ventricle, it is more difficult for blood to flow into it from the [[left atrium]]. In such a situation, filling can be maintained by a combination of coordinated left atrial pumping (i.e. beating) and a relatively slow heart rate. The former actively pumps blood into the stiff left ventricle, and the latter can allow for sufficient time for blood to passively enter the left ventricle from the left atrium.

==Risk Factors and Causes==
Any condition or process that leads to stiffening of the left ventricle can lead to diastolic dysfunction.

Some causes of left ventricular stiffening include:
* high blood pressure (i.e. [[hypertension]], where, as a result of left ventricular muscle [[hypertrophy]] to deal with the high pressure, the left ventricle has become stiff)
* [[aortic stenosis]] of any cause (here as with hypertension, the ventricular muscle has hypertrophied and thence become stiff, as a result of the increased pressure load placed on it by the stenosis)
* scarred heart muscle (e.g. occurring after a heart attack) (scars are relatively stiff)
* [[diabetes]] (stiffening occurs presumably as a result of [[glycosylation]] of heart muscle)
* severe systolic dysfunction that has led to ventricular dilation (i.e when the ventricle has been stretched to a certain point, any further attempt to stretch it more, as by blood trying to enter it from the left atrium, meets with increased resistance - it has become stiff
* reversible stiffening as can occur during periods of cardiac [[ischemia]]

One miscellaneous but important cause of diastolic dysfunction is [[mitral stenosis]]. In this case, the problem is not that the left ventricle is stiff. Rather, in mitral stenosis, blood cannot readily flow out from the left atrium into the left ventricle since the valve between those two heart chambers is blocked. Especially when the heart rate is elevated (as occurs in exercise and pregnancy), there will be insufficient time for blood to traverse the narrowed passageway (i.e. mitral valve) between the left atrium and left ventricle. As a consequence, the blood will back up into the left atrium and, eventually, the lungs. [[Pulmonary edema]] may result.

==Treatment==
By and large, diastolic dysfunction is chronic process (except during acute [[ischemia]] - see above). When this chronic condition is well tolerated by an individual, no specific treatment may be indicated. Rather, therapy should be directed at the root cause of the stiff left ventricle with things like high blood pressure and diabetes treated appropriately. Conversely, and as noted above, diastolic dysfunction tends to be better tolerated if the atrium is able to pump blood into the ventricles in a coordinated fashion. This does not occur in [[atrial fibrillation]] where there is no coordinated atrial activity. Hence, atrial fibrillation should be treated aggressively in people with diastolic dysfunction. In the same light, and also as noted above, if the atrial fibrillation persists and is leading to a rapid heart rate, treatment must be given to slow down that rate.

At this date, the role of specific treatments for diastolic dysfunction ''per se'' is unclear. There is some evidence that [[calcium channel blocker]] drugs may be of benefit in reducing ventricular stiffness in some cases. Likewise, treatment with [[angiotensin converting enzyme inhibitors]] such as [[enalapril]], [[ramipril]], and many others, may be of benefit due to their effect on [[ventricular remodeling]].

A major treatment consideration in people with diastolic dysfunction is when [[pulmonary edema]] develops. Unlike treatment of pulmonary edema occurring the setting of [[systolic]] dysfunction (where the primary problem is poor ventricular pumping as opposed to poor filling), the treatment of pulmonary edema complicating diastolic dysfunction emphasizes heart rate control (i.e. lowering it). [[Diuretics]] are often given as well. The role of afterload reduction in this setting is unknown.

==Prognosis==
Until recently, it was generally assumed that the prognosis for individuals with diastolic dysfunction and associated, intermittent pulmonary edema was better than those with systolic dysfunction. In fact, in two studies appearing in the [[New England Journal of Medicine]] in 2006, evidence was presented to suggest that the prognosis in diastolic dysfunction is the same as that in systolic dysfunction <ref>http://content.nejm.org/cgi/content/abstract/355/3/251.</ref> <ref>http://content.nejm.org/cgi/content/abstract/355/3/260</ref>

==References==
<references />
1. Owan TE, Hodge DO, Herges, RM, Jacobsen SJ, Roger VL, Redfield MM. Trends in Prevalence and outcome of heart failure with preserved ejection fraction. N Engl J Med 2006; 355:251-9.

2. Bhatia S, Tu JV, Lee DS, Austin PC, Fang J, Haouzi A, Gong Y, Liu PP. Outcome of heart failure with preserved ejection fraction in a population-based study. N Engl J Med 2006; 355:260-9.

[[Category:Cardiovascular diseases]]
[[Category:Cardiomyopathy]]
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Hypertrophic cardiomyopathy diastolic dysfunction

2011-08-13T01:18:14Z

C. Michael Gibson:

{{Hypertrophic cardiomyopathy}}

'''Editors-In-Chief:''' [[C. Michael Gibson, M.S., M.D.]] [mailto:mgibson@perfuse.org]
==Overview==
Although there may be structural or functional obstruction of the left ventricular outflow tract, symptoms may arise more often from [[diastolic dysfunction]].
==References==
{{Reflist|2}}

[[Category: Cardiology]]
[[Category: Cardiomyopathy]]
[[Category: Overview complete]]
[[Category: Template complete]]
[[Category: Genetic disorders]]

Hypertrophic cardiomyopathy anatomic abnormalities

2011-08-13T01:16:17Z

C. Michael Gibson:

{{Hypertrophic cardiomyopathy}}

'''Editors-In-Chief:''' [[C. Michael Gibson, M.S., M.D.]] [mailto:mgibson@perfuse.org]

==Overview==
Individuals with HCM have some degree of [[left ventricular hypertrophy]]. In approximately 2/3rds of cases this is an asymmetric hypertrophy, involving the inter-ventricular septum, and is known as [[asymmetric septal hypertrophy]] ([http://www.cardiomyopathy.org/html/which_card_hcm.htm ASH]). This is in contrast to the symmetric and concentric hypertrophy seen in [[aortic stenosis]] or [[hypertension]].

The degree of ventricular involvement is variable ranging from diffuse involvement of both ventricles to isolated involvement of a portion of one segment of the [[LV]].

Data from two large registries indicates that;
*55% of cases involve the septum and anterolateral free wall,
*20% involve the entire septum alone,
*10% are limited to the basal septum and 15% are limited to the apical or distal LV (Yamaguchi variant).

Some genetic variants may manifest very little overt [[LVH]] but have an increased risk of [[sudden cardiac death]] (SCD).
==References==
{{Reflist|2}}

[[Category: Cardiology]]
[[Category: Cardiomyopathy]]
[[Category: Overview complete]]
[[Category: Template complete]]
[[Category: Genetic disorders]]

Hypertrophic cardiomyopathy diastolic dysfunction

2011-08-13T01:15:23Z

C. Michael Gibson: New page: {{Hypertrophic cardiomyopathy}} '''Editors-In-Chief:''' C. Michael Gibson, M.S., M.D. [mailto:mgibson@perfuse.org] ==Overview== ==References== {{Reflist|2}} Category: Cardiology...

{{Hypertrophic cardiomyopathy}}

'''Editors-In-Chief:''' [[C. Michael Gibson, M.S., M.D.]] [mailto:mgibson@perfuse.org]
==Overview==

==References==
{{Reflist|2}}

[[Category: Cardiology]]
[[Category: Cardiomyopathy]]
[[Category: Overview complete]]
[[Category: Template complete]]
[[Category: Genetic disorders]]

Template:Hypertrophic cardiomyopathy

2011-08-13T01:14:31Z

C. Michael Gibson:

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Hypertrophic cardiomyopathy medical therapy

2011-08-13T01:12:11Z

C. Michael Gibson: /* Indications for and Timing of Initiation of Medical Therapy */

{{Hypertrophic cardiomyopathy}}

'''Editors-In-Chief:''' [[C. Michael Gibson, M.S., M.D.]] [mailto:mgibson@perfuse.org]
==Overview==
The medical management of the patient with hypertrophic cardiomyopathy involves minimizing diastolic dysfunction, reducing left ventricular outflow tract obstruction, optimizing [[heart failure]] management, maintaining [[normal sinus rhythm]], rate control and anticoagulation in the presence of [[atrial fibrillation]], and implantation of an [[automatic implantable cardiac defibrillator]] in those patients who survive [[sudden cardiac death]].

One of the funadamental goals of treatment is to relieve disabling [[dyspnea]] and improve exercise tolerance. It should be noted that the majority of patients do not have [[hypertrophic cardiomyopathy outflow obstruction|outflow tract obstruction]], and therefore would not benefit from [[Hypertrophic cardiomyopathy surgery|surgery]]. Medical therapy is therefore a mainstay of treatment. Given the limited number of patients with the condition, there are few randomized trials comparing strategies / agents in the management of HCM.

==Initiation of Medical Therapy==
Medical therapy is usually first initiated when signs and symptoms of [[exercise intolerance]] develop.

==Diuretics==
Treatment with diuretics (a mainstay of [[CHF]] treatment) will exacerbate symptoms in hypertrophic cardiomyopathy by decreasing ventricular volume and increasing outflow resistance.

==References==
{{Reflist|2}}

[[Category: Cardiology]]
[[Category: Cardiomyopathy]]
[[Category: Overview complete]]
[[Category: Template complete]]
[[Category: Genetic disorders]]

Hypertrophic cardiomyopathy medical therapy

2011-08-13T01:10:07Z

C. Michael Gibson: /* Overview */

{{Hypertrophic cardiomyopathy}}

'''Editors-In-Chief:''' [[C. Michael Gibson, M.S., M.D.]] [mailto:mgibson@perfuse.org]
==Overview==
The medical management of the patient with hypertrophic cardiomyopathy involves minimizing diastolic dysfunction, reducing left ventricular outflow tract obstruction, optimizing [[heart failure]] management, maintaining [[normal sinus rhythm]], rate control and anticoagulation in the presence of [[atrial fibrillation]], and implantation of an [[automatic implantable cardiac defibrillator]] in those patients who survive [[sudden cardiac death]].

One of the funadamental goals of treatment is to relieve disabling [[dyspnea]] and improve exercise tolerance. It should be noted that the majority of patients do not have [[hypertrophic cardiomyopathy outflow obstruction|outflow tract obstruction]], and therefore would not benefit from [[Hypertrophic cardiomyopathy surgery|surgery]]. Medical therapy is therefore a mainstay of treatment. Given the limited number of patients with the condition, there are few randomized trials comparing strategies / agents in the management of HCM.

==Indications for and Timing of Initiation of Medical Therapy==
Medical therapy is usually first initiated when signs and symptoms of [[exercise intolerance]] develop.

==Diuretics==
Treatment with diuretics (a mainstay of [[CHF]] treatment) will exacerbate symptoms in hypertrophic cardiomyopathy by decreasing ventricular volume and increasing outflow resistance.

==References==
{{Reflist|2}}

[[Category: Cardiology]]
[[Category: Cardiomyopathy]]
[[Category: Overview complete]]
[[Category: Template complete]]
[[Category: Genetic disorders]]

Hypertrophic cardiomyopathy medical therapy

2011-08-13T01:08:13Z

C. Michael Gibson: /* Overview */

{{Hypertrophic cardiomyopathy}}

'''Editors-In-Chief:''' [[C. Michael Gibson, M.S., M.D.]] [mailto:mgibson@perfuse.org]
==Overview==
The medical management of the patient with hypertrophic cardiomyopathy involves minimizing diastolic dysfunction, reducing left ventricular outflow tract obstruction, optimizing [[heart failure]] management, maintaining [[normal sinus rhythm]], rate control and anticoagulation in the presence of [[atrial fibrillation]], and implantation of an [[automatic implantable cardiac defibrillator]] in those patients who survive [[sudden cardiac death]].

One of the funadamental goals of treatment is to relieve disabling [[dyspnea]] and improve exercise tolerance. It should be noted that the majority of patients do not have [[hypertrophic cardiomyopathy outflow obstruction|outflow tract obstruction]], and therefore would not benefit from [[Hypertrophic cardiomyopathy surgery|surgery]]. Medical therapy is therefore a mainstay of treatment. Given the limited number of patients with the condition, there are few randomized trials comparing strategies / agents in the management of HCM.

==Diuretics==
Treatment with diuretics (a mainstay of [[CHF]] treatment) will exacerbate symptoms in hypertrophic cardiomyopathy by decreasing ventricular volume and increasing outflow resistance.

==References==
{{Reflist|2}}

[[Category: Cardiology]]
[[Category: Cardiomyopathy]]
[[Category: Overview complete]]
[[Category: Template complete]]
[[Category: Genetic disorders]]

Hypertrophic cardiomyopathy medical therapy

2011-08-13T01:06:36Z

C. Michael Gibson: /* Overview */

{{Hypertrophic cardiomyopathy}}

'''Editors-In-Chief:''' [[C. Michael Gibson, M.S., M.D.]] [mailto:mgibson@perfuse.org]
==Overview==
The medical management of the patient with hypertrophic cardiomyopathy involves minimizing diastolic dysfunction, reducing left ventricular outflow tract obstruction, optimizing [[heart failure]] management, maintaining [[normal sinus rhythm]], rate control and anticoagulation in the presence of [[atrial fibrillation]], and implantation of an [[automatic implantable cardiac defibrillator]] in those patients who survive [[sudden cardiac death]].

One of the funadamental goals of treatment is to relieve disabling [[dyspnea]] and improve exercise tolerance. It should be noted that the majority of patients do not have [[hypertrophic cardiomyopathy outflow obstruction|outflow tract obstruction]], and therefore would not benefit from [[Hypertrophic cardiomyopathy surgery|surgery]]. Medical therapy is therefore a mainstay of treatment.

==Diuretics==
Treatment with diuretics (a mainstay of [[CHF]] treatment) will exacerbate symptoms in hypertrophic cardiomyopathy by decreasing ventricular volume and increasing outflow resistance.

==References==
{{Reflist|2}}

[[Category: Cardiology]]
[[Category: Cardiomyopathy]]
[[Category: Overview complete]]
[[Category: Template complete]]
[[Category: Genetic disorders]]

Hypertrophic cardiomyopathy medical therapy

2011-08-13T01:05:31Z

C. Michael Gibson: /* Overview */

{{Hypertrophic cardiomyopathy}}

'''Editors-In-Chief:''' [[C. Michael Gibson, M.S., M.D.]] [mailto:mgibson@perfuse.org]
==Overview==
The medical management of the patient with hypertrophic cardiomyopathy involves minimizing diastolic dysfunction, reducing left ventricular outflow tract obstruction, optimizing [[heart failure]] management, maintaining [[normal sinus rhythm]], rate control and anticoagulation in the presence of [[atrial fibrillation]], and implantation of an [[automatic implantable cardiac defibrillator]] in those patients who survive [[sudden cardiac death]].

One of the funadamental goals of treatment is to relieve disabling [[dyspnea]] and improve exercise tolerance. It should be noted that the majority of patients do not have [[hypertrophic cardiomyopathy outflow obstruction|outflow tract obstruction]], and therefore would not benefit from surgery. Medical therapy is therefore a mainstay of treatment.

==Diuretics==
Treatment with diuretics (a mainstay of [[CHF]] treatment) will exacerbate symptoms in hypertrophic cardiomyopathy by decreasing ventricular volume and increasing outflow resistance.

==References==
{{Reflist|2}}

[[Category: Cardiology]]
[[Category: Cardiomyopathy]]
[[Category: Overview complete]]
[[Category: Template complete]]
[[Category: Genetic disorders]]

Hypertrophic cardiomyopathy medical therapy

2011-08-13T01:05:02Z

C. Michael Gibson: /* Overview */

{{Hypertrophic cardiomyopathy}}

'''Editors-In-Chief:''' [[C. Michael Gibson, M.S., M.D.]] [mailto:mgibson@perfuse.org]
==Overview==
The medical management of the patient with hypertrophic cardiomyopathy involves minimizing diastolic dysfunction, reducing left ventricular outflow tract obstruction, optimizing [[heart failure]] management, maintaining [[normal sinus rhythm]], rate control and anticoagulation in the presence of [[atrial fibrillation]], and implantation of an [[automatic implantable cardiac defibrillator]] in those patients who survive [[sudden cardiac death]].

One of the funadamental goals of treatment is to relieve disabling [[dyspnea]] and improve exercise tolerance. It should be noted that the majority of patients do not have [[hypertrophic cardiomyopathy outflow tract obstruction|outflow tract obstruction]], and therefore would not benefit from surgery. Medical therapy is therefore a mainstay of treatment.

==Diuretics==
Treatment with diuretics (a mainstay of [[CHF]] treatment) will exacerbate symptoms in hypertrophic cardiomyopathy by decreasing ventricular volume and increasing outflow resistance.

==References==
{{Reflist|2}}

[[Category: Cardiology]]
[[Category: Cardiomyopathy]]
[[Category: Overview complete]]
[[Category: Template complete]]
[[Category: Genetic disorders]]

Hypertrophic cardiomyopathy medical therapy

2011-08-13T01:03:58Z

C. Michael Gibson: /* Overview */

{{Hypertrophic cardiomyopathy}}

'''Editors-In-Chief:''' [[C. Michael Gibson, M.S., M.D.]] [mailto:mgibson@perfuse.org]
==Overview==
The medical management of the patient with hypertrophic cardiomyopathy involves minimizing diastolic dysfunction, reducing left ventricular outflow tract obstruction, optimizing [[heart failure]] management, maintaining [[normal sinus rhythm]], rate control and anticoagulation in the presence of [[atrial fibrillation]], and implantation of an [[automatic implantable cardiac defibrillator]] in those patients who survive [[sudden cardiac death]].

One of the funadamental goals of treatment is to relieve disabling [[dyspnea]] and improve exercise tolerance. It should be noted that the majority of patients do not have [[outflow tract obstruction]], and therefore would not benefit from surgery. Medical therapy is therefore a mainstay of treatment.

==Diuretics==
Treatment with diuretics (a mainstay of [[CHF]] treatment) will exacerbate symptoms in hypertrophic cardiomyopathy by decreasing ventricular volume and increasing outflow resistance.

==References==
{{Reflist|2}}

[[Category: Cardiology]]
[[Category: Cardiomyopathy]]
[[Category: Overview complete]]
[[Category: Template complete]]
[[Category: Genetic disorders]]

Presyncope

2011-08-13T00:58:33Z

C. Michael Gibson: ←Redirected page to Syncope

#redirect:[[Syncope]]