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==Angina pectoris==
==Angina pectoris==
*The hypertrophied left ventricle and the prolonged ejection time (the time for the heart to eject blood) result in an increased myocardial oxygen requirements. The elevated diastolic filling pressure also reduces the gradient between the aorta and the right atrium ("the height of the waterfall") which normally drives coronary blood flow. The hypertrophied ventricle may also compress the capillaries. All of the above reasons lead to a reduction in coronary blood flow even in the absence of obstructive epicardial stenoses. This may result in subendocardial [[ischemia]] during stress or exercise.<ref name="pmid6215582">{{cite journal| author=Marcus ML, Doty DB, Hiratzka LF, Wright CB, Eastham CL| title=Decreased coronary reserve: a mechanism for angina pectoris in patients with aortic stenosis and normal coronary arteries. | journal=N Engl J Med | year= 1982 | volume= 307 | issue= 22 | pages= 1362-6 | pmid=6215582 | doi=10.1056/NEJM198211253072202 | pmc= | url= }} </ref><ref name="pmid11870246">{{cite journal| author=Carabello BA| title=Clinical practice. Aortic stenosis. | journal=N Engl J Med | year= 2002 | volume= 346 | issue= 9 | pages= 677-82 | pmid=11870246 | doi=10.1056/NEJMcp010846 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11870246  }} </ref>.
*Left untreated, the average survival is 5 years after the onset of angina in the patient with aortic stenosis.
*Left untreated, the average survival is 5 years after the onset of angina in the patient with aortic stenosis.
*The hypertrophied left ventricle and the prolonged ejection time (the time for the heart to eject blood) results in increased myocardial oxygen requirements.  The elevated diastolic filling pressure also reduces the gradient between the aorta and the right atrium ("the height of the waterfall") that drives coronary blood flow.  There may be a relative reduction in the density of the capillary network.  The hypertrophied ventricle may also compress the capillaries. All of the above lead to a reduction in coronary blood flow even in the absence of obstructive epicardial stenoses. This may lead to subendocardial [[ischemia]] during stress or exercise.<ref name="pmid6215582">{{cite journal| author=Marcus ML, Doty DB, Hiratzka LF, Wright CB, Eastham CL| title=Decreased coronary reserve: a mechanism for angina pectoris in patients with aortic stenosis and normal coronary arteries. | journal=N Engl J Med | year= 1982 | volume= 307 | issue= 22 | pages= 1362-6 | pmid=6215582 | doi=10.1056/NEJM198211253072202 | pmc= | url= }} </ref><ref name="pmid11870246">{{cite journal| author=Carabello BA| title=Clinical practice. Aortic stenosis. | journal=N Engl J Med | year= 2002 | volume= 346 | issue= 9 | pages= 677-82 | pmid=11870246 | doi=10.1056/NEJMcp010846 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11870246  }} </ref>.


==Syncope==
==Syncope==

Revision as of 20:00, 16 October 2012

Aortic Stenosis Microchapters

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Mohammed A. Sbeih, M.D. [2]; Lakshmi Gopalakrishnan, M.B.B.S. [3]; Assistant Editor-In-Chief: Kristin Feeney, B.S. [4]

Overview

The main symptoms of aortic stenosis are angina, syncope and congestive heart failure. Left untreated, the average survival is 5 years after the onset of angina, 3 years after the onset of syncope, and 1 year after the onset of congestive heart failure [1][2][3]. Other symptoms of aortic stenosis are dyspnea on exertion, orthopnea and paroxysmal nocturnal dyspnea.

Angina pectoris

  • The hypertrophied left ventricle and the prolonged ejection time (the time for the heart to eject blood) result in an increased myocardial oxygen requirements. The elevated diastolic filling pressure also reduces the gradient between the aorta and the right atrium ("the height of the waterfall") which normally drives coronary blood flow. The hypertrophied ventricle may also compress the capillaries. All of the above reasons lead to a reduction in coronary blood flow even in the absence of obstructive epicardial stenoses. This may result in subendocardial ischemia during stress or exercise.[4][5].
  • Left untreated, the average survival is 5 years after the onset of angina in the patient with aortic stenosis.

Syncope

Left untreated, the average survival is 3 years after the onset of syncope in the patient with aortic stenosis. The mechanism of syncope secondary to aortic stenosis remains unclear. Three theroeis have been hypothesized to explain the relationship between aortic stenosis and syncope.

Severe Aortic Stenosis Results in a Nearly Fixed Cardiac Output

When the patient exercises, their peripheral vascular resistance will decrease as the blood vessels of the skeletal muscles dilate to allow the muscles to receive more blood to allow them to do more work. This decrease in peripheral vascular resistance is normally compensated for by an increase in the cardiac output. Since patients with severe aortic stenosis cannot increase their cardiac output, the blood pressure falls and the patient will develop syncope due to decreased blood flow to the brain.

During exercise High Pressures Generated by the Hypertrophy of the Left Ventricle can Result in a Vasodepressor Response Resulting in Secondary Peripheral Vasodilation and Decreased Overall Blood Flow to the Brain

During exercise, the high pressures generated in the hypertrophied left ventricle may cause a vasodepressor response, which subsequently results in peripheral vasodilation which in turn causes decreased blood flow to the brain. Therefore, due to the fixed obstruction to blood flow out from the stenosed aortic valve, it may be impossible for the heart to increase its output to offset peripheral vasodilation.

Left Ventricular Hypertrophy may result in a Decrement in the Functional Integrity of the Coronary Arteries and Blood Flow may be Inadequate to Supply the Walls of the Myocardium Resulting in Syncope

Due to the hypertrophy of the left ventricle in aortic stenosis, including the consequent inability of the coronary arteries to adequately supply blood to the myocardium, myocardial ischemia may develop which can lead to syncope.

Heart Block

Finally, among patients with senile calcific aortic stenosis, calcification in and around the aortic valve can progress and extend to involve the electrical conduction system of the heart. If that occurs, the result may be heart block.

Congestive Heart Failure

Left untreated, the average survival is 5 years after the onset of angina, 3 years after the onset of syncope, and 1 year after the onset of congestive heart failure [1][2][3]. Among such patients, if the aortic valve is not replaced, they tend to have a 50% 2-year mortality rate. CHF in the setting of aortic stenosis is due to a combination of systolic dysfunction (a decrease in the ejection fraction) and diastolic dysfunction (elevated filling pressure of the left ventricle).

Symptoms of left ventricular failure include the following:

Associated Conditions

Heyde's Syndrome

Von Willebrand Disease

References

  1. 1.0 1.1 Ross J, Braunwald E (1968). "Aortic stenosis". Circulation. 38 (1 Suppl): 61–7. PMID 4894151.
  2. 2.0 2.1 Kelly TA, Rothbart RM, Cooper CM, Kaiser DL, Smucker ML, Gibson RS (1988). "Comparison of outcome of asymptomatic to symptomatic patients older than 20 years of age with valvular aortic stenosis". Am J Cardiol. 61 (1): 123–30. PMID 3337000.
  3. 3.0 3.1 Iivanainen AM, Lindroos M, Tilvis R, Heikkilä J, Kupari M (1996). "Natural history of aortic valve stenosis of varying severity in the elderly". Am J Cardiol. 78 (1): 97–101. PMID 8712130.
  4. Marcus ML, Doty DB, Hiratzka LF, Wright CB, Eastham CL (1982). "Decreased coronary reserve: a mechanism for angina pectoris in patients with aortic stenosis and normal coronary arteries". N Engl J Med. 307 (22): 1362–6. doi:10.1056/NEJM198211253072202. PMID 6215582.
  5. Carabello BA (2002). "Clinical practice. Aortic stenosis". N Engl J Med. 346 (9): 677–82. doi:10.1056/NEJMcp010846. PMID 11870246.


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