Aortic stenosis symptoms
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Aortic Stenosis Microchapters |
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Diagnosis |
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Treatment |
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Percutaneous Aortic Balloon Valvotomy (PABV) or Aortic Valvuloplasty |
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Transcatheter Aortic Valve Replacement (TAVR) |
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Case Studies |
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Aortic stenosis symptoms On the Web |
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American Roentgen Ray Society Images of Aortic stenosis symptoms |
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Risk calculators and risk factors for Aortic stenosis symptoms |
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 include 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 include dyspnea on exertion, orthopnea and paroxysmal nocturnal dyspnea.
Angina pectoris
- Angina in the setting of heart failure has shown to increase mortality risk. Among patients with angina, in the absence of intervention, the 5 year mortality rate has shown to be ~50%.
- 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.[4][5].
Syncope
The mechanism of syncope secondary to aortic stenosis remains unclear. Three theroeis have been hypothesized to explain the relationship between aortic stenosis and syncope.
1. Severe aortic stenosis produces 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 syncopize due to decreased blood perfusion to the brain.
2. During exercise, high pressures generated by the hypertrophy of the left ventricular can result in a vasodepressor response resulting in secondary peripheral vasodilation and decreased overall blood flow to the brain
A second explanation as to why syncope may occur in aortic stenosis includes that during exercise, the high pressures generated in the hypertrophied left ventricle causes 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.
3. Left ventricular hypertrophy may result in a decrement in the functional integrity of the coronary arteries and blood may be inadequate in supplying the walls of the myocardium resulting in syncope
A third mechanism may sometimes be operative. 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, arrhythmias may develop which can lead to syncope.
Finally, in calcific aortic stenosis at least, the 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 - a potentially lethal condition of which syncope may be a symptom.
Aortic Stenosis and Congestive Heart Failure
- Presence of congestive heart failure carries a grave prognosis in patients with aortic stenosis.
- 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:
- Orthopnea
- Paroxysmal nocturnal dyspnea
- Pulmonary edema
- Pulmonary hypertension that can lead to:
- Right ventricular failure
- Systemic venous hypertension
- Hepatomegaly
- Atrial fibrillation
- Tricuspid regurgitation
Associated Conditions
Heyde's Syndrome
- In Heyde's syndrome, aortic stenosis is associated with angiodysplasia of the colon.
- Presenting symptoms include: hematemesis, melena
Von Willebrand Disease
- Aortic stenosis may result in a form of von Willebrand disease due to an increased turbulence around the stenosed aortic valve WHICH subsequently triggers a break down of coagulation factor VIII-associated antigen, (also called von Willebrand factor) and results in a variant of von Willebrand disease.
References
- ↑ Ross J, Braunwald E (1968). "Aortic stenosis". Circulation. 38 (1 Suppl): 61–7. PMID 4894151.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ Carabello BA (2002). "Clinical practice. Aortic stenosis". N Engl J Med. 346 (9): 677–82. doi:10.1056/NEJMcp010846. PMID 11870246.