The classic triad of symptoms of aortic stenosis occur on exertion and include dyspnea, syncope, and angina. The development of aortic stenosis takes many years and is initially asymptomatic. Dyspnea is the first symptom of aortic stenosis in about 50% of the cases while syncope and angina account for 35% and 15% of initial symptoms respectively. The clinical significance of a patient with aortic stenosis exhibiting symptoms cannot be underemphasized since the onset of symptoms is accompanied by a dramatic increase in mortality. According to one large series, if aortic valve replacement is not performed, patients presenting with dyspnea have a mean life expectancy of 2 years, those with syncope about 3 years, and those presenting with angina have an average of 5 years.
Angina in aortic stenosis frequently occurs in the absence of coronary artery disease. Instead, myocardial ischemia develops when the oxygen demand of the severely hypertrophied left ventricle exceeds oxygen supply. The Law of Laplace explains this phenomenon:
Note: LV wall stress is directly proportional to myocardial O2 demand, more specifically: O2 demand = wall stress X HR
Using the above equation, we can understand the pathologic process that develops over many years in patients with aortic stenosis. As LV pressure slowly increases over time due to worsening aortic stenosis, a parallel increase in LV wall thickness occurs (concentric hypertrophy) in order to maintain the LV wall stress at a constant level (since LV wall stress is an important determinant of myocardial O2 demand). Eventually, the LV is unable to hypertrophy any further, but the LV pressure continues to rise as the aortic stenosis worsens. This leads to a rise in LV wall stress and thus a rise in LV myocardial oxygen demand. When the heart rate increases in response to exertion (heart rate is also a determinant of O2 demand), a significant supply versus demand mismatch occurs resulting in myocardial ischemia and the clinical symptoms of angina.
Effort syncope occurs in aortic stenosis due to a sudden decrease in cerebral perfusion upon exertion. During exercise, the total peripheral resistance (TPR) decreases significantly since blood is being shunted toward working muscles. In the presence of significant aortic stenosis, the cardiac output cannot increase enough to accommodate this decreased TPR and cerebral perfusion is compromised resulting in syncope. This idea can be further reinforced by recalling the following equation:
MAP = CO X TPR
MAP = mean arterial pressure CO = cardiac output
So if the cardiac output is not able to increase due to severe aortic stenosis and the TPR decreases during exertion, the MAP will subsequently be reduced leading to decreased cerebral perfusion and syncope. It is important to note that another cause of syncope in patients with aortic stenosis is arrhythmias, especially atrial fibrillation and AV nodal blocks, as will be described later.
Dyspnea on exertion is due to heart failure. Both systolic and diastolic dysfunction typically contributes to heart failure in patients with aortic stenosis. Other classic symptoms of heart failure are also common and include orthopnea, PND, and signs of right sided heart failure (i.e. peripheral edema).
Other rare initial symptoms in a patient with aortic stenosis include embolic phenomenon from calcified aortic valve plaques or massive GI bleeding due to angiodysplasia (Heyde's syndrome). Heyde's syndrome is thought to be due to disruption of the pentamer structure of the von Willebrand factor as it traverses the severely stenotic aortic valve leading to an increase tendency to bleed from angiodysplasias.
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Review Questions - Multiple Choice
Review Questions - Cases
Aortic Stenosis Jeopardy
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