Epidemiological studies have determined that more than one in eight people aged 75 and older have moderate or severe aortic stenosis (AS). The most common cause of aortic stenosis is progressive calcification and senile degeneration. Congenital defects—particularly bicuspid aortic valves—also increase the risk of stenosis. Rheumatic heart disease also predisposes to AS but is almost always linked to significant mitral valve disease. Cardiac auscultation reveals a systolic ejection murmur that radiates to the carotid artery.
The pathophysiologic progression of aortic stenosis is typically slow, evolving over decades before the patient become symptomatic. AS imposes a chronic systolic pressure afterload on the left ventricle. This constant pressure causes the ventricle to hypertrophy in a concentric pattern. Changes in the left ventricular myocardium follow Laplace’s law, where wall tension is directly proportional to the product of pressure and chamber radius but inversely proportional to wall thickness. Consequently, the muscle fibers duplicate in parallel to compensate for the increased wall tension, leading to left ventricular hypertrophy as evident on the pressure-time tracing (Figure 65-1(A)). Stroke volume and ejection fraction are well preserved in AS; however, the ejection phase occurs at a much higher pressure. As the left ventricle becomes less compliant, the diastolic pressure–volume loop shifts upwards and rotates counterclockwise, resulting in elevated left ventricular end-diastolic pressure (Figure 65-1(B)). Although forward flow is affected, there is little change to the other cardiac chambers as long as the mitral valve remains competent.
Aortic stenosis: pressure-time tracing (A) and pressure-volume loop (B). (A, Reproduced with permission from Hammer GD, McPhee SJ, eds. Pathophysiology of Disease: An Introduction to Clinical Medicine, 7th ed. New York, NY: McGraw-Hill Education, Inc.; 2014: Fig. 10-22 B&C. B, Reproduced with permission from Cheitlin MD et al. Clinical Cardiology, 6th ed. New York, NY: McGraw-Hill Companies; 1993: Fig. 13-2 A.)
Concentric LV hypertrophy leads to diastolic dysfunction and deficient filling capacity. Consequently, the atrial contribution to ventricular filling (“atrial kick”) is critical in aortic stenosis. Atrial contribution comprises 40% of ventricular filling in patients with AS, while the contribution is as low as 15% in patients with a normal aortic valve.
Patients with aortic stenosis carry a higher risk for myocardial ischemia. Increased left ventricular end-diastolic pressure leads to a diminished perfusion gradient for coronary blood flow. Patients with AS most commonly present with the triad of syncope, angina, and dyspnea. Angina develops from increased myocardial oxygen demand (due to LV hypertrophy) and decreased supply to the coronary circulation (due to elevated LVEDP). Increased muscle mass from chronically elevated systolic pressures requires more energy to maintain forward flow across the stenotic valve. Up to one-third of patients with AS can have angina with no evidence of coronary artery disease.
Echocardiography can determine the severity of aortic stenosis. The normal ...