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  • Congenital bicuspid aortic valve (usually asymptomatic until middle or old age).

  • “Degenerative” or calcific aortic stenosis; similar risk factors as atherosclerosis (symptoms usually in the elderly).

  • Visual observation of immobile aortic valve plus a valve area of less than 1.0 cm2 define severe disease; low-gradient but severe aortic stenosis can thus be recognized.

  • Delayed and diminished carotid pulses.

  • Soft, absent, or paradoxically split S2.

  • Harsh systolic murmur, sometimes with thrill along left sternal border, often radiating to the neck; may be louder at apex in older patients.

  • ECG usually shows LVH; calcified valve on radiography or fluoroscopy.

  • Echocardiography/Doppler is diagnostic.

  • Surgery typically indicated for symptoms. TAVR is approved for patients with calcific aortic stenosis.

  • Intervention appropriate even in asymptomatic patients with super-severe aortic stenosis (mean gradient greater than 55 mm Hg) or when undergoing heart surgery for other reasons (eg, coronary artery bypass grafting [CABG]).

  • BNP is a marker of early LV myocardial failure, and high levels suggest poor prognosis.


There are two common clinical scenarios in which aortic stenosis is prevalent (eFigure 10–33). The first is due to a congenitally abnormal unicuspid or bicuspid valve, rather than tricuspid. Symptoms can occur in young or adolescent individuals if the stenosis is severe, but more often emerge at age 50–65 years when calcification and degeneration of the valve become manifest. A dilated ascending aorta, due to an intrinsic defect in the aortic root media and the hemodynamic effects of the eccentric aortic jet, may accompany the bicuspid valve in about half of these patients. Coarctation of the aorta is also seen in a number of patients with congenital aortic stenosis. Offspring of patients with a bicuspid valve have a much higher incidence of the disease in either the valve, the aorta, or both (up to 30% in some series).

eFigure 10–33.

Aortic stenosis. A: Drawing of the left heart in left anterior oblique view showing anatomic features of aortic stenosis. Note structures enlarged: left ventricle (thickened); poststenotic dilation of the aorta. (Reproduced, with permission, from Hammer GD, McPhee SJ. Pathophysiology of Disease, 8th ed. McGraw-Hill, 2019.) B: Drawing showing auscultatory and hemodynamic features of predominant aortic stenosis. Cardinal features include left ventricular hypertrophy and systolic ejection murmur. (EC, ejection click; SM, systolic murmur; P, pulmonary valve; A, aortic valve.) (Redrawn, with permission, from Cheitlin MD et al, eds. Clinical Cardiology, 6th ed. Originally published by Appleton & Lange. Copyright © 1993 by The McGraw-Hill Companies, Inc.) C: Pressure-volume loop in aortic stenosis. The left ventricle becomes thickened and less compliant, forcing the diastolic pressure-volume curve upward, which results in elevated left ventricular end-diastolic pressure (a′). Because the left ventricle must pump against a fixed gradient (increased afterload), b increases to b′. Finally, the hypertrophy of the ventricle results in increased inotropic force, which shifts the isovolumic pressure curve leftward.

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