What causes aortic stenosis (AS) in noncardiac surgery patients?

Updated: Jul 16, 2021
  • Author: Lindsay A (Finger) Raleigh, MD; Chief Editor: Sheela Pai Cole, MD  more...
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Over time, inflammation, atherosclerosis and calcification thicken the aortic valve leaflets and restrict mobility. In patients with a bicuspid aortic valve (BAV), these degenerative changes occur at an earlier age as a consequence of the abnormal hemodynamics across the valve leaflets. Rheumatic heart disease, infection, and systemic lupus erythematosus (SLE) are other, albeit rare, causes of AS.

Regardless of the etiology, calcification of the aortic valve leads to stenosis, inevitably resulting in a fixed obstruction to LV emptying. In response to the progressive narrowing of the aortic valve opening, the LV myocardium becomes hypertrophic in order to generate increased pressure during systole and thus force blood past the obstruction.

Initially, these compensatory changes allow the LV to maintain cardiac output, and patients are asymptomatic. Over time, chronic pressure overload and compensatory LV hypertrophy result in reduced compliance of the LV, with the subsequent development of diastolic dysfunction and increased LV end-diastolic pressure (LVEDP). Additionally, myocardial hypertrophy results in increased wall tension and myocardial oxygen consumption.

If the ventricular wall hypertrophy is not able to compensate for the increase in afterload, LV systolic function may decrease, and heart failure can ensue. As the stenosis progresses, patients are unable to increase stroke volume, and as a result, they are unable to increase cardiac output so as to compensate for increases in myocardial oxygen demand.

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