What is the pathophysiology of aortic stenosis (AS)?

Updated: May 07, 2019
  • Author: Xiushui (Mike) Ren, MD; Chief Editor: Terrence X O'Brien, MD, MS, FACC  more...
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When the aortic valve becomes stenotic, resistance to systolic ejection occurs and a systolic pressure gradient develops between the left ventricle and the aorta. This outflow obstruction leads to an increase in left ventricular (LV) systolic pressure. As a compensatory mechanism to normalize LV wall stress, LV wall thickness increases by parallel replication of sarcomeres, producing concentric hypertrophy. At this stage, the chamber is not dilated and ventricular function is preserved, although diastolic compliance is reduced.

Eventually, however, LV end-diastolic pressure (LVEDP) rises, which causes a corresponding increase in pulmonary capillary arterial pressures and a decrease in cardiac output due to diastolic dysfunction. The contractility of the myocardium may also diminish, which leads to a decrease in cardiac output due to systolic dysfunction. Ultimately, heart failure develops.

In most patients with aortic stenosis, LV systolic function is preserved and cardiac output is maintained for many years despite an elevated LV systolic pressure. Although cardiac output is normal at rest, it often fails to increase appropriately during exercise, which may result in exercise-induced symptoms.

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