Aortic stenosis pathophysiology

Aortic Stenosis Microchapters
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editors-In-Chief: Claudia P. Hochberg, M.D. [2]; Abdul-Rahman Arabi, M.D. [3]; Keri Shafer, M.D. [4]; Priyamvada Singh, MBBS [5]; Assistant Editor-In-Chief: Kristin Feeney, B.S. [6]

Overview

Aortic stenosis results in the onset of a chronic pressure overload of the left ventricle. As the disease progresses, an aortic stenosis can result in compromised functional integrity of the surrounding mitral valve. The most common complication of aortic stenosis is hypertrophy.

Pathophysiology

When the aortic valve becomes stenosed, it can result in the formation of a pressure gradient between the left ventricle (LV) and the aorta. The more constricted the valve, the higher the gradient between the LV and the aorta. For instance, with a mild AS, the gradient may be 20 mmHg. This means that, at peak systole, while the LV may generate a pressure of 140 mmHg, the pressure that is transmitted to the aorta will only be 120 mmHg. So, while a blood pressure cuff may measure a normal systolic blood pressure, the actual pressure generated by the LV would be considerably higher.

In individuals with AS, the left ventricle (LV) has to generate an increased pressure in order to overcome the increased afterload caused by the stenotic aortic valve and eject blood out of the LV. The more severe the aortic stenosis, the higher the gradient is between the left ventricular systolic pressures and the aortic systolic pressures. Due to the increased pressures generated by the left ventricle, the myocardium (muscle) of the LV undergoes hypertrophy (increase in muscle mass). This is seen as thickening of the walls of the LV. The type of hypertrophy most commonly seen in AS is concentric hypertrophy, meaning that all the walls of the LV are (approximately) equally thickened.