How aortic valve stenosis causes heart failure

Your left ventricle's job is to pump enough blood through your aortic valve to meet your body's needs. If your valve opening is narrow, your left ventricle has to work harder to pump enough blood.

When this happens, pressure builds up inside the left ventricle. The ventricle compensates for the buildup, called pressure overload, by becoming thicker (hypertrophy). Left ventricular hypertrophy allows the heart to generate enough pressure to maintain adequate blood flow across the narrowed valve.

With higher pressure in the left ventricle and hypertrophied heart muscle, the heart can compensate for aortic valve stenosis and the resulting pressure overload for a long time. In fact, your heart compensates so well that you may not feel any symptoms of stenosis for many years, even decades. But eventually the valve becomes too narrow and your heart can no longer keep up. The effort of pumping so hard under pressure year after year will wear out your heart muscle prematurely.

At first, the intense pressure inside your ventricle is transmitted back into the left atrium and lungs, leading to shortness of breath, usually with exertion. Late in the course of stenosis, the pressure can begin to stretch the muscle out of shape, expanding the ventricle, a condition called dilation. As your left ventricle dilates, it will eventually reach a point where it can't pump enough to meet your body's needs. This loss of function is called heart failure.

In this process from compensation to failure, it is extremely important to distinguish between your left ventricle's initial loss of pumping ability, which is reversible, and the point at which your left ventricle suffers permanent irreversible damage from dilation, leading to heart failure. This distinction is crucial, because when you first experience symptoms of aortic stenosis, it means that your heart is losing its ability to compensate.

Experts estimate that in most cases it takes about 3 to 6 months before this loss of function turns into permanent damage associated with heart failure.

Last Updated: November 4, 2009

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