Q. Pathophysiology of aortic regurgitation?

Left ventricle responds to chronic aortic regurgitation by chamber dilatation and an increase in its compliance so that end diastolic pressure does not increase. This is accompanied by rearrangement of muscle fibers and addition of new sarcomeres leading to eccentric hypertrophy.

As the chamber dilates-with preserved systolic function - stroke volume increases compensating the regurgitant volume. However, dilated chamber increases wall stress and afterload and to compensate for the increased afterload concentric hypertrophy ensues. Thus, chronic aortic regurgitation represents combined volume and pressure overload. During this compensatory phase involving preload reserve and concentric and eccentric hypertrophy, patient remains asymptomatic with preserved left ventricular systolic function but with dilated left ventricle. This can go on for many years. Patient becomes symptomatic as the preload reserve gets exhausted and end diastolic pressure increases. Further increase in afterload leads to afterload mismatch and left ventricular systolic function declines. The changes occur very insidiously and patient may remain asymptomative till severe LV dysfunction sets in. As the chamber enlargement proceeds and geometry alters depressed myocardial function occurs and predominates over afterload mismatch.

Though both mitral and aortic regurgitation cause volume overload to left ventricle-aortic regurgitation has additional pressure overload as the increased stroke volume has to be ejected into high impedance aorta. This is also borne out by the increased left ventricular end systolic wall stress. In mitral regurgitation, the initial compensatory mechanism is increased ejection fraction with little ventricular dilatation but in aortic regurgitation it is ventricular dilatation with preserved ejection fraction.

In aortic regurgitation, coronary perfusion is impaired due to decreased aortic diastolic pressure and increased oxygen demands. This in severe cases leads to sub endocardial ischaemia.