Abstract

Although aortic regurgitation imposes a volume load on the left ventricle, it became clear more than two decades ago that the resulting large stroke volume and wide pulse pressure also lead to systolic hypertension and concomitant left ventricular pressure overload.1,2 In fact, afterload is much higher in aortic regurgitation than in mitral regurgitation and may be as high as that in the more typically recognized pressure overload of aortic stenosis.3 The excess afterload in aortic regurgitation, in turn, forms the basis for the idea that afterload-reducing agents, such as vasodilators, might be beneficial in the medical treatment of this . . .

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