Cardiac hypertrophy and arterial compliance following drug treatment in hypertension.

The load of the heart in hypertension is related both to increased peripheral vascular resistance and decreased aortic compliance. From noninvasive studies involving determinations of pulse-wave velocity and systolic-diastolic variations of aortic arch diameter, it can be shown that increased aortic elastic modulus is strongly related to increased cardiac mass. The relationship is observed even after adjustment for the level of mean arterial pressure. It is suggested that decreased aortic compliance in hypertension causes a disproportionate increase in systolic pressure and end-systolic stress, thus contributing to promote cardiac hypertrophy. Such a possibility may have consequences for long-term antihypertensive therapy. Following converting enzyme inhibition and calcium blockade, important dissociations may be observed between the antihypertensive effect and the cardiac and arterial changes.