Cardiac Hypertrophy and Aortic Distensibility in Essential Hypertension

Abstract

Reduced aortic distensibility and compliance may participate in the genesis of cardiac hypertrophy in hypertension. In patients with borderline hypertension, indices of aortic distensibility are often altered, but are poorly related to the degree of septal hypertrophy, which is considered to be a marker of cardiac hypertrophy in this particular population. In patients with sustained essential hypertension, the degree of cardiac hypertrophy seems to correlate strongly with the increase in aortic rigidity. Dihydralazinelike substances are unable to modify arterial stiffness, whereas calcium-entry blockers and converting-enzyme inhibitors improve arterial stiffness when achieving the same degree of blood pressure reduction. Modifications in aortic rigidity must be considered in order to understand reversion of cardiac hypertrophy as a result of antihypertensive treatment.