Arterial distensibility and left ventricular hypertrophy in patients with sustained essential hypertension.

Reduced aortic distensibility and compliance may participate in the genesis of cardiac hypertrophy in patients with hypertension. In these patients the increase in end-systolic stress, a determinant factor contributing to the development of cardiac hypertrophy, is influenced not only by the geometric properties of the ventricle but also by the level of systolic pressure. In patients with sustained essential hypertension, the degree of cardiac hypertrophy correlates significantly with the increase in aortic rigidity, which is assessed by the calculation of the characteristic impedance, by the measurement of carotid-femoral pulse-wave velocity, or by the calculation of the Peterson elastic modulus at the level of the aortic arch. Dihydralazine-like 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 the stiffness of the aorta and other large arteries must be considered to understand reversion of cardiac hypertrophy as a result of antihypertensive treatment.