Cardiac volume load as a determinant of the response of cardiac mass to antihypertensive therapy.

Abstract

Whereas chronic pressure overload induces left ventricular hypertrophy in a predictable way, the same lowering of systolic blood pressure by different antihypertensive drug classes is not associated with the same regression of LV mass. In particular, arterial vasodilators may not induce regression or even cause progression despite persistent decreases in blood pressure. It has been commonly assumed that different activation of non-haemodynamic mechanisms may explain such a dissociation. However, different effects on the other haemodynamic determinant of cardiac mass, cardiac volume overload, have not been taken into account. Our results in normotensive and hypertensive humans and rats indicate that arterial vasodilators induce a pattern of changes in cardiac anatomy, compatible with cardiac volume overload being a major contributor to these changes. Cardiac sympathetic hyperactivity may also contribute, possibly more in hypertension than in normotension.