Regression of Cardiac Hypertrophy and Left Ventricular Pumping Ability Postregression

Abstract

As a result of the increasing afterload imposed upon the left ventricle in hypertension, the heart adapts structurally and functionally. Structural changes involve an increased muscle mass achieved by left ventricular hypertrophy (LVH). Unless therapy is interdicted, left ventricular failure will ensure as the major cardiac hemodynamic consequence. LVH is also associated with a risk that is independent of the pressure. Although antihypertensive therapy reduces risk from the hemodynamic alterations, the independent risk of LVH has not been demonstrated. Moreover, should risk be demonstrated with therapy, before it can be ascribed to any specific agent(s), it must be dissociated from its effects on pressure, coronary blood flow (and flow reserve), or electrophysiological effects and be directly related to its action on reducing mass and reversing hypertrophy. Current investigative areas, involving new concepts of molecular biology of the cardiac myocyte, may provide great promise to the quest of unraveling these heretofore unexplainable and newly postulated questions.