REVERSAL OF HYPERTROPHY - AN ACTIVE BIOLOGIC PROCESS

Evidence from in vivo, in vitro, and genetic studies suggests that the reversal as well as the development of left ventricular hypertrophy d o not depend solely on hemodynamic load; other factors are involved. S everal humoral agents that may affect mitogenesis of cardiac myocytes and nonmyocitic elements have been identified, including the local ren in-angiotensin system, norepinephrine, endothelins, transforming growt h factor beta, insulin-like growth factor, bradykinin, prostaglandins, and nitric oxide. Animal studies using various models of left ventric ular hypertrophy are beginning to suggest that reversal of hypertrophy may decrease mortality, improve coronary flow reserve, and maintain c ardiac performance. Studies in humans are less supportive, and more ar e needed before it may be concluded that reduction of left ventricular mass decreases the cardiovascular morbidity and mortality associated with cardiac hypertrophy.