抄録
This review provides a brief summary of molecular and pathophysiological events involved in the development and reversal of hypertensive left ventricular hypertrophy (LVH). Data gathered in our laboratory over the years are emphasized. Since ventricular hypertrophy confers considerable risk for increased premature cardiovascular morbidity and mortality, particular atttention has been given to reversal of hypertrophy and those factors that may determine the outcome of the reversal process. Our data show that reversal of hypertrophy and ventricular function postregression depend not only on hemodynamic factors but also on nonhemodynamic factors. Thus, various antihypertensive agents have demonstrated differences in their ability to promote LVH reversal and affect ventricular function. The possible roles of the local myocytic renin-angiotensin system, alterations in calcium metabolism, accumulation of collagen and changes in coronary circulation that accompany LVH in determining ventricular function and the magnitude of risk associated with LVH are discussed. Finally, a brief overview of molecular mechanisms that mediate alterations in gene expression and initiation of growth after hemodynamic stress is given. (Hypertens Res 1993; 16: 163-177)
