Cardiac remodeling in systemic hypertension.

Experimental and clinical studies provide evidence that hypertension is causally related to adverse cardiac structural changes, such as LA enlargement, LV hypertrophy and myocardial fibrosis, and functional changes inclusive of LV systolic and diastolic dysfunction. These changes are induced by both hemodynamic and nonhemodynamic factors. There is accumulating evidence from several small and large clinical trials that various classes of antihypertensive therapy prevent and regress LVH and myocardial fibrosis. Prevention and reversal of LVH are associated with an improvement in cardiac function and with a decline in risk of adverse cardiovascular outcomes. Prevention of LVH should be a priority in subjects with hypertension. In patients with hypertensive heart disease, the components of therapy must comprise optimization of BP and regression of LVH. Future targets of therapy in hypertensive heart disease may include regression of myocardial fibrosis, normalization of LA size, and improvement in LV diastolic function.