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(Circulation. 1998;98:1987-1989.)
© 1998 American Heart Association, Inc.

Editorial

Regression of Left Ventricular Hypertrophy in Patients With Hypertension

Blockade of the Renin-Angiotensin-Aldosterone System

Bertram Pitt, MD

From the Cardiology Division, University of Michigan Medical Center, Ann Arbor.

Correspondence to Bertram Pitt, MD, Cardiology Division, University of Michigan Medical Center, 1500 E Medical Center Dr, Ann Arbor, MI 48109-0366.

Key Words: Editorials • hypertrophy • hypertension

Left ventricular hypertrophy in patients with hypertension is of importance because of its association with an increase in the incidence of heart failure and other cardiovascular events, such as myocardial infarction and sudden cardiac death. Not all antihypertensive agents, however, have been suggested to be equally effective in causing regression of left ventricular hypertrophy or preventing its progression.¹ Although several classes of antihypertensive agents are effective in causing regression of ventricular hypertrophy, it is uncertain whether all strategies are equally effective and, more importantly, whether strategies equally effective in causing regression of ventricular hypertrophy will be equally effective in preventing the consequences of ventricular hypertrophy, such as myocardial infarction and sudden cardiac death.

The mechanism of ventricular hypertrophy in patients with hypertension is as yet uncertain; however, activation of the renin-angiotensin-aldosterone system (RAAS) as a result of myocardial stretch and other factors is recognized as playing an important role. Angiotensin II has been shown to stimulate various growth factors, cytokines, fibroblast activity, myocyte hypertrophy, and myocardial fibrosis. Strategies to prevent activation of the RAAS and/or its effects would therefore appear attractive in preventing ventricular hypertrophy and its consequences in patients with hypertension.

ACE inhibitors have been shown to cause a reduction in myocardial cytokines, growth factors, oxygen free radical production, collagen formation, and myocyte growth. They increase nitric oxide release and reduce morbidity, ischemic events, and mortality in patients with heart failure, including those with a history of hypertension. A meta-analysis of all antihypertensive agents has suggested that ACE inhibitors . . . [Full Text of this Article]

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