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(Circulation. 1997;95:1983-1985.)
© 1997 American Heart Association, Inc.

Articles

Do Antihypertensive Drugs Differ in Their Ability to Regress Left Ventricular Hypertrophy?

Richard B. Devereux, MD

From the Department of Medicine, The New York Hospital-Cornell Medical Center, New York, NY.

Correspondence to Richard B. Devereux, MD, Division of Cardiology, Box 222, The New York Hospital–Cornell Medical Center, 525 E 68th St, New York, NY, 10021. E-mail rbdevere@mail.med.cornell.edu

Key Words: Editorials • echocardiography • hypertrophy • hypertension

	Introduction

 
Numerous studies have documented a strong relationship between left ventricular (LV) hypertrophy and the risk of cardiovascular events in hypertensive patients.^{1 2 3 4 5 6} Furthermore, initial evidence suggests that whether LV hypertrophy is reduced or progresses over time directly influences the risk of subsequent complications.^{7 8 9 10} In this context, it is understandable that considerable attention has been devoted to determining whether different forms of antihypertensive therapy differ with regard to their ability to induce regression of hypertensive LV hypertrophy. Some progress has been made, but important questions remain unanswered after the recent appearance of a meta-analysis of randomized double-blind studies of LV hypertrophy regression¹¹ as well as detailed analyses of echocardiographic data from the Treatment of Mild Hypertension Study (TOMHS) and other large trials^{12 13} and, in this issue of Circulation, from the long-awaited Veterans Administration study of single-drug antihypertensive treatment.¹⁴ To place this recent evidence in context, it is useful to consider the characteristics of optimal study designs for trials of LV hypertrophy regression that help make their results conclusive and generalizable.

	Criteria for an Optimal Study of LV Hypertrophy Regression

 
To add useful information to the existing large but flawed literature, studies of LV hypertrophy regression should at least be randomized and double-blind and use an anatomically validated method of measuring LV mass to compare an active agent with either a placebo or one or more other active agents over 6 months in hypertensive women and men, many or all of whom have LV hypertrophy at baseline.¹⁵ Relatively small studies of this type, with 20 to 30 patients per treatment arm, . . . [Full Text of this Article]

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