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Circulation. 1999;100:685-688

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(Circulation. 1999;100:685-688.)
© 1999 American Heart Association, Inc.


Correspondence

Influence of the Angiotensin II Antagonist Valsartan on Left Ventricular Hypertrophy in Patients With Essential Hypertension

John S. Gottdiener, MD

Cardiology Division St Francis Hospital, Roslyn, NY


*    Introduction
 
To the Editor:

The recent article by Thürmann et al1 is of substantial interest in documenting efficacy of a relatively new angiotensin II antagonist for reduction of left ventricular mass in hypertensive patients. However, some features of the study cast doubts on the validity of the results. Moreover, misstatements of fact concerning existing literature further impair the interpretation of these data.

Although the authors report the efficacy of valsartan for regression of left ventricular hypertrophy (LVH), in fact, only the mean reduction of left ventricular (LV) mass is reported rather than the number of individuals with LVH who had sufficient reductions of LV mass to revert to normal. More importantly, despite the emphasis on the efficacy of valsartan, the investigators' data indicate that LV mass was reduced with atenolol as well. It is unclear whether the reduction of LV mass with atenolol was significantly less than that with valsartan. It can be questioned whether the {approx}10 g average difference in LV mass reduction between valsartan- and atenolol-treated patients is biologically or even statistically meaningful. Additionally, there appeared to be equivalent reduction of LV wall thickness with atenolol and with valsartan.

More importantly, the study was not a comparison of single-drug therapy. A third of the patients in both groups received hydrochlorothiazide to achieve hypertension control. Other patients received pretreatment with diuretics, which was considered acceptable because the investigators believed that the effects of diuretics on LV mass and wall thickness have been shown to be negligible. In fact, single-drug comparative . . . [Full Text of this Article]

Petra A. Thürmann, MD

Hospital Wuppertal GmbH Philipp Klee Institute of Clinical Pharmacology, Wuppertal, Germany

Peter Kenedi, MD

Department of Internal Medicine Diakonissenkrankenhaus, Frankfurt, Germany

Andor Schmidt, MD

Offenbach/Main, Germany

Sebastian Harder, MD; Norbert Rietbrock, MD

Institute of Clinical Pharmacology, University Hospital, Frankfurt, Germany




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