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(Hypertension. 2004;43:936.)
© 2004 American Heart Association, Inc.

Editorial Commentary

Is the Female Heart More Sensitive to Aldosterone for Early Remodeling?

From the Cardiovascular Division, University of Minnesota, Minneapolis.

Correspondence to Dr Daniel A. Duprez, Cardiovascular Division, VCRC, Room 270, University of Minnesota, MMC 508, 420 Delaware Street SE, Minneapolis, MN 55455. E-mail dupre007@umn.edu

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Seldom is there such a renewed interest in the study of a compound isolated more than a half century ago as we see now with aldosterone. A new era has begun in the study of aldosterone in individuals free of myocardial infarction and of heart failure.¹

The mineralocorticoid hormone aldosterone was thought to be produced uniquely in the adrenal cortex and to act exclusively on epithelia to promote sodium retention and potassium excretion. However, it is now known that aldosterone also acts on nonepithelial tissues, such as brain, heart, and blood vessels. In addition, enzymes required for aldosterone biosynthesis are expressed in these same tissues, which may be consistent with local aldosterone production acting in a paracrine fashion.²

With the introduction of angiotensin-converting enzyme (ACE) inhibitors and their presumptive elimination of angiotensin II, a major determinant of aldosterone production by the adrenal glands, the perception of the pathophysiologic importance of aldosterone in congestive heart failure has been minimized during the past 20 years. However, recent evidence has revived interest in aldosterone and its role in congestive heart failure.

The Randomized Aldactone Evaluation Study (RALES) and Eplerenone Post–Acute Myocardial Infarction Heart Failure Efficacy and Survival Study (EPHESUS) clearly demonstrated that antagonizing aldosterone on top of inhibition of the ACE or on top of blocking of the angiotensin II receptor had a major beneficial effect in risk reduction of cardiovascular morbidity and mortality in severe heart failure and postmyocardial infarction.^3,4

Ventricular remodeling is the process by which mechanical, neurohormonal, and possibly genetic . . . [Full Text of this Article]

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