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(Circulation. 2005;112:2380-2382.)
© 2005 American Heart Association, Inc.

Editorial

Angiotensin-Converting Enzyme Inhibitors or ß-Blockers in Heart Failure

Does It Matter Who Goes First?

James C. Fang, MD

From the Cardiovascular Division, Brigham and Women’s Hospital, Boston, Mass.

Correspondence to James C. Fang, MD, Cardiovascular Division, Brigham and Women’s Hospital, 75 Francis St, Boston, MA 02115. E-mail jfang@partners.org

Key Words: Editorials • heart failure • drugs • adrenergic beta-antagonists • angiotensin-converting enzyme inhibitors

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

Angiotensin-converting enzyme (ACE) inhibitors and ß-blockers are potent therapies in heart failure. They lower total mortality and heart failure hospitalizations by 25% to 40% across all ages, functional capacities, degrees of left ventricular dysfunction, and causes.^1,2 But does it matter which intervention is given first? There are 2 primary reasons why clinicians initiate heart failure therapy with ACE inhibitors for patients with systolic dysfunction: (1) ACE inhibitors were the first agents to demonstrate a mortality benefit in heart failure and therefore have since served as background therapy for all heart failure trials, and (2) heart failure is a hemodynamic as well as a neurohormonal condition that acutely improves with vasodilation.³ In acutely decompensated patients, initial hemodynamic stabilization through vasodilation improves the neurohormonal profile, including a reduction in norepinephrine levels.⁴ This stabilization may allow the subsequent introduction of ß-blockers, which are acutely associated with a decline in ventricular function.^5,6

Article p 2426

However, when a patient has compensated heart failure, would a ß-blocker first be tolerated, safe, and even better? There are putative reasons why ß-blockers first may lead to greater survival and improved quality of life. The adrenergic system is activated earlier than the renin-angiotensin system (RAS)⁷ and is an important stimulus for RAS activation. Norepinephrine is a potent predictor of mortality.⁸ Enhanced sympathetic renal activity may contribute to sodium and water avidity.⁹ Evidence suggests that there is less "escape" and greater suppression of angiotensin II by ACE inhibitors when the adrenergic system is also blocked.¹⁰ Cardiorenal complications of heart . . . [Full Text of this Article]

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Circulation 2005 112: 2377. [Extract] [Full Text]

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