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Circulation. 2002;106:1055-1057
Published online before print August 5, 2002, doi: 10.1161/01.CIR.0000030935.89559.04
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(Circulation. 2002;106:1055.)
© 2002 American Heart Association, Inc.


Brief Rapid Communications

Elevated Plasma Aldosterone Levels Despite Complete Inhibition of the Vascular Angiotensin-Converting Enzyme in Chronic Heart Failure

Ulrich P. Jorde, MD; Timothy Vittorio, MD; Stuart D. Katz, MD; Paolo C. Colombo, MD; Farhana Latif, MD; Thierry H. Le Jemtel, MD

From the Division of Circulatory Physiology, Department of Medicine, Columbia University College of Physicians and Surgeons, New York, NY (U.P.J., T.V., P.C.C.); the Section of Cardiovascular Medicine, Department of Medicine, Yale University School of Medicine, New Haven, Conn (S.D.K.); and the Division of Cardiology, Department of Medicine, Albert Einstein College of Medicine, New York, NY (F.L., T.H.L.J.).

Correspondence to Thierry H. Le Jemtel, MD, Albert Einstein College of Medicine, 1300 Morris Park Ave, Bronx, NY 10461. E-mail lejemtel{at}aecom.yu.edu

Background— Plasma aldosterone levels are elevated in patients with chronic heart failure (CHF) taking angiotensin-converting enzyme (ACE) inhibitors. Elevated aldosterone levels may reflect incomplete inhibition of the vascular converting enzyme during long-term ACE inhibition. We simultaneously measured plasma aldosterone levels and the degree of inhibition of the vascular converting enzyme in patients with CHF.

Methods and Results— Thirty-four subjects with CHF receiving the maximum recommended doses of ACE inhibitors for a duration of 3 to 105 months were studied. The pressor response to exogenous angiotensin I (AI) was measured and normalized for the pressor response to angiotensin II (AII) to assess inhibition of the vascular converting enzyme (AII/AI ratio). Aldosterone levels were determined by solid-phase radioimmunoassay. Eleven of the 34 subjects had plasma aldosterone levels above the upper limit of normal, ie, >15.0 ng/dL. Seven of these 11 subjects (64%) had an AII/AI ratio <=0.05, indicating complete inhibition of the vascular converting enzyme. In the entire cohort, the AII/AI ratio did not correlate with the duration of ACE inhibitor therapy.

Conclusions— Plasma aldosterone levels are elevated in patients with CHF during long-term ACE inhibitor therapy despite complete inhibition of the vascular converting enzyme. Complete inhibition of the vascular converting enzyme does not obviate the need for aldosterone receptor blockade in patients with CHF.


Key Words: heart failure • angiotensin • aldosterone




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