Inverse relation between aldosterone and venous capacitance in chronically treated congestive heart failure

Ernst R. Rietzschel, Daniel A. Duprez, Marc L. De Buyzere, Denis L. Clement

Research output: Contribution to journalArticlepeer-review

7 Scopus citations

Abstract

The purpose of this study was to examine if there is a relation between the aldosterone escape phenomenon and venous capacitance of the upper and lower limbs in patients with long-term congestive heart failure (CHF) receiving chronic treatment with angiotensin-converting enzyme (ACE) inhibitors. The study group consisted of 16 subjects with ischemic CHF in New York Heart Association functional class II (age 59 ± 2 years, ejection fraction 24 ± 4%), stabilized under a constant drug regimen comprising furosemide, captopril 50 mg 3 times daily, and digoxin for at least 3 months. Thirteen apparently healthy volunteers, aged 50 ± 4 years acted as controls. Forearm and calf venous capacitances were measured simultaneously by venous occlusion plethysmography using mercury-in-silastic strain gauges. The equilibration technique was used to derive venous capacitance from the recorded pressure-volume curves. Active renin, angiotensin II, and aldosterone levels were determined on venous blood samples obtained in the supine position. Angiotensin II (p <0.05) and aldosterone (p <0.01) were statistically significantly higher in patients with CHF under long-term ACE inhibition than in controls (aldosterone escape phenomenon). In CHF, forearm venous capacitance was 2.19 ± 0.18 ml/100 ml; calf venous capacitance was 2.83 ± 0.27 ml/100 ml. Aldosterone significantly and inversely correlated with venous capacitance in both upper (r = -0.586; p = 0.017) and lower (r = -0.625; p = 0.01) limbs. No correlations were found between forearm or calf venous capacitance and renin or angiotensin II. In patients with heart failure chronically treated with diuretics and full ACE inhibition, venous capacitance is inversely correlated with aldosterone through the mechanism of aldosterone escape, creating the potential for further deterioration of the CHF process. Copyright (C) 2000 Excerpta Medica Inc.

Original languageEnglish (US)
Pages (from-to)977-980
Number of pages4
JournalAmerican Journal of Cardiology
Volume85
Issue number8
DOIs
StatePublished - Apr 15 2000

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