Document Detail


Inverse relation between aldosterone and venous capacitance in chronically treated congestive heart failure.
MedLine Citation:
PMID:  10760338     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
E Rietzschel; D A Duprez; M L De Buyzere; D L Clement
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  The American journal of cardiology     Volume:  85     ISSN:  0002-9149     ISO Abbreviation:  Am. J. Cardiol.     Publication Date:  2000 Apr 
Date Detail:
Created Date:  2000-06-26     Completed Date:  2000-06-26     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  0207277     Medline TA:  Am J Cardiol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  977-80     Citation Subset:  AIM; IM    
Affiliation:
Department of Cardiology and Angiology, University Hospital, Gent, Belgium.
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MeSH Terms
Descriptor/Qualifier:
Aldosterone / blood*
Angiotensin-Converting Enzyme Inhibitors / therapeutic use*
Diuretics / therapeutic use
Extremities / blood supply
Furosemide / therapeutic use
Heart Failure / drug therapy*,  physiopathology
Humans
Middle Aged
Vascular Capacitance / physiology*
Vasoconstriction / physiology
Chemical
Reg. No./Substance:
0/Angiotensin-Converting Enzyme Inhibitors; 0/Diuretics; 52-39-1/Aldosterone; 54-31-9/Furosemide
Comments/Corrections
Erratum In:
Am J Cardiol 2000 Aug 15;86(4):484

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