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Regional and systemic metabolic effects of angiotensin-converting enzyme inhibition during exercise in patients with severe heart failure.

Authors
  • Kugler, J
  • Maskin, C
  • Frishman, W H
  • Sonnenblick, E H
  • LeJemtel, T H
Type
Published Article
Journal
Circulation
Publication Date
Dec 01, 1982
Volume
66
Issue
6
Pages
1256–1261
Identifiers
PMID: 6291801
Source
Medline
License
Unknown

Abstract

The acute hemodynamic and metabolic effects of captopril therapy were studied in 12 patients with severe heart failure during maximal exercise performed on an upright bicycle ergometer. During the control period, exhaustion occurred after 4.2 +/- 2.7 minutes of exercise. Cardiac index increased from 1.54 +/- 0.36 l/min/m2 at rest to 3.39 +/- 1.54 l/min/m2 (p less than 0.001) at exhaustion; systemic arteriovenous oxygen difference increased from 8.8 +/- 2.1 to 12.8 +/0 2.4 ml/100 ml (p less than 0.001) and oxygen uptake from 3.4 +/- 0.5 to 10.8 +/- 3.0 ml/kg/min (p less than 0.001). Pulmonary arterial oxygen content decreased from 7.3 +/- 1.3 to 3.7 +/- 1.5 ml/100 ml (p less than 0.001) and femoral vein oxygen content from 5.0 +/- 1.7 to 2.5 +/- 1.2 ml/100 ml (p less than 0.001). During captopril therapy, cardiac index significantly increased both at rest (1.83 +/- 0.54 vs 1.54 +/- 0.36 l/min/m2, p less than 0.01) and during maximal exercise (3.67 +/- 1.51 vs 3.39 +/- 1.54 l/min/m2, p less than 0.01). Systemic arteriovenous oxygen difference decreased significantly at rest, from 8.8 +/- 2.1 to 7.7 +/- 2.1 ml/100 ml (p less than 0.01) and during maximal exercise from 12.8 +/- 2.4 to 12.3 +/- 2.2 ml/100 ml (p less than 0.01). Pulmonary arterial oxygen content at exhaustion was significantly higher during captopril therapy than during the control period (4.1 +/- 1.1 vs 3.7 +/- 1.5 ml/100 ml, p less than 0.05), while femoral venous blood content was unchanged. Captopril therapy did not significantly increase maximal oxygen uptake or exercise duration. Thus, the acute administration of captopril to patients with severe heart failure does not increase exercise capacity despite improved cardiac performance. Moreover, captopril therapy does not acutely result in metabolic benefits to the skeletal muscles during exercise.

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