Key result
Enalapril treatment for 3 months in patients with chronic heart failure did not improve the decreased activity of oxidative enzymes or capillarization, though muscle fibre area increased.
Why the study?
Does enalapril treatment improve skeletal muscle metabolism and histology in patients with congestive heart failure?
Observational (n=46)
Does enalapril treatment improve skeletal muscle metabolism and histology in patients with congestive heart failure?
Enalapril treatment in heart failure patients improves functional class and increases muscle fibre area, but does not reverse the underlying deficits in skeletal muscle oxidative enzymes and capillarization.
Enalapril increases fibre area without restoring oxidative enzymes or capillarization in heart failure; leaves open whether longer ACE inhibition improves skeletal muscle metabolism.
To evaluate if enalapril treatment can influence skeletal muscle metabolism and histology we investigated 26 patients with congestive heart failure and 20 normal subjects. The patients were treated with enalapril for 3 months in addition to diuretics and digitalis. Biopsies from the lateral vastus muscle were taken before and after treatment. Citrate synthetase, 3-hydroxyacyl-CoA dehydrogenase and phosphorylase activities were significantly decreased in the patients compared with controls. The number of capillaries per fibre and the number of capillaries surrounding each fibre were significantly decreased among patients. After 3 months of enalapril treatment functional class improved significantly. The lactate dehydrogenase activity increased whereas the oxidative enzymes did not change significantly. The type I, II and II A fibre areas increased significantly after enalapril treatment. We conclude that patients with chronic heart failure have decreased activity of oxidative enzymes and of phosphorylase in skeletal muscle. They also have decreased capillarization in skeletal muscle. These changes were not influenced by enalapril treatment. The increase in muscle fibre area seen after enalapril treatment could be due to increased physical activity. The cause of increased muscle lactate dehydrogenase activity after enalapril treatment needs further investigation.
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Schaufelberger et al. (1996) conducted an observational in Congestive heart failure (n=46). Enalapril vs. Normal subjects (baseline) and pre-treatment (follow-up) was evaluated on Skeletal muscle metabolism and histology (oxidative enzymes, phosphorylase, capillarization, and fibre area). Enalapril treatment for 3 months in patients with chronic heart failure did not improve the decreased activity of oxidative enzymes or capillarization, though muscle fibre area increased.
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