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  • Title: Are alterations of skeletal muscle ultrastructure in patients with heart failure reversible under treatment with ACE-inhibitors?
    Author: Münzel T, Kurz S, Drexler H.
    Journal: Herz; 1993 Dec; 18 Suppl 1():400-5. PubMed ID: 8125419.
    Abstract:
    In patients with chronic heart failure, exercise capacity and clinical symptoms correlate poorly, if at all with the degree of left ventricular dysfunction. These observations might indicate that peripheral alterations (e.g. reduced perfusion of the exercising muscle) contribute to the functional state and exercise capacity of patients with chronic heart failure. Acute improvements in hemodynamics by means of therapy with vasodilators or positive inotropes, however, could not be translated into an enhanced oxygen consumption. These studies have prompted the hypothesis that in the setting of heart failure, intrinsic abnormalities of the exercising muscle develop that prevent acute improvement in peak VO2. Indeed, ultrastructural analysis of a large cohort of patients with chronic heart failure revealed that volume density of mitochondria and surface density of mitochondrial cristae (both are parameters for the oxidative capacity of skeletal muscle) were reduced by more than 20% as compared to healthy control subjects. In contrast to left ventricular contractility parameters, ultrastructural changes of the skeletal muscle correlated closely with peak oxygen consumption, indicating that abnormalities of the exercising muscle contribute to a decreased exercise capacity in this patient group. Chronic but not acute treatment with angiotensin converting enzyme (ACE) inhibitors increases blood flow to the exercising muscle and improves peak oxygen consumption. These protracted effects of ACE-inhibitors might be due to an inhibitory effect on the vascular renin angiotensin system leading to a beneficial remodelling of the vessel wall. Forearm vessels of patients with heart failure do not respond adequately to acetylcholine and reactive hyperemia, indicating an impaired endothelial function.(ABSTRACT TRUNCATED AT 250 WORDS)
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