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From tissue wasting to cachexia: changes in peripheral blood flow and skeletal musculature

R Sharma1 and S.D Anker*,1,2

a Clinical Cardiology, National Heart & Lung Institute, Imperial College School of Medicine, London, U.K.
b Franz Volhard Klinik (Charité, Campus Berlin-Such) at Max Delbrück Centrum for Molecular Medicine, Berlin, Germany

* Correspondence: Dr Stefan Anker, MD PhD, Clinical Cardiology, NHLI London, Dovehosue Street, London SW3 6LY, U.K.

Abstract

Chronic heart failure (CHF) is characterized by a limitation in exercise capacity caused by breathlessness and fatigue. There is substantial evidence to suggest that these symptoms are largely determined by abnormalities of peripheral blood flow and skeletal muscle function, as opposed to central haemodynamic disturbances. Muscle atrophy and loss of strength, decreased oxidative capacity and structural changes in the skeletal musculature have all been reported in CHF. Abnormalities in peripheral blood flow also predict reduced exercise capacity, particularly in patients with cardiac cachexia. Endothelial dysfunction is present in CHF, together with an increase in peripheral vasomotor tone. The factors that regulate endothelial function in CHF are complex and poorly understood. The present review addresses abnormalities in endothelial function, regional blood flow and skeletal muscle in CHF, and their contributions to tissue wasting and cachexia.

Key Words: Blood flow chronic heart failure • endothelial function skeletal muscle


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