Objective-In congestive heart failure (CHF) the skeletal muscle of the lower limbs develops a myopathy with atrophy and shift from the slow type to the fast type fibres.

No abstract

Objective-To see whether cardiac morphological and functional abnormalities in uraemic patients are determined by high blood pressure or if they are an expression of a specific cardiomyopathy. Design-Cross sectional study. Setting-City general hospital in Italy. Haemodialysis for chronic renal failure still carries high mortality (10% per year). Cardiovascular events are the main cause of death (50-60% against 15% in control populations).' Accelerated coronary atherosclerosis, which has been claimed to be linked to lipid abnormalities, high blood pressure, diabetes, altered oxygen delivery at cellular level, and to an unknown uraemic factor, seems to be closely related to this excessive mortality.23The natural course of disease in these patients is also characterised by congestive heart failure, possibly as a result of a specific uraemic cardiomyopathy.

Six months' treatment with L and with E produces an improvement in EC of similar magnitude. These changes are accompanied by a reshift of MHCs of leg skeletal muscle toward the slow, more fatigue-resistant isoforms. Magnitude of MHC1 changes correlates with the net peak V(O2) gain, which suggests that improved EC may be caused by favorable biochemical changes occurring in the skeletal muscle.