Background: Heart failure (HF) is accompanied by elevated levels of pro-inflammatory cytokines. Skeletal muscle myopathy with atrophy of fibres, decreased oxidative metabolism and preferential synthesis of fast myosin heavy chains (MHCs) occurs, which contributes to the worsening of symptoms. l-Carnitine has been shown to be protective against the apoptosis-induced atrophy of fibres and fast MHCs shift.
Aims: To investigate the interrelationship between TNFalpha and sphingosine (SPH), which induce muscle wastage, and plasma levels of l-carnitine.
Methods: We studied 18 heart failure patients and correlated NYHA class and ventricular function with the plasma concentration of these molecules.
Results: TNFalpha and SPH levels were raised and correlated with the severity of HF. l-Carnitine levels were increased in HF patients, but decreased according to the severity of cardiac decompensation.
Conclusions: The increased levels of l-carnitine are likely due to release from the damaged muscle, reduced urinary excretion, decreased dietary intake and liver synthesis (malnutrition). It is possible that the cytokine-induced muscle wastage is not counterbalanced by the beneficial metabolic effects of l-carnitine, the metabolism of which is profoundly perturbed in CHF. l-Carnitine supplementation may produce positive effects on the skeletal muscle, as has been shown in animal models of HF.
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