Inflammation and perturbation of the l‐carnitine system in heart failure

Abstract

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. To investigate the interrelationship between TNFalpha and sphingosine (SPH), which induce muscle wastage, and plasma levels of l-carnitine. We studied 18 heart failure patients and correlated NYHA class and ventricular function with the plasma concentration of these molecules. 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. 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.