© 2005 European Society of Cardiology
Inflammation and perturbation of the L-carnitine system in heart failure
a Internal Medicine 1, S. Bortolo Hospital Vicenza, Italy
b CNR Institute of Neurosciences, Unit for Neuromuscular Biology and Pathophysiology, Department of Biomedical Sciences, University of Padua Viale G. Colombo 3, 35100 Padova, Italy
* Corresponding author. Tel.: +39 49 8276031; fax: +39 49 8276040. E-mail address: ldl{at}bio.unipd.it
| Abstract |
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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 TNF
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: TNF
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.
Key Words: Heart failure L-carnitine TNF
Sphingosine Inflammation
Received September 15, 2004; Revised November 24, 2004; Accepted November 25, 2004
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