Effects of Levocarnitine on Brachial-Ankle Pulse Wave Velocity in Hemodialysis Patients: A Randomized Controlled Trial

Abstract

Background and Aims: Atherosclerotic cardiovascular disease is the most common cause of mortality in patients with end-stage kidney disease. Chronic kidney disease patients often exhibit a deficiency in l-carnitine due to loss during hemodialysis (HD). We studied the effects of l-carnitine supplementation on brachial-ankle pulse wave velocity (baPWV), a marker of atherosclerosis, in HD patients. Methods: This was a prospective, open-label, randomized, parallel controlled, multi-center trial testing the anti-atherosclerotic efficacy of oral l-carnitine administration (20 mg/kg/day). HD patients (n = 176, mean age, 67.2 ± 10.3 years old; mean duration of HD, 54 ± 51 months) with plasma free l-carnitine deficiency (<40 μmol/L) were randomly assigned to the oral l-carnitine group (n = 88) or control group (n = 88) and monitored during 12 months of treatment. Results: There were no significant differences in baseline clinical variables between the l-carnitine and control groups. l-carnitine supplementation for 12 months significantly increased total, free, and acyl carnitine levels, and reduced the acyl/free carnitine ratio. The baPWV value decreased from 2085 ± 478 cm/s at baseline to 1972 ± 440 cm/s after six months (p < 0.05) to 1933 ± 363 cm/s after 12 months (p < 0.001) of l-carnitine administration, while no significant changes in baPWV were observed in the control group. Baseline baPWV was the only factor significantly correlated with the decrease in baPWV. Conclusions: l-carnitine supplementation significantly reduced baPWV in HD patients. l-carnitine may be a novel therapeutic strategy for preventing the progression of atherosclerotic cardiovascular disease.

Associations between acylcarnitine to free carnitine ratio and adverse prognosis in heart failure patients with reduced or preserved ejection fraction

“…Carnitine transports long‐chain fatty acids into the mitochondria for β‐oxidation and protects the myocardium against ischaemic injury, the occurrence of angina, diastolic dysfunction, and HF 2, 3. Carnitine deficiency results in impaired mitochondrial β‐oxidation, decreased glucose oxidation, and accelerated cellular apoptosis 4, 5. In HF patients, decreased myocardial carnitine levels accompanied by increased plasma carnitine levels, potentially reflecting increased leakage of carnitine through damaged cardiomyocyte membranes, have been reported 1, 6.…”

Decreased level of serum carnitine might lead to arteriosclerosis progression via the accumulation of advanced glycation end products in maintenance hemodialysis patients

“…Previous studies showed that carnitine administration attenuated the progression of atherosclerosis and improved cardiovascular dysfunction in HD patients [28,29]. Given that serum level of carnitine is significantly reduced in most HD patients [14], administering carnitine to this population could potentially prevent the progression of arteriosclerosis and improve prognosis.…”

Hemodiyaliz Hastalarında Karnitin Kullanımı

“…Ancak yapılan karnitin desteği prostaglandin I 2 ve nitrik oksit üretimini tekrar artırabilmekte ve ROS üretimini azaltmaktadır. Dahası proinflamatuvar sitokinlerin plazma ve miyokardial ekspresyonunu azaltarak kardiyovasküler hastalıklara karşı koruyucu bir rol oynamaktadır (16,17).…”

“…Ayrıca başlangıçta ayak bileği brakial basıncı daha yüksek olanlarda karnitin suplementasyonu ile birlikte bu indeks daha fazla oranda azalmıştır. Bu nedenle L-karnitin tedavisinin antiaterosklerotik özellikte olduğu söylenebilir (16).…”