Effects of &lt;i&gt;L&lt;/i&gt;-Carnitine Supplementation on Cardiac Morbidity in Hemodialyzed Patients

Matsumoto, Yoshihiro; Sato, Motoyoshi; Ohashi, Hiroshige; Araki, Hajime; Tadokoro, Mitsunobu; Osumi, Yukio; Ito, Hiroyasu; Morita, Hiroyuki; Amano, Izumi

doi:10.1159/000013584

Cited by 52 publications

(35 citation statements)

References 34 publications

(41 reference statements)

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“…4 Inhibition of fatty acid metabolism in the carnitine-lacking myocardium could be a pathogenic mechanism in uremic cardiomyopathy, 35 and a risk factor for cardiomegaly in patients on maintenance HD. 34 In the present study, although no correlation was found between plasma free carnitine level and the echocardiographic parameters studied, there was a significant decrease in some of the cardiac diameters (LA, RV, LVED and LVES) and an increase in diastolic function (E/A ratio) after 2 months of oral L-carnitine supplementation. However, these parameters, except for E/A ratio, were still significantly different from those of the controls.…”

Section: Discussioncontrasting

confidence: 75%

“…However, these parameters, except for E/A ratio, were still significantly different from those of the controls. Consistent with this finding, researchers 2,6,34,36,37 have reported a reduction of cardiomegaly, improvement of left ventricular function and performance, improvement of the metabolic and hemodynamic cardiac parameters, and improvement of cardiac complications (arrhythmia, reduced output, and low cardiothoracic ratio) in HD patients after L-carnitine treatment. However, cardiac thickness (RVAW, IVS, LVPW), left ventricular systolic function (FS and EF) and indices (MI, EDVI, ESVI) showed no significant changes after treatment and still these values continued to be significantly higher than controls.…”

Section: Discussionmentioning

confidence: 67%

“…33 There are factors related specifically for life on HD include myocardial stress such as recurrent volume expansion, accumulation of advanced glycation end products and deficit of certain substances that are essential for myocardial cells to perform their metabolic function. 34 The myocardium and skeletal muscles display the highest intracellular concentration of L-carnitine. 32 Approximately 60% of total energy metabolism is provided by the oxidation of fatty acids as a primary energy source in the normal heart muscle.…”

Section: Discussionmentioning

confidence: 99%

“…35 As L-carnitine plays a role in the utilization of fatty acids and glucose in the myocardium, 35 carnitine deficiency is an important factor in cardiac morbidity. 34 The myocardial ischemia generates acylcarnitine products and intracellular lactate production. 4 Inhibition of fatty acid metabolism in the carnitine-lacking myocardium could be a pathogenic mechanism in uremic cardiomyopathy, 35 and a risk factor for cardiomegaly in patients on maintenance HD.…”

Section: Discussionmentioning

confidence: 99%

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Dyslipidemia, Oxidative Stress and Cardiac Dysfunction in Children with Chronic Renal Failure: Effects of L-Carnitine Supplementation

2003

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Background: Secondary carnitine deficiency may develop in chronic renal failure (CRF) patients undergoing longterm hemodialysis (HD), with a resulting higher incidence of cardiovascular diseases, dyslipidemia and oxidative stress. We studied the efficacy of 12 months of L-carnitine supplementation on the amelioration of dyslipidemia, oxidative stress and cardiac dysfunction in 24 CRF children undergoing long-term HD compared with 24 age-and sex-matched controls. Methods: Plasma samples were analyzed spectrophotometerically before and after dialysis sessions and after 2-month supplementation with oral L-carnitine (50 mg/kg/day) for free carnitine (FC), the lipid profile, and oxidative stress markers. Echocardiography the day following dialysis measured cardiac diameters, wall thicknesses, left ventricular mass index (Ml), end diastole and systole volume indices and functions. Results: The pre-dialysis FC concentration was substantially lower than controls and decreased significantly at the end of the dialysis session. Pre-and post-dialysis plasma levels of free fatty acids (FFAs), trigyleride (TG), total cholesterol (TC) and oxidative stress markers significantly increased while high-density lipoprotein cholesterol (HDL-C) and phospholipids significantly decreased compared to controls. Echocardiography detected a significant increase in cardiac diameters and thickness, and systolic and diastolic cardiac dysfunction. After L-carnitine supplementation, plasma levels of FC increased to normal levels. FFAs, TC and HDL-C returned to control levels while TG, phospholipids, and the oxidative stress markers decreased but remained significantly higher than controls. There was a significant decrease in cardiac diameters and an increase in left ventricular diastolic function (E/A ratio), but no correlation between FC levels and echocardiographic parameters. Pre-dialysis, post-dialysis and after treatment, plasma FC level showed a significant positive correlation with HDL-C and phospholipids and a significant negative correlation with each of oxidative stress markers, FFAs, TG and TC. On the other hand, FFAs showed a significant positive correlation with TG, TC, DC, NO and a significant negative correlation with HDL-C and phospholipids. Conclusion: This study demonstrates that CRF children under regular HD suffer from a decrease in the level of plasma FC, dyslipidemia, oxidative stress, and an increase in cardiac diameters and thickness with impairment of cardiac functions. Oral L-carnitine supplementation at a dose of 50 mg/kg for 2 months can increase plasma FC level, improve dyslipidemia, decrease oxidative stress with reduction of cardiac diameters and increase in diastolic function.

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Section: Discussioncontrasting

confidence: 75%

Section: Discussionmentioning

confidence: 67%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Dyslipidemia, Oxidative Stress and Cardiac Dysfunction in Children with Chronic Renal Failure: Effects of L-Carnitine Supplementation

2003

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“…10 We previously reported that L-carnitine administration ameliorated myocardial fatty acid metabolism in patients undergoing HD. 11 There were also reports of improvement of cardiac dysfunction by L-carnitine supplementation, especially in patients with declined cardiac systolic function or with symptoms of heart failure; [12][13][14][15] however, when patients with normal myocardial function were studied, no benefit of carnitine was seen. 13,16 Left ventricular hypertrophy (LVH) is common and is an independent predictor of cardiac death in patients undergoing dialysis.…”

mentioning

confidence: 99%

L-Carnitine Supplementation Decreases the Left Ventricular Mass in Patients Undergoing Hemodialysis

Sakurabayashi

Miyazaki

Yuasa

et al. 2008

Circ J

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Background Patients on long-term hemodialysis become deficient in carnitine and are frequently treated with carnitine supplementation to offset their renal anemia, lipid abnormality and cardiac dysfunction. The therapeutic value of carnitine supplementation on left ventricular hypertrophy (LVH) in patients with normal cardiac systolic function remains uncertain. Methods and ResultsThe cardiac morphology and function of 10 patients given 10 mg/kg of L-carnitine orally, immediately after hemodialysis sessions 3 times per week for a 12-month period were compared with 10 untreated control patients. Using echocardiography, left ventricular fractional shortening (LVFS) and left ventricular mass index (LVMI) were measured before and after the study period. As a result, amounts of serum-free carnitine increased from 28.4±4.7 to 58.5±12.1 mol/L. The LVMI decreased significantly from 151.8±21.2 to 134.0±16.0 g/m 2 in treated patients (p<0.01), yet the LVMI in untreated control patients did not change significantly (ie, from 153.3±28.2 to 167.1±43.1 g/m 2 ). However, LVFS values remained unchanged in both groups. Although L-carnitine promoted a 31% reduction in erythropoietin requirements, hematocrit and blood pressure did not change during the study period. Conclusions Supplementation with L-carnitine induced regression of LVH in patients on hemodialysis, even for those with normal systolic function. (Circ J 2008; 72: 926 -931)

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The use of levo-carnitine in children with renal disease: a review and a call for future studies

et al. 2005

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Carnitine is an amino acid derivative that has a key role in the regulation of fatty acid metabolism and ATP formation. Carnitine deficiency has been described in various conditions, including chronic kidney disease (CKD) and end stage renal disease (ESRD). The deficiency of this micronutrient is postulated to lead to adverse effects across multiple organ systems. There is a paucity of information on carnitine deficiency and its effects in the pediatric CKD and ESRD populations. Currently, there is no evidence supporting the routine use of carnitine supplementation in children with ESRD. In this article, we review the pathophysiology, pharmacokinetics and the potential effects of levo-carnitine supplementation with a focus on the pediatric CKD and ESRD populations. Finally, potential future directions of research are discussed.

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Effects of <i>L</i>-Carnitine Supplementation on Cardiac Morbidity in Hemodialyzed Patients

Cited by 52 publications

References 34 publications

Dyslipidemia, Oxidative Stress and Cardiac Dysfunction in Children with Chronic Renal Failure: Effects of L-Carnitine Supplementation

Dyslipidemia, Oxidative Stress and Cardiac Dysfunction in Children with Chronic Renal Failure: Effects of L-Carnitine Supplementation

L-Carnitine Supplementation Decreases the Left Ventricular Mass in Patients Undergoing Hemodialysis

The use of levo-carnitine in children with renal disease: a review and a call for future studies

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