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Review Article | DOI: https://doi.org/10.31579/IJBR-2021/006
*Corresponding Author: Aamir J. A. Mosawi. Advisor Doctor,Baghdad Medical City and the National Center for Training and Development of Iraqi Ministry of Health, Iraq
Citation: Aamir J. A. Mosawi (2021) The uses of L-Carnitine in cardiology. International Journal of Biomed Research. 1(1).DOI: 10.31579/IJBR-2021/006
Copyright: © 2021, Aamir J. A. Mosawi, This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Received: 01 March 2021 | Accepted: 12 March 2021 | Published: 16 March 2021
Keywords: l-carnitine, cardiology, heart disease
L-carnitine is a non-protein amino acid synthesized from the essential amino acids lysine and methionine or obtained from dietary sources. Accumulating scientific research evidence suggests that L-carnitine has beneficial cardiovascular effects, and a potential in the management of a variety of cardiovascular disorders including congestive heart failure. The aim of this paper is to review the uses of L-Carnitine in cardiology.
Conclusion: Chronic heart diseases remain an important cause of morbidity and mortality in Iraq and many other countries in the world suggesting a need for advancing their medical therapy, possibly through emphasis on impairment in substrate metabolism and heart energy and substrate utilization which contribute to contractile dysfunction, and not expected to improve with traditional therapies. Fat is the most important energy source for heart muscle , and carnitine is vital for normal fatty acid beta-oxidation, and inadequate carnitine can cause cardiac dysfunction.
There is convincing evidence from experimental and clinical research that L-Carnitine has a beneficial effect when used in the treatment of a variety of heart diseases including congestive heart failure, myocardial infarction, and angina. The effect of L-Carnitine can be attributed to cardio-protective effects against ischemia and increasing the rate of fatty acid transport into mitochondria. It can improve exercise tolerance and oxygen consumption leading to symptomatic improvement and mortality reduction. As an anti-anginal agent, it can reduce ST segment depression and left ventricular end-diastolic pressure. L-Carnitine can also improve myocardial ischemia by relieving inhibition of mitochondrial adenine nucleotide translocase.
L-carnitine is a non-protein amino acid synthesized from the essential amino acids lysine and methionine or obtained from dietary sources. There are two main natural forms of L-carnitine, Acetyl-L-carnitine and propionyl-L-carnitine. Physiological roles of L-carnitine include [1-12]:
1-L-carnitine has an important role in fatty acid metabolism as it is an essential cofactor of carnitine palmitoyltransferanse 1 (CPT1), which allows fatty acid transport into mitochondria and the incorporation of long chain fatty acids into the β-oxidation cycle to obtain acetyl-CoA.
2-L-carnitine has an important role in glucose metabolism through as modulates the intra-mitochondrial acetyl-CoA/CoA ratio and the pyruvate dehydrogenase complex (PDH).
3-L-carnitine reduces the accumulation of the intermediate products of β-oxidation by increasing the efflux of acyl and acetyl groups (acyl-carnitines and acetyl-carnitine) out of cells into the plasma.
Failure of this physiologic role with the accumulation of β-oxidation intermediates may contribute to the development of insulin resistance in heart and skeletal muscle and of heart failure and ischemia.
Therefore, L-carnitine supplementation may have beneficial effects in the treatment of insulin resistance and cardiovascular diseases, by restoring tissue carnitine of skeletal muscle and myocardium.
4-L-carnitine helps cardiomyocytes in meeting their absolute need for ATP, and thus preserving the pulsatile cardiac function, and help in maintaining cell and tissue viability.
As early as 1960s, experimental evidence from animal study on guinea pigs suggested abnormal metabolism of long chain fatty acids in heart failure associated with chronic constriction of the ascending aorta. Theses abnormalities were attributed to reduction in the level of myocardial carnitine which controls the oxidation rate of long chain fatty acids, a decrease in palmitic acid oxidation, and increased rate of palmitate incorporation into triglycerides and lecithin. Wittels and Spann (1968) exogenous carnitine can restore defective palmitate metabolism [1].
Morand et al (1979) reported the occurrence of lipidic myopathy diagnosed by muscle biopsy and associated with severe cardiomyopathy caused by a generalized carnitine deficiency in a girl who presented initially with nausea, vomiting and intermittent hypoglycemia. At the age of five years, the girl developed generalized muscular weakness with severe amyotrophy, and cardiomegaly. Thereafter, she developed severe heart failure. Treatment with carnitine chlorhydrate and a diet low in lipids and high in medium chain triglycerides was associated with rapid improvement in myopathy and heart failure [2].
Early during the 1980s, the occurrence of myocardial carnitine deficiency in chronic heart failure has been emphasized, and the possibility of using carnitine in heart failure has been suggested. A role in the prevention of arrhythmias in acute myocardial infarct has also been suggested (Lanni et al, 1980; Suzuki et al, 1982) [3, 4, 5].
Experimental evidence from animal study on hamster, suggested that cardiomyopathy associated with congestive heart failure resulting from carnitine deficiency (York and colleagues, 1983) [6].
Ramos et al (1983) reported a protective effect of carnitine in patients with diphtheric myocarditis in a controlled study which included 132 diphtheric patients, 73 patients of them were treated with DL-carnitine, 100 mg/kg/day during 4 days after hospitalization. Treatment reduced the incidence of heart failure (P = 0.0475), of pacemaker implants (P = 0.0256), and of lethality indexes due to myocarditis (P = 0.013) [7].
Experimental evidence from animal study on turkeys with spontaneous cardiomyopathy and turkeys with furazolidone-induced cardiomyopathy associated with heart failure suggested that liver synthesis of carnitine increases in response to hypotension to promote beta-oxidation of fatty acids as a cardiac energy source (Pierpont et al, 1985) [8].
Ghidini et al (1985) reported a controlled study which included 38 patients (22 men, 16 women) with heart failure, secondary to ischemic and/or hypertensive heart disease. Their age raged from 65 to 82 years. Treatment included digitalis, diuretics, and antiarrhythmic agents). 21 patients received also oral L-carnitine 1-g doses twice daily for 45 days, while 17 received placebo. L-carnitine treatment resulted in a distinct improvement with reduced heart rate, edema and dyspnea, and increased diuresis and a marked reduction in daily digitalis requirement. L-carnitine treatment was also associated with a significant lowering of cholesterol and triglyceride levels, and was not associated with adverse effects in any patient [9].
A double-blind clinical study reported the treatment of 115 patients with septic, cardiac and traumatic shock, with bolus intravenous dose of acetyl-L-carnitine followed by infusion for 12 hours. Treatment was associated with improvement in blood oxygenation and significant reduction in heart rate and right atrial pressure in patients cardiogenic shock. In patients with septic shock, treatment increased systolic and mean arterial pressures (Gasparett et al, 1991) [10].
Kobayashi and colleagues (1992) treated patients with ischemic heart disease with oral L-carnitine for 12 weeks. Treatment was associated with significant improvement in exercise tolerance of patients with effort angina. Of 9 treated patients with chronic congestive heart failure, 5 patients (55%) moved to a lower NYHA class and the overall condition was improved in 6 patients (66%) [11].
Fernandez and Proto (1992) reported that treatment of patient with chronic myocardial ischemia with 2 g daily of L-carnitine during 1 year was associated with lowering of rate of anginal pains, reducing the requirement of nitrates, and also improvement of physical performance [12].
Bartels (1992) emphasized the importance of myocardial carnitine content in controlling myocardial oxidative metabolism and energy transfer. They used L-propionylcarnitine, a potent analogue of L-carnitine in attempt to improve heart function through a possible positive inotropic effect in 32 fasting normotensive patients with coronary artery disease. They treated sixteen patients with L-propionylcarnitine (15 mg/kg), while sixteen control patients received a vehicle mannitol/acetate, infused over five minutes.
In the control group, heart contractility was reduced by 5% with a significant 11% reduction in stroke volume. While patients treated L-propionylcarnitine didn’t experience change in isovolumetric contractility indices, but the peak ejection and filling rates improved by 16% at 45 minutes. In addition, the cardiac output in the treated patients increased by 8%. However, treatment had no effect systemic or coronary hemodynamics and myocardial oxygen consumption, but lactate uptake increased by 42%. [13]
Mancini et al (1992) reported a controlled study which included 60 patients (48 and 73 years) with mild to moderate (II and III NYHA class) congestive heart failure whom were treated with digitalis and diuretics for at least three months, but remained symptomatic. Thirty patients were additionally treated with oral mg of propionyl-L-carnitine, three times a day for 180 days. After one month, treatment was associated with significant increases in the maximum exercise and ventricular ejection fraction. Accordingly, Mancini et al thought that propionyl-L-carnitine has undoubted therapeutic benefit in patients with congestive heart failure, and it can be efficaciously added to the standard therapy [14].
Pucciarelli et al (1992) reported a controlled study which included 50 patients (48-69 years) with mild-moderate congestive heart failure and were treated with digitalis and diuretic. 25 patients were treated with oral propionyl-L-carnitine 2 g in two divided doses. Treatment increased maximum exercise time on the treadmill increased 11.1
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