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In addition to increasing the rate of fatty acid transport into mitochondria, levocarnitine reduces the intramitochondrial ratio of acetyl\u2010CoA to free CoA, thus stimulating the activity of pyruvate dehydrogenase and increasing the oxidation of pyruvate. Supplementation of the myocardium with levocarnitine results in an increased tissue carnitine content, a prevention of the loss of high\u2010energy phosphate stores, ischemic injury, and improved heart recovery on reperfusion. Clinically, levocarnitine has been shown to have anti\u2010ischemic properties. In small short\u2010term studies, levocarnitine acts as an antianginal agent that reduces ST segment depression and left ventricular end\u2010diastolic pressure. These short\u2010term studies also show that levocarnitine releases the lactate of coronary artery disease patients subjected to either exercise testing or atrial pacing. These cardioprotective effects have been confirmed during aortocoronary bypass grafting and acute myocardial infarction. In a randomized multicenter trial performed on 472 patients, levocarnitine treatment (9 g\/day by intravenous infusion for 5 initial days and 6 g\/day orally for the next 12 months), when initiated early after acute myocardial infarction, attenuated left ventricular dilatation and prevented ventricular remodeling. In treated patients, there was a trend towards a reduction in the combined incidence of death and CHF after discharge. Levocarnitine could improve ischemia and reperfusion by (1) preventing the accumulation of long\u2010chain acyl\u2010CoA, which facilitates the production of free radicals by damaged mitochondria; (2) improving repair mechanisms for oxidative\u2010induced damage to membrane phospholipids; (3) inhibiting malignancy arrhythmias because of accumulation within the myocardium of long\u2010chain acyl\u2010CoA; and (4) reducing the ischemia\u2010induced apoptosis and the consequent remodeling of the left ventricle. Propionyl\u2010l\u2010carnitine is a carnitine derivative that has a high affinity for muscular carnitine transferase, and it increases cellular carnitine content, thereby allowing free fatty acid transport into the mitochondria. Moreover, propionyl\u2010l\u2010carnitine stimulates a better efficiency of the Krebs cycle during hypoxia by providing it with a very easily usable substrate, propionate, which is rapidly transformed into succinate without energy consumption (anaplerotic pathway). Alone, propionate cannot be administered to patients in view of its toxicity. The results of phase\u20102 studies in chronic heart failure patients showed that long\u2010term oral treatment with propionyl\u2010l\u2010carnitine improves maximum exercise duration and maximum oxygen consumption over placebo and indicated a specific propionyl\u2010l\u2010carnitine effect on peripheral muscle metabolism. A multicenter trial on 537 patients showed that propionyl\u2010l\u2010carnitine improves exercise capacity in patients with heart failure, but preserved cardiac function.\n                  <\/jats:p>","DOI":"10.1196\/annals.1320.007","type":"journal-article","created":{"date-parts":[[2004,12,8]],"date-time":"2004-12-08T18:33:28Z","timestamp":1102530808000},"page":"79-91","source":"Crossref","is-referenced-by-count":191,"title":["Therapeutic Effects of l\u2010Carnitine and Propionyl\u2010l\u2010carnitine on Cardiovascular Diseases: A Review"],"prefix":"10.1111","volume":"1033","author":[{"given":"ROBERTO","family":"FERRARI","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"E","family":"MERLI","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"G","family":"CICCHITELLI","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"D","family":"MELE","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"A","family":"FUCILI","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"C","family":"CECONI","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2009,7,8]]},"reference":[{"key":"e_1_2_7_2_2","first-page":"134","article-title":"Primary and secondary disorders of carnitine metabolism","volume":"5","author":"Vivo D.C.","year":"1990","journal-title":"Int. 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