BACKGROUND AND AIM: We evaluated the impact of triple nutrient supplementation (TNS: carnitine, taurine and coenzyme Q(10)) vs. carnitine alone (CARN) or placebo on survival, infarct size, cardiac function and metabolic gene expression using a model of myocardial infarction (MI) in rats. METHODS AND RESULTS: Male Wistar rats were randomized to three groups divided in two independent studies prior to ligation of the left anterior descending coronary artery (LAD): TNS vs. Placebo and TNS vs. CARN. Nutrient supplementation [L-carnitine (300 mg/day), coenzyme Q(10) (15 mg/kg body weight/day) and taurine (0.1M)] was administered daily for four weeks prior to and for 10 days after MI. At that time, cardiac function and infarct size were measured. Metabolic gene (mRNA) expression in the peri-infarct tissue of left ventricle from TNS, placebo or corresponding time-control rats (TNS or placebo without LAD ligation) was measured 10 days after MI. When compared to placebo, TNS significantly improved survival (60% vs. 34%, p<0.02), cardiac function, and reduced infarct size (30+/-7% vs. 42+/-9%, p<0.001). Although CARN improved survival like TNS (45% vs. 50%, not significant), it did not reduce infarct size (32+/-14% vs. 19+/-10%, p<0.05) or delay myocardial remodeling. In the placebo group, MI was associated with a significantly altered pattern of metabolic gene expression (glucose transporter 1, liver carnitine palmitoyl transferase 1, medium-chain acyl-CoA dehydrogenase; p<0.01 for all three) in the left ventricle peri-infarct tissue. In contrast, gene expression was normalized in the group receiving TNS. CONCLUSIONS: Our results support the potential cardioprotective impact of TNS during myocardial ischemia. In contrast to carnitine supplementation alone, TNS improved survival as well as cardiac function, gene expression and delayed remodeling.
BACKGROUND AND AIM: We evaluated the impact of triple nutrient supplementation (TNS: carnitine, taurine and coenzyme Q(10)) vs. carnitine alone (CARN) or placebo on survival, infarct size, cardiac function and metabolic gene expression using a model of myocardial infarction (MI) in rats. METHODS AND RESULTS: Male Wistar rats were randomized to three groups divided in two independent studies prior to ligation of the left anterior descending coronary artery (LAD): TNS vs. Placebo and TNS vs. CARN. Nutrient supplementation [L-carnitine (300 mg/day), coenzyme Q(10) (15 mg/kg body weight/day) and taurine (0.1M)] was administered daily for four weeks prior to and for 10 days after MI. At that time, cardiac function and infarct size were measured. Metabolic gene (mRNA) expression in the peri-infarct tissue of left ventricle from TNS, placebo or corresponding time-control rats (TNS or placebo without LAD ligation) was measured 10 days after MI. When compared to placebo, TNS significantly improved survival (60% vs. 34%, p<0.02), cardiac function, and reduced infarct size (30+/-7% vs. 42+/-9%, p<0.001). Although CARN improved survival like TNS (45% vs. 50%, not significant), it did not reduce infarct size (32+/-14% vs. 19+/-10%, p<0.05) or delay myocardial remodeling. In the placebo group, MI was associated with a significantly altered pattern of metabolic gene expression (glucose transporter 1, liver carnitine palmitoyl transferase 1, medium-chain acyl-CoA dehydrogenase; p<0.01 for all three) in the left ventricle peri-infarct tissue. In contrast, gene expression was normalized in the group receiving TNS. CONCLUSIONS: Our results support the potential cardioprotective impact of TNS during myocardial ischemia. In contrast to carnitine supplementation alone, TNS improved survival as well as cardiac function, gene expression and delayed remodeling.