Coenzyme Q10 in patients undergoing CABG: Effect of statins and nutritional supplementation.

BACKGROUND: The hydroxymethylglutaryl coenzyme A reductase inhibitors (statins) are effective cholesterol lowering medications, however, statins may interfere with CoQ(10) biosynthesis. We examined the effect of statin therapy as well as nutritional supplements on plasma, cardiac and skeletal muscle concentrations of CoQ(10). METHODS: Forty patients with left ventricular dysfunction had fasting blood samples collected at baseline and following four weeks of supplementation (150mg/day of CoQ(10)). Cardiac and skeletal muscle biopsies were collected at the time of surgery and frozen in liquid nitrogen until analyzed for CoQ(10) levels by high performance liquid chromatography. RESULTS: Nutrient supplementation significantly increased plasma [(1.8 (1.2, 2.7) vs 0.8 (0.6, 0.94) mug/ml plasma, median+IQR; p=0.001)] and cardiac tissue concentrations of CoQ(10) [(120.5 (76.5, 177.1) vs 87.3 (60.5, 110.8) nmol/g wet weight, p=0.04)]. No effect of supplementation was seen on samples of skeletal muscle from the chest wall. Statin therapy was not found to influence plasma, cardiac or chest wall levels of CoQ(10). CONCLUSION: Nutrient supplementation significantly increased plasma and cardiac tissue levels of CoQ(10) but did not influence chest wall muscle concentrations. Statin therapy did not significantly influence tissue concentrations of CoQ(10). Longer term studies are needed to confirm this observation.

Effect of NaHCO3 on cardiac energy metabolism and contractile function during hypoxemia.

OBJECTIVE: To examine the impact of administration of NaHCO3 on contractility and energy metabolism of the myocardium during hypoxemia. METHODS: Regional myocardial hypoxia was induced in the left anterior descending (LAD) artery myocardium in anesthetized, open-chest dogs, using a perfusion circuit between the right atrium and the LAD artery, and a membrane oxygenator. The rate of flow in LAD artery was maintained constant with the use of a roller pump. During hypoxia, eight dogs were administered isotonic NaHCO3 in the circuit and six other dogs received equimolar NaCl. Myocardial contractile function was assessed using sonomicrometry for measurement of percentage of systolic shortening and preload recruitable stroke work. Oxygen consumption and the rate of appearance of lactate were measured. Clamp-frozen tissue samples were obtained at the end of the experiment from the hypoxic LAD myocardium and the nonhypoxic circumflex myocardium for measurement of tissue lactate level. RESULTS: During hypoxia, there was a significant decrease in oxygen consumption by the LAD myocardium (35 +/- 7 micromol/min in the NaCl group and 40 +/- 7 micromol/min in the NaHCO3 group during hypoxia vs. 131 +/- 11 micromol/min during aerobic perfusion). There was also a significant decrease in myocardial contractility as measured by percentage of systolic shortening (14 +/- 3% to -8 +/- 3%); NaHCO3 infusion during hypoxia did not improve myocardial contractility (-7 +/- 2%). Similar results were obtained with measurements of preload recruitable stroke work. The rate of production of lactate during hypoxia was substantially lower than expected, based on the calculated oxygen deficit, and was not significantly increased by the administration of NaHCO3 (33 +/- 9 micromol/min in the NaCl group and 51 +/- 5 micromol/min in the NaHCO3 group). Tissue lactate was not statistically different in the hypoxic myocardium supplied by the LAD artery and the nonhypoxic myocardium supplied by the circumflex artery in either group. CONCLUSION: The response of the myocardium to hypoxia is to decrease its mechanical work and metabolic demand. The infusion of NaHCO3 did not enhance myocardial contractile function or flux in glycolysis during hypoxia. We speculate that this diminished mechanical work and metabolic demand may represent an adaptive response to preserve cellular integrity until oxygen delivery is restored.