The role of coenzyme Q10 in the pathophysiology and therapy of experimental congestive heart failure in the dog

Background: Coenzyme Q(10) (CoQ(10)) is essential for ATP generation and has antioxidant properties. Decreased CoQ(10) levels have been reported in human heart failure (CHF), but it remains unclear if this is a conserved feature of CHF. The objective of the study was to determine if tnchycardia-induced CHF in the dog is associated with reduced CoQ(10) levels. Furthermore, it was hypothesized that CoQ(10) supplementation may improve CHF severity by preventing CoQ(10) deficiency (if present) or via antioxidant effects. Methods and Results: Serum and myocardial levels of CoQ(10) were examined in normal dogs (n = 6), dogs with CHF (control, n = 5), and dogs with CHF treated with CoQ(10) (CoQ(10); 10 mg/kg/day, n = 5). Serum CoQ(10) levels did not change with CHF in control dogs, and myocardial levels were similar to those of normal dogs. CoQ(10) therapy increased serum but not myocardial levels of CoQ(10). In early CHF, CoQ(10)-treated dogs had lower filling pressures, and, in severe CHF, CoQ(10)-treated dogs had less hypertrophy as compared with untreated dogs. Other indices of CHF severity were similar in control and CoQ(10)-treated dogs. Conclusion: These data indicate that CoQ(10) deficiency is not present in this model of CHF. Although dramatic effects on hemodynamics were not observed, CoQ(10) supplementation did appear to attenuate the hypertrophic response associated with CHF.