Abstract

Heart failure is a complex clinical syndrome increasingly recognized as a state of myocardial energy starvation driven by mitochondrial dysfunction and reduced ATP production. While standard pharmacotherapy targets neurohormonal pathways, it often leaves the metabolic deficit of the failing heart unaddressed. This mini review examines the pathophysiological rationale of CoQ10 supplementation - a critical component of the mitochondrial electron transport chain and a potent antioxidant- and evaluates its clinical utility in HF management. Myocardial biopsies indicate that CoQ10 deficiency correlates with increased heart failure severity. Clinical evidence, anchored by the landmark Q- Symbio trial, demonstrates that long-term adjunctive CoQ10 therapy significantly reduces MACE and cardiovascular mortality compared to placebo. Furthermore, CoQ10 supplementation is associated with improved NYHA functional class, and potential recovery in left ventricular ejection fraction. Emerging research also suggests that CoQ10 levels influence the functionality of the anti-aging and cardioprotective protein Sirtuin1. This review notes that while CoQ10 demonstrates an excellent safety profile with no significant adverse events, data regarding its efficacy in HFpEF remain scarce and inconclusive. The supplementation of CoQ10 in addition to traditional pharmacotherapy is a scientifically sound, valuable adjunctive therapy, though further large-scale, rigorous trials are needed to standardize dosage and confirm benefits across all HF phenotypes.

Keywords:Coenzyme Q10; Heart failure; MACE; HFpEF; Ubiquinone; Ubiquinol

Abbreviations: ATP: Adenosine Triphosphate; CoQ10: Coenzyme Q10; CoQH2: Ubiquinol; HF: Heart failure; HFpEF: Heart Failure with Preserved Ejection Fraction; LDL: Low-density lipoprotein; MACE: Major Adverse Cardiovascular Events; NAD: Nicotinamide Adenine Dinucleotide; NYHA: New York Heart Association; Sirt1: Sirtuin 1; YLD: Years Lived with Disability