Coenzyme Q10 for heart failure and symptomatic cardiovascular diseases

Coenzyme Q10 (CoQ10, ubiquinone), embedded within the inner mitochondrial membrane, fulfills a dual physiological mandate as an essential electron shuttle in the oxidative phosphorylation cascade and an endogenous antioxidant.Heart failure (HF) and ischemic heart disease (IHD) are characterized by profound tissue CoQ10 depletion.Pivotal randomized controlled trials, including the landmark Q-SYMBIO study, in which 93% of participants had heart failure with reduced ejection fraction (HFrEF), have demonstrated that exogenous CoQ10 supplementation ameliorates functional capacity and significantly mitigates the risks of cardiovascular mortality and HF rehospitalization.Furthermore, CoQ10 confers robust anti-anginal and anti-ischemic cytoprotection in patients with coronary artery disease by preserving endothelial nitric oxide synthase coupling, suppressing lipid peroxidation, and augmenting ischemic preconditioning.3hydroxy-3-methylglutaryl-coenzyme A reductase inhibition suppresses mevalonate pathway downstream synthesis of CoQ10, occasionally precipitating statin-associated muscle symptoms or statin-induced cardiomyopathy-a rare yet severe metabolic complication readily reversible upon prompt CoQ10 repletion.Despite these benefits, substantial clinical knowledge gaps persist regarding the therapeutic efficacy of CoQ10 in microvascular angina and HF with preserved ejection fraction.This narrative review critically evaluates the biomechanical mechanisms of CoQ10 in cardiomyocyte contractility, synthesizes rigorous clinical trial evidence across HFrEF and IHD, examines statin-induced mitochondrial depletion, and delineates future translational directions for addressing unmet needs in cardiovascular medicine.