Coenzyme Q10 in Heart Failure: Mechanisms and Therapeutic Potential

Heart failure (HF) is a progressive and debilitating condition characterized by the heart’s inability to meet the body’s metabolic demands, often due to impaired cardiac contractility and energy depletion. Mitochondrial dysfunction and oxidative stress are central to the pathophysiology of HF, leading to disrupted bioenergetics and exacerbating cardiac damage. Coenzyme Q10 (CoQ10), a key component of the mitochondrial electron transport chain, has garnered attention for its potential therapeutic role in HF due to its dual functions in adenosine triphosphate production and antioxidant defense. Clinical trials, notably the CoQ10 as adjunctive treatment of chronic HF focusing on changes in Symptoms, BIomarker status, and long-term Outcome (Q-SYMBIO) trial, have demonstrated that long-term CoQ10 supplementation significantly reduces cardiovascular and all-cause mortality in patients with chronic HF. Additionally, CoQ10 improves functional capacity and ejection fraction, with minimal side effects. Despite its promise, further large-scale trials are needed to confirm these findings and determine optimal dosing. CoQ10’s potential to modulate mitochondrial function and oxidative stress makes it a promising adjunctive therapy in the management of HF.