The Effect of coenzyme Q10 on morbidity and mortality in chronic heart failure. Results from Q-SYMBIO: a randomized double-blind trial

Abstract

Chronic heart failure (CHF) is a common, costly, disabling, and potentially fatal condition that affects around two per cent of the adult population in developed countries [1]. CHF is when the heart fails to supply organs and tissues with oxygen and nutrients. The heart’s inability to contract with sufficient force to circulate blood returning from the body and lungs to the heart leads to fluid retention caused by leaky blood vessels. Subsequent symptoms include shortness of breath, weakness, fatigue, and chest pain. Around half of those who develop CHF die within five years of their diagnosis. Heart failure has multiple causes, and treatment strategies may include lifestyle modifications, heart transplant, and medication. Standard CHF treatment aims at blocking, rather than enhancing, cellular processes. This may cause dysfunction of bioenergetics, leading to energy starvation of the cardiac muscle [2,3]. In recent years, scientists have become increasingly aware of the role of coenzyme Q10 (CoQ10) as an essential cofactor for energy production and also a powerful antioxidant. A low level of myocardial CoQ10 is related to the severity of CHF [4]. Previous randomized controlled trials of CoQ10 in CHF, however, have been underpowered to address major clinical endpoints. In Q-Symbio, 420 patients with moderate to severe HF were randomly assigned to 100 mg CoQ10 three times daily or placebo in a 2-year prospective trial, as add-on therapy to their standard therapy. Primary short-term endpoints at 16 weeks included changes in NYHA functional classification, six-minute walk test, and levels of NT-pro BNP. Primary long-term endpoint at two years was occurrence of MACE (Major Adverse Cardiovascular Events). [...].