Despite numerous evidence-based medical and device therapies for patient with heart failure (HF) and reduced ejection fraction (HFrEF), the outcomes of these patients remain poor. HF is an energy-depleted state associated with low myocardial adenosine triphosphate (ATP) production, mitochondria dysfunction, abnormal calcium handling, increased reactive oxygen species generation, and endothelial dysfunction. Many of the disease modifying therapies in chronic HF act by modulation of maladaptive neurohormonal pathways, such as the renin–angiotensin–aldosterone axis. Such therapies are limited by side effects, including hypotension leading to calls for new drugs with hemodynamically neutral profiles.1 Coenyzme Q10 (CoQ10) may represent a therapeutic option to treat individuals with HF. Preclinical data suggest that CoQ10 has a critical role in ATP production, a potent anti-inflammatory agent, and may improve endothelial function. Lower CoQ10 levels are seen in patients with advanced HF symptoms and with lower ejection fractions. A recent randomized controlled trial has suggested that there may be a mortality benefit in patients with HFrEF with CoQ10 supplementation. Furthermore, there does not seem to be an adverse hemodynamic profile or safety concern about CoQ10 use.2 This review summarizes the literature about the mechanisms, clinical data, and safety profile of CoQ10 supplementation in HF.
Mitochondria, Energy, and HF
Patients with chronic HF typically have a relapsing and remitting disease course, with periods of decompensation causing worsening symptoms, such as dyspnea and peripheral edema, resulting in increases in therapy or hospitalization.3 Furthermore, despite drug therapies that can reduce morbidity and mortality, the management of chronic symptoms such as fatigue and exercise intolerance remains challenging. One novel therapeutic avenue is to modulate cardiac energetics. Regardless of cause, it has been hypothesized that the failing heart is energy starved.4,5 HF is associated with abnormal calcium handling,6 ATP depletion,4 and mitochondria dysfunction7 within cardiomyocytes leading to a perturbation of the cardiac metabolic pathways.6 These alterations result in energy depletion and negatively affects on cardiac contractile function.6 Therapies that can prevent cardiac energy depletion may play a role in the treatment and management of HF.
Read more via: https://acrobat.adobe.com/id/urn:aaid:sc:US:4343f3bb-ba6c-479e-877a-dbe3cb030c42