Antioxidant treatment for heart failure: friend or foe

Increasing studies demonstrate a pivotal role for oxidant stress in the pathophysiology of heart failure (HF). Recent meta-analyses also reveal the potential pitfall of a mono-dimensional antioxidant approach. This review article summarizes the main biological pathways involved in oxidant stress and HF, the possible deleterious nature of certain antioxidant monotherapy and proposes potential antioxidant strategies necessary to challenge specific HF aetiology and progression.

Oxidant stress is well established in the aetiology of cardiovascular disease (CVD) and increasingly implicated in congestive heart failure (CHF). Human and animal models of CHF demonstrate enhanced reactive oxygen species (ROS) production, reduced antioxidant reserve and ROS-mediated cardiac injury. Similarly, various ‘antioxidant’ agents used in the treatment of CHF appear to confer cardio-protective benefits. In contrast, recent meta-analyses have suggested a deleterious effect of vitamin E in heart failure (HF), warranting reappraisal of ‘antioxidant’ use in this context.