Targeting mitochondrial dysfunction in the treatment of heart failure.

INTRODUCTION: Heart failure (HF) has reached epidemic proportions worldwide. Despite the availability of drugs that reduce mortality and afford good symptom relief, HF continues to exact a considerable clinical and economic burden. Current HF therapies elicit benefit by reducing cardiac workload by lowering heart rate and loading conditions, thereby reducing myocardial energy demands. Areas covered: Recent recognition that the failing heart is 'energy deprived' and its primary energy source, the mitochondria, is dysfunctional, has focused attention on mitochondria as a worthy therapeutic target. In HF, mitochondrial dysfunction leads to reduced adenosine triphosphate (ATP) synthesis and excessive formation of damaging reactive oxygen species (ROS), a combination the failing heart can ill afford. Expert commentary: Correcting mitochondrial dysfunction can help forge a new therapeutic approach based on readily available energy that can meet increasing cardiac demands. This paradigm shift, once implemented successfully, is likely to elicit better overall cardiac function, better quality of life, and improved survival for patients with HF.