Abstract
Despite our continued advances in the management of coronary artery disease, there have been no significant reductions in the morbidity or mortality related to end‐stage heart failure. The syndrome of heart failure represents a common endpoint for several disease processes, however, at the molecular level there are certain biochemical similarities common to all failing myocardium. Targeting these derangements with gene therapy represents a promising option in the treatment of heart failure. In this review, we will discuss the common biochemical changes that occur in the failing heart, novel therapeutic targets, including the β‐adrenergic receptor system and intracellular calcium regulation, and the vectors and transfer methodology responsible for delivering these transgenes to the myocardium.