Abstract

More than 1.3 million percutaneous interventions (PCIs) and 400,000 coronary artery bypass graft procedures for cardiac revascularization are performed in the United States annually. Although restoring blood flow is the best method for reducing the extent of heart muscle damage after myocardial infarction (MI), reperfusion of ischemic myocardium itself can be injurious. Reperfusion-related complications after PCI for MI and coronary artery bypass grafting include myocardial stunning, the no-reflow phenomenon, reperfusion arrhythmias, and lethal cardiac ischemia-reperfusion (IR) injury, which results in irreversible injury and death of cardiomyocytes. Identified mechanisms that contribute to IR injury include adenosine triphosphate depletion, oxidative stress, inflammation, and intracellular calcium ion overload. At present, although multiple modalities targeting these and other IR injury mechanisms have been tested, effective, proved approaches are lacking, and the need to develop cardioprotective agents to reduce infarct size in patients with MI and prevent perioperative MIs in patients who undergo heart surgery remains unmet. Several pharmacotherapies that have shown promise in preclinical studies, such as MC-1, cariporide, and pexelizumab, have failed to live up to that promise in phase III clinical trials, highlighting the need for clinically relevant, disease-specific models for translating experimental data to efficacy in patients. The development of new pharmacologic agents also will depend on a better understanding of the underlying cellular and subcellular mechanisms of IR injury. This interactive program highlights novel investigational approaches to protection against IR injury.

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