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May guide future cardioprotective therapies in ACS; leaves open clinical translation of these pathways.
Acute coronary syndromes and heart failure arising as a consequence of ischemic injury to the myocardium account for a large proportion of all hospital admissions and of all causes of death in industrialized nations. Medical and surgical management of these conditions consumes enormous resources each year, but current therapeutic measures fall far short of reducing death and disability from ischemic heart disease to acceptable levels. Several recently successful advances in therapy of acute coronary syndromes are based on limiting the extent of myocardial damage that ensues following occlusion of a major coronary artery by rapid restoration of blood flow. However, many patients are not suitable candidates for thrombolytic drugs or revascularization procedures, and these approaches often are applied too late to prevent irreversible damage to the myocardium. A greater understanding of the mechanisms of ischemic injury, and of endogenous defense mechanisms, could foster additional improvements in clinical care.
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Williams et al. (2000) studied this question.
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