Abstract Chronic stable angina is the first manifestation of ischemic heart disease in one half of patients; in the United States, the annual incidence of angina in 213 of 1000 of the population is over 30 years of age. The morbidity associated with ischemic heart disease is considerable: each years millions of patients have an MI, or are hospitalised for unstable angina. In recent years less attention has been paid to chronic ischemic syndrome; a possible explanation is that most patients with angina, refractory to medical treatment, are referred for myocardial revascularization in order to improve symptoms and to prevent death and myocardial infarction. Unfortunately available data do not support this common belief. The current evidence allows us to conclude that percutaneous transluminal coronary angioplasty (PTCA) in chronic coronary artery disease does not reduce the rate of subsequent MI or mortality and that PTCA results in superior symptomatic relief of angina and improved exercise tolerance compared with medical therapy, but the difference narrows with time. Several mechanisms may be considered to explain the persistence of angina/ischemia after a revascularization procedure, including incomplete revascularization, graft/PTCA failure, and disease progression in native coronary arteries. Microvascular dysfunction may play a prominent role in the unexpected prevalence of angina after the removal of obstructions in the major coronary branches. A better understanding of the metabolism derangements associated with ischemia and reperfusion allowed the development of new pharmacological approaches. In contrast to classic "hemodynamic" agents, metabolic agents have no hemodynamic, inotropic or chronotropic effect and interfere with cardiac energy metabolism.
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