Clinical epidemiology of acute myocardial infarction

In the United States by mid-century, cardiovascular disease accounted for more than half of all deaths. In the second half of this century, 85% of reduction in age-adjusted mortality rates from all causes can be ascribed to the decline in death from cardiovascular disease and stroke. Approximately half of such dramatic decline in mortality rates from ischemic heart disease (IHD) can be explained by primary and secondary prevention and half by therapeutic improvements. Epidemiology of therapeutic regimens in acute myocardial infarction (AMI) indicates substantial increases in the use of thrombolytic therapy, aspirin, beta-blockers and, in some countries, coronary angioplasty. The long-term results of several thrombolytic trials have shown the persistence of early benefit until 10 years after AMI. However, approximately half of the patients with AMI are admitted to the hospital too late to fully benefit from thrombolytic therapy, and one fourth of eligible patients do not receive any form of reperfusion. Primary angioplasty is advocated by some as the treatment of choice in AMI. The present results are not convincing enough to induce the enormously complex and costly reorganization of the health system, allowing the immediate access to coronary angiography for all or most patients with AMI. However, stenting the infarct coronary artery at the site of previous occlusion appears to improve the immediate and medium-term results of coronary revascularization procedures. Approximately half of the AMI survivors are rehospitalized within 1 year after the index event, and postinfarction mortality rate remains exceedingly high. After AMI, prognostic and therapeutic procedures have been introduced in the absence of evidence from controlled trials of their effectiveness profile. Outcome research is needed to standardize effective post-AMI policies. Moreover, new strategies are needed to reduce the incidence and mortality rates of acute ischemic events. A number of new candidate risk factors for IHD are emerging; they are associated with endothelial dysfunction, thrombogenic state, and inflammatory state. It is hoped that advances in molecular approach to cardiovascular disease, molecular genetics and transgenic techniques will allow better understanding and more effective therapeutic strategies to prevent and control IHD.