The aggressive treatment of acute myocardial infarction.

NOT SINCE Herrick's description of acute myocardial infarction (AMI) have so many options been available for the treatment of this condition. For decades management of AMI consisted of bed rest, oxygen, prevention of thromboembolic complications, and treatment of arrhythmias and heart failure. Despite the marked reduction of mortality consequent to primary arrhythmias, AMI remains the most common cause of in-hospital death in industrialized nations and both mortality rates and morbidity in survivors are unacceptably high. Recently, a number of aggressive therapies designed to reperfuse evolving infarction have been developed. While there is considerable dispute concerning the role that these newer modes of treatment should play in the management of AMI, there is general agreement on the following three basic principles and their corollaries: (1) Mortality of patients after AMI both early and late is influenced importantly by the degree of dysfunction of the left ventricle, which in turn is dependent on the size of the initial infarct and on the quantity of myocardium that becomes infarcted later.' Therefore, limiting the size of the initial infarct and prevention of subsequent infarction are important goals of efforts to improve patient survival. (2) The time interval between the onset of coronary occlusion and any intervention likely to be successful in limiting the size of the resultant infarct is brief, usually not more than about four hours, and often even shorter. Accordingly, any strategy designed to limit infarct size, if it is to be useful in a large fraction of patients with AMI, must be applied immediately upon the development of symptoms.' (3) After infarction some patients remain at high risk of experiencing additional coronary events. Therefore, efforts designed to identify high-risk pa-