[Results and limits of fibrin-unspecific thrombolysis in acute myocardial infarct].

Acute myocardial infarction is caused by thrombotic occlusion of a coronary vessel. Mortality and quality of life are both determined by the extent of infarction. It is possible to interrupt the development of necrosis by early fibrinolytic therapy. If reperfusion is initiated within three to six hours, a significant reduction in mortality is likely. Currently available fibrin-unspecific plasminogen activators such as streptokinase and urokinase are effective thrombolytic agents but do not fulfill all the criteria of an ideal plasminogen activator. Recanalisation rates are relatively low after intravenous administration, since the agents are not fibrin-specific and because the effect is delayed. Serious hemorrhagic complications may occur, since therapeutically effective dosage results in a hemostatic defect. The possible advantages of reduction in blood viscosity for collateral circulation in the ischemic region and a possible antithrombotic effect have not been defined. A complex strategy is necessary for optimal treatment of acute myocardial infarction. Early intervention is decisive in regard to recanalisation rate, infarct size, left ventricular function and mortality, while delayed interventions serve to maintain the advantages of early recanalisation by limiting angina pectoris and preventing reinfarction. Therefore, a combination of early intravenous administration of a fibrinolytic agent with subsequent invasive intervention appears reasonable and advantageous. Progress in the treatment of acute myocardial infarction will depend on development of effective plasminogen activators capable of achieving rapid and complete recanalisation without major side effects after intravenous administration.