CHANGING PARADIGMS IN THROMBOLYSIS IN ACUTE MYOCARDIAL-INFARCTION

Acute myocardial infarction occurs when a ruptured coronary artery pla que causes sudden thrombotic occlusion of a coronary artery and cessat ion of coronary artery blood flow. This paper reviews the underlying c oronary pathology in progressive coronary atherosclerosis, mechanisms of plaque rupture and arterial occlusion and the time relationship bet ween coronary occlusion and myocardial necrosis. Reperfusion can be ac hieved by chemical thrombolysis with different thrombolytic agents. Ea rly lysis is achieved best by prehospital administration, a transtelep honic monitor, a mobile intensive care unit, active general practition er treatment or by warning the emergency room of impending arrival of a patient. Thrombolytic therapy may be unsuccessful and not achieve Gr ade III TIMI flow in less than 4 h (or even 2 h) due to inadequate or intermittent perfusion or reocclusion. Adjuvant therapy includes aspir in and platelet receptor antagonists. Bleeding is a constant danger. D irect percutaneous transluminal coronary angioplasty (PTCA) may be as effective or better than chemical thrombolysis. Reperfusion protects t he myocardium and salvages viable tissue. It also improves mechanical remodelling of the ventricle. Long-term follow-up has shown that quant um leaps of fresh coronary occlusion causes step-wise progression in p atient disability and that further early, prompt reperfusion can salva ge myocardium and prevent this inexorable progress of the disease. (C) 1997 Elsevier Science Ireland Ltd.