Changing paradigms in thrombolysis in acute myocardial infarction

Mervyn S. Gotsman, Yoseph Rozenman, Dan Admon, Morris Mosseri, Chaim Lotan, Doron Zahger, A. Teddy Weiss

Research output: Contribution to journalArticlepeer-review

6 Scopus citations


Acute myocardial infarction occurs when a ruptured coronary artery plaque causes sudden thrombotic occlusion of a coronary artery and cessation of coronary artery blood flow. This paper reviews the underlying coronary pathology in progressive coronary atherosclerosis, mechanisms of plaque rupture and arterial occlusion and the time relationship between coronary occlusion and myocardial necrosis. Reperfusion can be achieved by chemical thrombolysis with different thrombolytic agents. Early lysis is achieved best by prehospital administration, a transtelephonic monitor, a mobile intensive care unit, active general practitioner treatment or by warning the emergency room of impending arrival of a patient. Thrombolytic therapy may be unsuccessful and not achieve Grade III TIMI flow in less than 4 h (or even 2 h) due to inadequate or intermittent perfusion or reocclusion. Adjuvant therapy includes aspirin and platelet receptor antagonists. Bleeding is a constant danger. Direct percutaneous transluminal coronary angioplasty (PTCA) may be as effective or better than chemical thrombolysis. Reperfusion protects the myocardium and salvages viable tissue. It also improves mechanical remodelling of the ventricle. Long-term follow-up has shown that quantum leaps of fresh coronary occlusion causes step-wise progression in patient disability and that further early, prompt reperfusion can salvage myocardium and prevent this inexorable progress of the disease.

Original languageEnglish
Pages (from-to)227-242
Number of pages16
JournalInternational Journal of Cardiology
Issue number3
StatePublished - 23 May 1997
Externally publishedYes


  • Acute myocardial infarction
  • Coronary pathology
  • Reperfusion
  • Thrombolysis
  • Thrombotic occlusion


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