[Physiopathologic basis of the use of thrombolytic agents during the acute phase of myocardial infarction].

Experimental animal studies have shown that coronary occlusion is followed by myocardial infarction and that coronary reperfusion can limit infarction size. Myocardial necrosis and the recovery of function are progressive phenomena in these animal models. Similarly, human myocardial infarction is caused by coronary occlusion and the size and severity of the infarct can be reduced by spontaneous or therapeutic coronary reperfusion. However, there are important differences between the animal models and clinical myocardial infarction. The results of randomised therapeutic trials of thrombolytic drugs show that the theoretical equation between reperfusion, myocardial protection and reduction of mortality has not yet been fully validated. This may be explained either by the fact that the intermediary criteria of assessment (patency at 90 minutes and ejection fraction at the 3rd week) have been badly chosen or by the fact that some of the therapeutic benefit of thrombolytics on mortality is not due to reperfusion or myocardial protection. The physiopathological rationale behind the use of thrombolytics in the acute phase of myocardial infarction is coronary reperfusion, but is reperfusion beneficial in all myocardial infarcts? What is or are the intermediary factors between reperfusion and the decrease in mortality? Is reperfusion the only benefit of thrombolysis? Clear answers to these questions are not yet available.