[Ischemic syndrome: reperfusion and myocardial cytoprotection]

With regard to the concept of reperfusion injury, there is no doubt that the benefit of reperfusion can cause serious arrhythmias, mechanical stunning, myovascular damage, new necrosis, or as some people consider more likely, apotosis. Advances in cell biology of cardiomyocytes have been remarkable in recent years. However, it is still impossible to monitor all the events that occur in these cells, especially in relation to their function and dysfunction. Our understanding of cellular dysfunction would be enhanced if different types of morphological changes could be related to specific metabolic and functional disorders of the cells. The most important of these changes are those leading to cell necrosis. In terms of therapy, it is essential to identify and prevent the progression of these lethal processes. The concepts of modern interventional cardiology have shown that steps such as thrombolysis, primary angioplasty, relief of coronary spasm-calcium antagonists and drugs such as trimetazidine (myocardial protection) are all important to promote coronary flow and to improve tissue metabolism. The pre-treatment and treatment with trimetazidine during the experimental period is almost totally able to prevent ischemic contracture. The mode of action is metabolic. The site of action is not clear. There is a very interesting trial called EMIP, presently under way in Europe, on the use of trimetazine in early thrombolysis that may help to show that this drug could prevent reperfusion injury. The results have not yet been disclosed.