الفهرس 
Role of Trimetazidine in the treatment of ischemic heart disease: Pharmacology of TrimetazidineOnly 14 pages are availabe for public view
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Abstract
It is well known that myocardial cell cannot survive under prolonged ischemia and coronary reperfusion appears to be the appropriate therapy (Leizorovicz et al., 1992). Unfortunately reperfusion may prevent or reduce the development of necrosis, but may determine the reperfusion damage (Amborosio et al., 1987).
The reperfusion damage which frequently occurs when early reperfusion is performed, are mainly related to Ca overload, high level of oxygen free radicals, inflammation and acidosis (Lagadic-Gossman et al., 1996).
Trimetazidine is a metabolic agent belongs to the piperazine group of compounds, which was proven to have anti-ischemic anti-anginal properties without any hemodynamic effect (Stanely, 2002 and Marzilli and Klein, 2003).
Trimetazidine improved post-ischemic recovery during reperfusion through its direct action on myocardial cell, it prevents intracellular ATP decrease (Allibardi et al., 1998), limits the intracellular acidosis (El Banani et al., 2000), corrects disturbances of transmembrane ion exchanges leading to Ca overload (Guarnieri et al., 1997), protects against induced toxicity of excessive production of oxygen free radicals (Maupoil et al., 1990), and inhibits neutrophil infiltration (Williams et al., 1993).
Clinical studies that evaluated the effectiveness of Trimetazidine in the setting of acute myocardial infarction has been reported that Trimetazidine improves segmental left ventricular function (Meneveau and Khalife, 1997),