Abstract
The review presents data on alterations of mitochondrial oxidative metabolism occuring due to heart failure, mechanisms of cytoprotective agent trimetazidine associated with a partial inhibition of the fatty acid oxidation and increased metabolism of pyruvate, reduction of cardiomyocyte apoptosis and oxidative stress are described. The results of clinical studies showing the effectiveness of trimetazidine therapy in ischemic heart decease are reported, as well as the latest data on the effects of prolonged use of trimetazidine on prognosis in patients with heart failure.
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