Why the study?
Does trimetazidine improve myocardial protection and clinical outcomes in patients with ischemic heart disease and heart failure?
Does trimetazidine improve myocardial protection and clinical outcomes in patients with ischemic heart disease and heart failure?
Trimetazidine provides comprehensive cytoprotection during ischemia-reperfusion by optimizing energy metabolism and reducing oxidative stress, translating to clinical benefits in angina, coronary interventions, and heart failure.
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May support trimetazidine in refractory angina or HF; leaves open confirmation by prospective RCTs before practice change.
The review presents, as the classical data on the mechanism of action of metabolic cytoprotector trimetazidine in acute ischemia/reperfusion injury associated with a partial inhibition of the oxidation of long chain fatty acids and increased metabolism of pyruvate, as well as new concepts of reducing the level of oxidative stress, reduction of cardiomyocyte apoptosis, elimination areas of myocardial stunning and hibernation state. Described cytoprotective effects associated with inhibition of activation of mitochondrial pore with transient (temporary) permeability. Presented clinical studies showing significant anti-anginal and anti-ischemic effect of the trimetazidine in patients with stable angina, to decrease myocardial damage in acute coronary syndrome, during intervention on the coronary arteries. Particular attention is given to the latest data on the positive effects of prolonged use of trimetazidine on the course and prognosis in patients with heart failure.
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Глезер et al. (2014) studied this question.
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