Open AccessThe mechanism of action of metabolic cytoprotector trimetazidine in acute ischemia-reperfusion injury
Author(s) -
М. Г. Глезер,
Глезер Мария Генриховна,
Е. И. Асташкин,
Асташкин Евгений Иванович,
M. V. Novikova,
Новикова Марина Вячеславовна
Publication year - 2014
Publication title -
cardiosomatika
Language(s) - English
Resource type - Journals
eISSN - 2658-5707
pISSN - 2221-7185
DOI - 10.26442/cs45079
Subject(s) - trimetazidine , medicine , ischemia , cardiology , reperfusion injury , oxidative stress , myocardial infarction , beta oxidation , pharmacology , metabolism
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.