2014


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2014/№1

Role of trimetazidine in optimization of therapy for acute coronary syndrome with respect to the effect on endothelial dysfunction and systemic inflammation

Davydov S. I., Titova V. V., Gordeeva M. A., Tarasov A. A., Babaeva A. R.

Keywords: dysfunction of endothelium, ACS, systemic inflammation, trimetazidine

DOI: 10.18087/rhj.2014.1.1802

Background. At the present time, the ongoing search for drugs is focused on the drugs that can suppress activities of proinflammatory cytokines and improve the endothelial function to prevent formation of thrombus in acute coronary syndrome (ACS). Evidence is available that trimetazidine inhibits LV remodeling by restricting oxidative stress, apoptosis and inflammation and also by influencing the expression of endothelial nitric oxide synthase. However, the effect of trimetazidine on inflammation and endothelial function in ACS is understudied. Aim. To study the effect of trimetazidine MB treatment on markers of endothelial dysfunction and systemic inflammation. Materials and methods. The study included 60 patients with ACS. All patients received a standard therapy for ACS. The patients were divided into two groups using the “envelope” method and based on the administered treatment. The main group additionally received trimetazidine МВ (drug Productal MB) 35 mg twice daily whereas the control group did not receive this drug. Standard laboratory and instrumental tests were performed for all patients. Serum levels of endothelin-1, von Willebrand factor, tumor necrosis factor-α (TNF-α), interleukin-1 (IL-1), and interleukin-6 (IL-6) were measured in all patients using the enzyme-linked immunosorbent assay (ELISA). Results. Different clinical variants of ACS were associated with significant increases in laboratory markers for endothelial dysfunction, including endothelin and von Willebrand factor. Blood levels of proinflammatory cytokines (TNF-α, IL-1, IL-6) were also significantly increased in relation to the severity of myocardial ischemia and injury. The addition of trimetazidine MB to the standard therapy for ACS improved outcomes of the treatment; manifestations of anginal syndrome were significantly less pronounced and the endothelial function was stabilized as indicated by the decreased level of von Willebrand factor and a greater decrease in endothelin than in the control group. The observed changes in proinflammatory cytokines (TNF-α, IL-1, and IL-6) induced by the combination therapy including trimetazidine MB, which were greater in ST elevation myocardial infarction, evidenced a beneficial effect of the drug on pathogenetic aspects of inflammation in patients with ACS. Conclusion. The combination of trimetazidine MB antianginal effect with its observed beneficial effect on endothelial function and mechanisms of systemic inflammation suggests that supplementation of standard therapy with this drug can be useful for improvement of therapy for ACS and prevention of repeated exacerbations of IHD.
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Davydov S. I., Titova V. V., Gordeeva M. A. et al. Role of trimetazidine in optimization of therapy for acute coronary syndrome with respect to the effect on endothelial dysfunction and systemic inflammation. Russian Heart Journal. 2014;75 (1):18–25

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