Load Amount Of Trimetazidine's Influence On Endothelial Function In Patients With Chd And Hypertension

Objective: Coronary atherosclerotic heart disease refers to heart diseases caused by myocardial ischemia and hypoxia even necrosis due to coronary atherosclerosis which leads to lumen stenosis or obstruction, or (and) functional changes in coronary arteries. These diseases are collectively called coronary heart disease (CHD). They are also known as ischemic heart disease. With regard to the mechanism of this disease in recent years, most scholars support the "endothelial injury hypothesis," believing that the major risk factors for this disease will eventually damage arteries intima, while the formation of atherosclerotic lesions is the result of arterial reation to intima injury in the course of inflammation-fibrous hyperplasia. Hypertension is a major risk factor for coronary heart disease, and endothelial cell injury plays a very important role in the genesis and development of high blood pressure. Endothelial cell injury is the dynamic factor and the carrier of the " endothelia-high blood pressure-cardiovascular events" chain[9]. High blood pressure can stimulate secretion of vascular endothelial cells, leading to endothelial dysfunction. Therefore, in addition to anti-myocardial ischemia, the improvement of endothelial cell function through drugs has become an effective means of prevention and treatment of coronary heart disease. Besides, improving myocardial cell metabolism and myocardial ischemia, trimetazidine can also activate nitric oxide synthase indirectly therefore mediate vascular relaxing factor generation which means improvement of endothelial function. This study checked and measured endothelium-dependent vasodilation as well as plasma nitric oxide (NO) to investigate the influence of trimetazidine on endothelial function in patients with CHD and essential hypertension and guide clinical treatment.Methods: 60 patients with coronary artery disease associated with essential hypertension were enrolled in this study (39 male, 21 female, aged 41-71). None of them had history of diabetes mellitus or hyperlipidemia. Plasma NO levels and flow-mediated dilatation rates of change (FMD, that is, endothelium-dependent vasodilation) were detected on the third day of hospitalization. Then the enrolled patients were given trimetazidine hydrochloride tablets (Vasorel, Wan Shuang Li, made by the French pharmaceutical firm Servier) 60mg immediately. Plasma NO levels and FMD value were detected again after 2 hours. The results were collected and dealed with paired t test results.Results: The results of plasma NO level and FMD value were higher 2 hours after the load amount of trimetazidine treatment than before, and there was statistical significance.1 Plasma NO level after trimetazidine treatment was 49.33±9.84μmol/L, while the level of plasma NO level before treatment was 48.15±11.35μmol/L, P<0.05, which was statistically significant.2 The baseline of brachial artery diameter after trimetazidine treatment was 4.61±0.83 mm, FMD value (expressed as a percentage) after treatment was 12.77±9.168%; the baseline of brachial artery diameter before treatment was 4.60±0.82 mm, FMD value was 10.99±8.733%, P <0.05, which was statistically significant.Conclusion:1 Plasma NO level after load amount of trimetazidine treatment was significantly higher than that before trimetazidine treatment, indicating that trimetazidine has protective effects on endothelial cells2 Brachial artery FMD value after trimetazidine treatment was significantly higher than that before trimetazidine treatment, indicating that trimetazidine can improve endothelium-dependent vasodilation.3 No adverse reaction related to trimetazidine was found.