Plasmic hemostasis and some biochemical indices in trimetasidine treatment in patients with chronic heart failure

Aim. The study of trimetasidine effects on plasmic hemostasis and blood biochemistry in patients with chronic heart failure (CCF) of NYHA functional class II-III. Materials and methods. The study enrolled 30 patients (24 mates and 6 females) aged 40-72 years with class II-III CCF, postinfarction cardiosclerosis and ejection fraction under 40%. Previously the patients received perindopril (the inhibitor of angiotensin converting enzyme) in daily close 2-4 mg, on-demand digoxin and diuretics. Trimetasidine,vas given in a daily dose 60 mg for 6 months. Before and after the treatment the patients' blood was examined for: levels of factors VII and X of antithrombin III coagulation, soluble fibrinomonomeric complexes (SFMC), fibrinogen, glucose, uric acid creatinines, total cholesterol, high density lipoprotein, triglycerides, AST, ALT, LDH, acid phosphotase, gamma-GT, sodium, potassium, activated partial thrombin time. Results. Initially, the patients had a 23.9% increase in the levels of factors VII and X, a 14.3% decrease of antithrombin III, 29.8 and 227.6% rise in concentrations of fibrinogen and SFMC respectively, compared to controls. After treatment values of fibrinogen, factors VII and X, SFMC fell by, 21.1, 17 and 35.5%, respectively. The thrombin time arose by 17.9% (p > 0.05). Insignificant inhibition was registered in the activity of acid phosphotase and gamma-GT. Glucose, AST, ALT, LDH levels remained unchanged. Plasma creatinine tended to lowering. Total cholesterol insignificantly increased at high levels of HDL cholesterol (p > 0.05) and reduced levels of triglycerides (p > 0.05). Conclusions, Trimetasidine therapy, given after conventional treatment with diuretics, digoxin, inhibitor of angiotensin-converting enzyme, aspirin has a beneficial effect in patients with circulatory deficiency through improving hemostatic and biochemical parameters.

Tereschenko S.N. , Drozdov V.N. , Levchuk N.N. , Demidova I.V.
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chronic cardiac failure; blood biochemistry; hemostasis; treatment; trimetazidine
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