Effects of trimetazidine on clinical symptoms and tolerance of exercise of patients with syndrome X: a preliminary study.

BACKGROUND: Trimetazidine diminishes angina and improves tolerance of exercise of patients with ischemic heart disease, and has no influence on blood pressure and heart rate. OBJECTIVE: To determine the effect of trimetazidine on angina symptoms and exercise tolerance in patients with syndrome X. METHODS: We investigated the effect of trimetazidine on the clinical symptoms and tolerance of exercise of 34 patients (20 women and 14 men, aged 32-60 years) with syndrome X (angina pectoris, positive result of exercise test, and normal coronary angiogram). The exercise test was performed before initiation of oral administration of trimetazidine therapy (20 mg three times a day) and 1 and 6 months thereafter. RESULTS: We obtained negative results of exercise treadmill tests for four patients (11.76%) after 1 month and five patients (14.71%) after 6 months of trimetazidine treatment. There was also a decrease in the incidence of effort angina after 6 months of treatment (26 patients or 76.47% before treatment versus 13 patients or 38.23% after 6 months of treatment). The drug had no significant influence on the heart rate and blood pressure. The duration for which patients could exercise was significantly prolonged by 1 month (652.9 +/- 206.2 versus 563.4 +/- 190.4 s, P = 0.0047) and 6 months (650.3 +/- 207.8 s, P = 0.0094) of treatment with trimetazidine. CONCLUSION: Treatment with trimetazidine decreases signs of angina during exercise and improves tolerance of exercise of patients with syndrome X.

The effects of dipyridamole stress test on plasma levels of soluble adhesion molecules intracellular adhesion molecule-1, vascular cell adhesion molecule-1, E-selectin and L-selectin in patients with ischemic heart disease and patients with syndrome X.

BACKGROUND: Adhesion of activated leukocytes to the endothelium as a result of myocardial ischemia/reperfusion has been shown to be involved in the development of tissue injury. Leukocyte adhesion to the endothelium occurs via adhesion molecules expressed on the surface of both cell types. Upon cell activation these proteins may be released into the circulation and measured in a soluble form. AIM: To verify whether the dipyridamole stress test, performed in patients with ischemic heart disease (IHD) and in patients with syndrome X, modifies plasma levels of the soluble adhesion molecules vascular cell adhesion molecule-1 (VCAM-1), intracellular adhesion molecule-1 (ICAM-1), E-selectin and L-selectin. METHODS: Plasma levels of the soluble endothelial adhesion molecules ICAM-1, VCAM-1 and E-selectin, as well as of the soluble leukocyte adhesion molecule L-selectin, were measured in venous blood samples taken before and 7 min after administration of dipyridamole in patients with IHD, patients with syndrome X and healthy individuals. Myocardial perfusion was evaluated using single photon emission tomography. The plasma levels of soluble VCAM-1, ICAM-1, E-selectin and L-selectin were all measured using enzyme-linked immunosorbent assays. RESULTS: After infusion of dipyridamole, plasma levels of ICAM-1 increased significantly in patients with IHD, whereas they remained unchanged in patients with syndrome X and in the control group. In patients with IHD, the initial plasma levels of VCAM-1, E-selectin and L-selectin, before administration of dipyridamole, were higher than those observed in patients with syndrome X and than those in the control group. Plasma levels of soluble VCAM-1, E-selectin and L-selectin decreased significantly in patients with IHD following the dipyridamole stress test, whereas they remained unchanged in patients with syndrome X, and in the control group. CONCLUSION: In patients with IHD, administration of dipyridamole induces myocardial ischemia resulting in modification of plasma levels of the soluble adhesion molecules.