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J Pieczul-Mróz

Publications and source records attributed to J Pieczul-Mróz.

At least 19 recordsLinked to original sources

Etofibrate decreases factor VII and fibrinogen levels in patients with polymetabolic syndrome.

Etofibrate is a hypolipemic drug belonging to the fibrate class. By improving the lipid profile, these drugs often exert a favorable influence on hemostatic risk factors of ischemic heart disease. We present a pilot study on the influence of etofibrate on lipids and lipoproteins in serum, as well as on factor VII and fibrinogen. The study group was comprised of 18 males, aged 52.5 +/- 7.3 years, with hypertriglyceridemia or mixed hyperlipoproteinemia and other risk factors of atherosclerosis, particularly insulin-dependent diabetes and arterial hypertension. The group was further divided into two subgroups depending on the coexistence of arterial hypertension. All patients received etofibrate 500 mg daily for 3 months. In comparison with initial values, a decrease in the following was noted for the whole study group: triglyceride level (226.0 +/- 27.1 vs. 288.0 +/- 51.9 mg/dl; p < 0.05), percent LDL-cholesterol (72.4 +/- 1.8 vs. 75.8 +/- 1.7; p < 0.05), apolipoprotein B (111.2 +/- 4.6 vs. 115.3 +/- 5.4 mg/dl; p < 0.05), atherogenic indices: LDL/HDL (5.06 +/- 0.58 vs. 5.95 +/- 0.50; p < 0.02) and apolipoprotein B and A (apoB/apoA) (0.92 +/- 0.04 vs. 1.02 +/- 0.06; p < 0.05). There was an increase in percent HDL-cholesterol (14.7 +/- 1.1 vs. 12.8 +/- 0.7; p < 0.05) and apoA (121.0 +/- 4.8 vs. 111.2 +/- 2.4 mg/dl; p < 0.05). A marked decrease in the level of factor VII (FVIIc) (114 +/- 5.9 vs. 136 +/- 5.3%; p < 0.001) and fibrinogen (2.95 +/- 0.17 vs. 3.58 +/- 0.17 g/l; p < 0.01) was found. Fibrinogen levels fell notably (3.09 +/- 0.30 vs. 3.87 +/- 0.34 g/l; p < 0.05) in the subgroup with arterial hypertension, and F1 + 2 markers tended to decline (2.32 +/- 0.53 vs. 2.74 +/- 0.37 nmol/l; NS). Patients with normals arterial pressure maintained their fibrinogen levels (3.23 +/- 0.24 vs. 3.36 +/- 0.26 g/l; NS). A positive correlation between FVIIc and F1 + 2 was observed during treatment. All results were expressed as arithmetic means +/- SE. The present study has demonstrated that etofibrate has hypolipemic, antithrombotic and antiatherosclerotic properties in patients with polymetabolic syndrome.

Arteriosclerosis↗

[Evaluation of platelet function and tissue plasminogen activator activity in ischemic heart disease depending on concurrence with hyperlipoproteinemia and aspirin therapy].

Platelet activation, impairment of fibrinolysis and dyslipidemia are important factors in the pathogenesis and progression of ischemic heart disease. Aspirin therapy will reduce platelet activation both by its negative effect on platelet aggregation (SPA) and by inhibition of granule release which liberates such mediators as platelet factor 4 (PF4) and plasminogen activator inhibitor 1 (PAI-1). The present study was performed in 57 patients with ischemic heart disease (IHD), divided into groups depending on coexistent hyperlipoproteinemia (HLP) and aspirin treatment. The control group included 21 healthy individuals, matched for age and sex. Parameters of hemostasis (SPA, PF4, PAI-1) and concentration of lipid fractions (TC, TG, LDL, HDL) were measured in plasma. Increased PF4 levels were found in all groups with IHD, irrespective of hyperlipoproteinemia or aspirin treatment. Enhanced SPA and higher PAI-1 were limited to group IHD-HLP without aspirin. Highest PAI-1 activities were observed after stimulation of platelets in vitro. In conclusion, patients with IHD and hyperlipoproteinemia presented most pronounced platelet activation and impairment of fibrinolysis. Aspirin had a beneficial effect on these changes. Lower activities of PAI-1, in patients treated with aspirin, can be ascribed to its reduced release from platelets. Aspirin did not satisfactorily reduce the level of PF4, although it strongly inhibited SPA.

Adult↗

[Heparin increases platelet aggregation and inhibits fibrinolysis, especially in primary hypertriglyceridemia and after myocardial infarction].

The authors presented the effect of unfractionated heparin on platelet aggregation and fibrinolysis. The studies have been performed in the control group and with primary hypertriglyceridemia as well as in patients after myocardial infarction. Adrenaline and ADP induced platelet aggregation was examined in plasma rich platelets; fibrinolysis was estimated in euglobulin test. These parameters have been determined before and after (10, 20, 60, 240, 360 min.) intravenous injection of 50 units heparin per kg body weight. We have observed, that heparin increased also platelet aggregation and inhibited fibrinolytic activity in persons with primary hypertriglyceridemia particularly and after myocardial infarction. Correlation was found between investigated parameters and products of heparin lipolytic activity, especially with level of free fatty acids.

Adult↗