To determine whether there is a correlation between fibrinolytic activity and dyslipidemia, we performed a study of 72 subjects (20 patients with hypercholesterolemia, 20 with hypertriglycerldemia, 12 with isolated low high-density lipoprotein (HDL)-cholesterol (mean age 47.7 +/- 6.3, body mass index 24.7 +/- 0.4) and 20 healthy controls. Plasminogen activator inhibitor-1 (PAI-1), tissue-plasminogen activator activity and plasmin-antiplasmin complexes (PAP) were detected at baseline and after venous occlusion test. We also measured at baseline lipidic pattern, soluble E and P selectins (sE-sel, sP-sel), prothrombin factor 1+2 (F1 + 2), lipoprotein(a), factor VII, plasma insulin, fibrinogen, homocysteine, and thrombin activable fibrinolysis inhibitor (TAFI) activity Fibrinolysis was significantly reduced In hypertriglyceriderritc patients compared with hypercholesterolemic patients and control subjects (PAP p 0<.01 and p <0.001) and was associated with increased PAI-1 (at baseline and after venous occlusion test, p <0.001). sP-sel, F1+2 and TAFI were not significantly different compared with controls, while hypercholesterolemic subjects showed a significant increase in these parameters (p <0.001), which were related to decreased PAP only at the upper low-density lipoprotein (LDL)-cholesterol levels (> 160 mg/dl) (p <0.007, r = -0.76). Moreover there was no significant difference in PAI-1 activity (at baseline and after venous occlusion test) compared with controls. In conclusion, endothelial dysfunction was the main mechanism of decreased fibrinolysis in subjects with hypertriglyceridemia and low HDL-cholesterol, while enhanced thrombin generation and TAF1 activity were the main determinants In hypercholesteridemia.

Puccetti, L., A. L., P., Pastorelli, M., G., B., M., C., A., P., et al. (2001). Different mechanisms of fibrinolysis impairment among dyslipidemic subjects. INTERNATIONAL JOURNAL OF CLINICAL PHARMACOLOGY RESEARCH, 21, 147-155.

Different mechanisms of fibrinolysis impairment among dyslipidemic subjects

PUCCETTI, LUCA;PASTORELLI, MARCELLO;BRUNI, FULVIO
2001

Abstract

To determine whether there is a correlation between fibrinolytic activity and dyslipidemia, we performed a study of 72 subjects (20 patients with hypercholesterolemia, 20 with hypertriglycerldemia, 12 with isolated low high-density lipoprotein (HDL)-cholesterol (mean age 47.7 +/- 6.3, body mass index 24.7 +/- 0.4) and 20 healthy controls. Plasminogen activator inhibitor-1 (PAI-1), tissue-plasminogen activator activity and plasmin-antiplasmin complexes (PAP) were detected at baseline and after venous occlusion test. We also measured at baseline lipidic pattern, soluble E and P selectins (sE-sel, sP-sel), prothrombin factor 1+2 (F1 + 2), lipoprotein(a), factor VII, plasma insulin, fibrinogen, homocysteine, and thrombin activable fibrinolysis inhibitor (TAFI) activity Fibrinolysis was significantly reduced In hypertriglyceriderritc patients compared with hypercholesterolemic patients and control subjects (PAP p 0<.01 and p <0.001) and was associated with increased PAI-1 (at baseline and after venous occlusion test, p <0.001). sP-sel, F1+2 and TAFI were not significantly different compared with controls, while hypercholesterolemic subjects showed a significant increase in these parameters (p <0.001), which were related to decreased PAP only at the upper low-density lipoprotein (LDL)-cholesterol levels (> 160 mg/dl) (p <0.007, r = -0.76). Moreover there was no significant difference in PAI-1 activity (at baseline and after venous occlusion test) compared with controls. In conclusion, endothelial dysfunction was the main mechanism of decreased fibrinolysis in subjects with hypertriglyceridemia and low HDL-cholesterol, while enhanced thrombin generation and TAF1 activity were the main determinants In hypercholesteridemia.
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Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/11365/43944
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