Unbound MEDLINE

Different mechanisms of fibrinolysis impairment among dyslipidemic subjects. International journal of clinical pharmacology research [Int J Clin Pharmacol Res] Journal article

 
TitleDifferent mechanisms of fibrinolysis impairment among dyslipidemic subjects.
Author(s)Puccetti L, Pasqui AL, Pastorelli M, Bova G, Cercignani M, Palazzuoli A, Auteri A, Bruni F 
InstitutionInstitute of Medical Semeiotics, Center for Metabolic Diseases and Atherosclerosis, University of Siena, Italy. puccetti@unisi.it
SourceInt J Clin Pharmacol Res 2001; 21(3-4):147-55.
MeSHAdult
Analysis of Variance
Female
Fibrinolysis
Humans
Hypercholesterolemia
Hyperlipidemias
Hyperlipoproteinemias
Hypertriglyceridemia
Male
Middle Aged
Plasminogen Activator Inhibitor 1
Statistics, Nonparametric
AbstractTo determine whether there is a correlation between fibrinolytic activity and dyslipidemia, we performed a study of 72 subjects (20 patients with hypercholesterolemia, 20 with hypertriglyceridemia, 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 hypertriglyceridemic 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 < 0.001, 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 TAFI activity were the main determinants in hypercholesterolemia.
Languageeng
Pub Type(s)Comparative Study
Journal Article
Research Support, Non-U.S. Gov't
PubMed ID12067144
  
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