4.6 Article

Effects of lipids and lipid-lowering therapy on hemostatic factors in patients with myocardial infarction

Journal

JOURNAL OF THROMBOSIS AND HAEMOSTASIS
Volume 2, Issue 5, Pages 718-725

Publisher

WILEY
DOI: 10.1111/j.1538-7836.2004.00658.x

Keywords

coagulation; D-dimer; lipid-lowering therapy; PAI-1

Funding

  1. NHLBI NIH HHS [HL-48259, T-32 HL-07152, HL-30616] Funding Source: Medline

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Background: The risk of cardiovascular disease (CVD) is associated with specific hemostatic markers and lipid profiles, and evidence indicates that there are associations between lipid profiles and the levels of certain hemostatic factors. The disturbances in hemostasis and the risk of CVD can be ameliorated by lipid-lowering therapy. Objective: We investigated the associations of lipid profiles with factor (F)VIIa, von Willebrand factor (VWF), D-dimer and plasminogen activator inhibitor-1 (PAI-1), and examined whether lipid-lowering statin therapy would affect the levels of these hemostatic markers. Patients and methods: This cross-sectional study analyzed 1045 postmyocardial infarction patients. Results: In multivariate regression analyses (without adjusting for clinical covariates) HDL-cholesterol (HDL-C) and HDL size were independent and significant predictors of FVIIa; HDL size was a predictor of VWF; HDL size, HDL-C and LDL size were predictors Of D-dimer; and triglyceride and HDL size were predictors of PAI-1. After adjusting for clinical covariates, HDL-C, lipoprotein (Lp)(a), apolipoprotein B (apoB) and warfarin were independent and significant predictors of FVIIa; HDL size, age, diabetes mellitus, insulin, race and warfarin were predictors of VWF; HDL-C, HDL size, LDL size, age, warfarin, hypertension and gender were predictors of D-dimer; and triglyceride, HDL size, body mass index, insulin and hypertension were predictors of PAI-1. Patients on statin therapy had significantly lower levels Of D-dimer than those who were not on this therapy. Conclusion: There are significant associations of lipid profiles with hemostatic factors, the directions of which suggest novel pathways by which dyslipidemia may contribute to coronary heart disease.

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