Protein S, von Willebrand Factor, and Euglobulin Lysis Time as Markers of Coronary Heart Disease

Background Associations of three markers of thrombotic tendency, von Willebrand factor, tissue plasminogen activator antigen and fibrin D-dimer, with coronary heart disease have been reported in meta-analyses. It is not known, however, whether findings are generalizable to older women. Design Prospective cohort of 3582 women aged 60-79 years randomly selected from 23 towns without evidence of cardiovascular disease at entry into the British Women's Heart and Health Study. Methods Women were followed for 4.7 years for incident coronary heart disease. Cox proportional hazard models were used to compare the hazard ratio of coronary heart disease per doubling for each thrombotic factor. Results In models adjusting for age and town only there was no association between von Willebrand factor or D-dimer and incidence of coronary heart disease, but there was a positive association of tissue plasminogen activator: coronary heart disease hazard ratio per doubling was 1.37 (95% confidence interval: 1.08-1.75). Adjustment for potential confounders (socio-economic position, smoking, lung function, physical activity, alcohol consumption, body mass index, waist-to-hip ratio) attenuated association to 1.20 (0.92-1.58). Further adjustment for risk factors that may be part of the same pathophysiological process linking tissue plasminogen activator to coronary heart disease (high density lipoprotein cholesterol, triglycerides, blood pressure, fasting glucose, insulin, C-reactive protein, fibrinogen) attenuated the hazard ratio to 1.05 (0.79-1.40). Conclusion In older women, tissue plasminogen activator was associated with incident coronary heart disease, but does not appear to be an independent risk factor for coronary heart disease as the association was attenuated by adjustment for confounding and other metabolic and vascular risk factors. Eur J Cardiovasc Prev Rehabil 14:638-645 © 2007 The European Society of Cardiology

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Decreased levels of von Willebrand factor-cleaving protease in coronary heart disease and thrombotic thrombocytopenic purpura: study of a simplified method for assaying the enzyme activity based on ristocetin-induced platelet aggregation

British Journal of Haematology ◽

10.1046/j.1365-2141.2003.04257.x ◽

2003 ◽

Vol 121 (1) ◽

pp. 123-129 ◽

Cited By ~ 9

Author(s):

Gina Yoo ◽

Margareta Blombäck ◽

Karin Schenck-Gustafsson ◽

Shu He

Keyword(s):

Coronary Heart Disease ◽

Enzyme Activity ◽

Heart Disease ◽

Platelet Aggregation ◽

Thrombotic Thrombocytopenic Purpura ◽

Von Willebrand Factor ◽

Thrombocytopenic Purpura ◽

Simplified Method ◽

Von Willebrand ◽

Willebrand Factor

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Venostasis but not DDAVP Infusion Provokes the Plasma Fibronectin Increase

Thrombosis and Haemostasis ◽

10.1055/s-0038-1647304 ◽

1990 ◽

Vol 64 (02) ◽

pp. 294-296 ◽

Cited By ~ 1

Author(s):

M Letowska ◽

K Bykowska ◽

J Sablinski ◽

S Lopaciuk ◽

M Kopeć

Keyword(s):

Von Willebrand Factor ◽

Vessel Wall ◽

Blood Donors ◽

Plasma Fibronectin ◽

Lysis Time ◽

Before And After ◽

Euglobulin Lysis Time ◽

Von Willebrand ◽

Willebrand Factor ◽

Factor Antigen

SummaryPlasma fibronectin (pFN), von Willebrand factor antigen (vWf: Ag), factor VIII procoagulant activity, fibrinogen, euglobulin lysis time (ELT) and hematocrit were determined in healthy blood donors before and after venostasis as well as after intravenous infusion of l-deamino-8-D-arginine vasopressin (DDAVP). Both venostasis and DDAVP provoked an increase in vWf : Ag and shortening in the ELT. In contrast, venostasis only but not DDAVP induced an increase in pFN levels which was statistically significant with and without correction for a concomitant hematocrit increment. The results indicate that there is a distinct difference in the patterns of venostasis and DDAVP mediated release of proteins from the vessel wall.

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Genetic variability of von Willebrand factor and risk of coronary heart disease: the Rotterdam Study

British Journal of Haematology ◽

10.1046/j.1365-2141.2003.04776.x ◽

2004 ◽

Vol 124 (3) ◽

pp. 343-347 ◽

Cited By ~ 29

Author(s):

Irene M. Van Der Meer ◽

Geert-Jan Brouwers ◽

Saskia Bulk ◽

Frank W. G. Leebeek ◽

Deirdre A. M. Van Der Kuip ◽

...

Keyword(s):

Coronary Heart Disease ◽

Heart Disease ◽

Genetic Variability ◽

Von Willebrand Factor ◽

Rotterdam Study ◽

Von Willebrand ◽

Willebrand Factor

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Correlation of von Willebrand factor gene polymorphism and coronary heart disease

Molecular Medicine Reports ◽

10.3892/mmr.2012.1037 ◽

2012 ◽

Vol 6 (5) ◽

pp. 1107-1110 ◽

Cited By ~ 1

Author(s):

AI-GUO XU ◽

RONG-MEI XU ◽

CHANG-QING LU ◽

MENG-YING YAO ◽

WEI ZHAO ◽

...

Keyword(s):

Coronary Heart Disease ◽

Heart Disease ◽

Gene Polymorphism ◽

Von Willebrand Factor ◽

Factor Gene ◽

Von Willebrand ◽

Willebrand Factor

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Family History of Coronary Heart Disease and Hemostatic Variables in Middle-Aged Adults

Thrombosis and Haemostasis ◽

10.1055/s-0038-1655912 ◽

1997 ◽

Vol 77 (01) ◽

pp. 087-093 ◽

Cited By ~ 23

Author(s):

James S Pankow ◽

Aaron R Folsom ◽

Michael A Province ◽

D C Rao ◽

John Eckfeldt ◽

...

Keyword(s):

Coronary Heart Disease ◽

Heart Disease ◽

Family History ◽

Risk Score ◽

Von Willebrand Factor ◽

Chd Risk ◽

History Of ◽

Chd Risk Factors ◽

Von Willebrand ◽

Willebrand Factor

SummaryIndividuals with a family history of coronary heart disease (CHD) may be predisposed to atherothrombosis. To investigate this hypothesis, a family CHD risk score was computed for approximately 13,000 men and women aged 45 to 64; hemostatic variables (fibrinogen, factor VIIc, factor VIIIc, von Willebrand factor, antithrombin III, protein C) were also measured in plasma. After adjustment for age and ethnicity, there was a statistically significant, positive association between the family risk score and four of the six hemostatic variables (fibrinogen, factor VIIc, factor VIIIc, von Willebrand factor) in women and all six hemostatic variables in men. In general, these associations were weak and substantially attenuated after adjustment for constitutional, lifestyle, and biochemical covariates. These results indicate that mean levels of selected hemostatic variables, like traditional CHD risk factors, are higher in individuals with a family history of heart disease.

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