Fibrin D-dimer, von Willebrand factor and tissue plasminogen activator inhibitor antigens are predictive of major ischaemic heart disease

1995 ◽  
Vol 6 (2) ◽  
pp. 156 ◽  
Author(s):  
G. D. O. Lowe ◽  
A. Rumley ◽  
J. W. G. Yarnell ◽  
P. M. Sweetnam ◽  
H. F. Thomas
Keyword(s):  
Heart Disease ◽  
Ischaemic Heart Disease ◽  
Plasminogen Activator ◽  
Von Willebrand Factor ◽  
Plasminogen Activator Inhibitor ◽  
Tissue Plasminogen ◽  
Von Willebrand ◽  
Willebrand Factor ◽  
Activator Inhibitor ◽  
D Dimer

Associations of von Willebrand factor, fibrin D-dimer and tissue plasminogen activator with incident coronary heart disease: British Women's Heart and Health cohort study

2007 ◽  
Vol 14 (5) ◽  
pp. 638-645 ◽  
Author(s):  
Margaret May ◽  
Debbie A. Lawlor ◽  
Rita Patel ◽  
Ann Rumley ◽  
Gordon Lowe ◽  
...  
Keyword(s):  
Coronary Heart Disease ◽  
Heart Disease ◽  
Plasminogen Activator ◽  
Tissue Plasminogen Activator ◽  
Von Willebrand Factor ◽  
Incident Coronary Heart Disease ◽  
Tissue Plasminogen ◽  
Von Willebrand ◽  
Willebrand Factor ◽  
D Dimer

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

von Willebrand Factor, Soluble P-Selectin, Tissue Plasminogen Activator and Plasminogen Activator Inhibitor in Atherosclerosis

1995 ◽  
Vol 74 (02) ◽  
pp. 626-630 ◽  
Author(s):  
A D Blann ◽  
M Dobrotova ◽  
P Kubisz ◽  
C N McCollum
Keyword(s):  
Plasminogen Activator ◽  
Tissue Plasminogen Activator ◽  
Von Willebrand Factor ◽  
Plasminogen Activator Inhibitor ◽  
Tissue Plasminogen ◽  
Soluble P ◽  
Von Willebrand ◽  
Willebrand Factor ◽  
Activator Inhibitor ◽  
Pai 1

SummaryTissue plasminogen activator antigen (tPA), plasminogen activator inhibitor antigen (PAI-1), soluble P-selectin and von Willebrand factor antigen (vWf) were measured by ELISA in 41 patients with peripheral vascular disease (PVD), 41 with ischaemic heart disease (IHD) and in 46 age and sex matched asymptomatic controls. Increased vWf was found in patients with IHD (p = 0.0002) and in patients with PVD (p = 0.0011) relative to the controls but levels did not differ between the two patients groups. Raised tPA found in both PVD (p = 0.0006) and IHD (p = 0.0061) compared to the controls also failed to differentiate the two groups of patients. Soluble P-selectin was also raised in both groups (p = 0.003 in IHD and p = 0.0102 in PVD) with no difference between the groups. There were no differences in levels of PAI-1 between the groups. In the subjects taken as a whole, there were significant Spearman’s correlations between tPA and vWf (r = 0.37, p <0.001), tPA and triglycerides (r = 0.38, p <0.001), tPA and P-selectin (r = 0.19, p = 0.032), vWf and age (r = 0.25, p = 0.005) and inversely between vWf and HDL (r = -0.25, p = 0.006). These data support the concept that increased levels of tPA may be important in atherosclerosis, and indicate that soluble P-selectin may be useful in further analysis of the role of platelets and the endothelial cell in this disease.

Fibrin D-dimer, Tissue Plasminogen Activator, Plasminogen Activator Inhibitor, and the Risk of Major Ischaemic Heart Disease in the Caerphilly Study

1998 ◽  
Vol 79 (01) ◽  
pp. 129-133 ◽  
Author(s):  
J. W. G. Yarnell ◽  
P. M. Sweetnam ◽  
A. Rumley ◽  
H. F. Thomas ◽  
P. C. Elwood ◽  
...  
Keyword(s):  
Risk Factors ◽  
Heart Disease ◽  
Ischaemic Heart Disease ◽  
Plasminogen Activator ◽  
Tissue Plasminogen Activator ◽  
Plasminogen Activator Inhibitor ◽  
Mean Difference ◽  
Tissue Plasminogen ◽  
Activator Inhibitor ◽  
D Dimer

SummaryPlasma levels of fibrin D-dimer, tissue plasminogen activator (tPA) and plasminogen activator inhibitor (PAI) have been associated with ischaemic heart disease (IHD). However their associations with incident IHD in samples of the general population are not established. D-dimer antigen, tPA antigen and PAI activity were measured in stored, fasting plasma samples from 1,998 men aged 45-65 examined between 1984 and 1988, during the first re-examination of the Caerphilly Study cohort. These variables were related to major IHD events (myocardial infarction or IHD death) which occurred in 129 men during a follow-up period which averaged 61 months. Mean fibrin D-dimer was higher in men who developed IHD events (90 vs. 71 ng/ml; age-adjusted logarithmic mean difference 0.21; 95% CI 0.11, 0.30; p <0.0001). This association remained after adjusting for baseline IHD and for other risk factors including fibrinogen: the adjusted relative odds of IHD in the highest fifth of D-dimer were 3.5 (95% CI 1.8, 6.9; p = 0.0003). Mean tPA antigen was also higher in men who developed IHD (12.6 vs. 11.6 ng/ml; mean difference 0.9; 95% CI 0.2, 1.7; p = 0.02); however this difference largely disappeared after adjusting for other risk factors. PAI activity was not associated with risk of IHD.

scholarly journals Continuous Active State of Coagulation System in Patients With Nonthrombotic Inflammatory Bowel Disease

2011 ◽  
Vol 17 (6) ◽  
pp. 600-604 ◽  
Author(s):  
Huseyin Alkim ◽  
Selime Ayaz ◽  
Canan Alkim ◽  
Aysel Ulker ◽  
Burhan Sahin
Keyword(s):  
Plasminogen Activator ◽  
Degradation Products ◽  
Plasminogen Activator Inhibitor ◽  
Protein S ◽  
Plasminogen Activator Inhibitor 1 ◽  
Inflammatory Bowel ◽  
Von Willebrand ◽  
Willebrand Factor ◽  
Activator Inhibitor ◽  
D Dimer

This study was planned for searching possible changes of the total coagulation and fibrinolysis system in inflammatory bowel disease (IBD) in order to obtain some clues for explaining the relation between IBD and hypercoagulability. A total of 24 patients with ulcerative colitis, 12 patients with Crohn disease, and 20 healthy controls were studied. Platelets; prothrombin time (PT); partial thromboplastin time (PTT); fibrinogen; d-dimer; fibrinogen degradation products; protein C; protein S; antithrombin; thrombin time; von Willebrand factor; coagulation factors V, VII, VIII, IX, XI, and XIII; plasminogen; antiplasmin; tissue plasminogen activator; plasminogen activator inhibitor 1; and prothrombin fragments 1 + 2 were studied. Most of the procoagulants (platelets, fibrinogen, von Willebrand factor, coagulation factor IX, and plasminogen activator inhibitor 1) were found increased together with decreases in some anticoagulants (protein S and antithrombin) in IBD. Also the activation markers of coagulation (d-dimer, fibrinogen degradation products, and prothrombin fragments 1 + 2) were all increased. The parameters of the total coagulation–fibrinolysis system were increased in IBD, regardless of the form and the activity of the disease.

Von Willebrand Factor, Plasminogen Activator Inhibitor-1 and C-Reactive Protein Are Markers of Thrombolytic Efficacy in Acute Myocardial Infarction

1992 ◽  
Vol 68 (06) ◽  
pp. 678-682 ◽  
Author(s):  
F Andreotti ◽  
D R Hackett ◽  
A W Haider ◽  
M C Roncaglioni ◽  
G J Davies ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Plasminogen Activator ◽  
Von Willebrand Factor ◽  
Plasminogen Activator Inhibitor ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
Von Willebrand ◽  
Willebrand Factor ◽  
Activator Inhibitor

SummaryPlasma von Willebrand factor, plasminogen activator inhibitor activity and C-reactive protein were assessed as markers of coronary recanalisation in 30 patients with acute myocardial infarction receiving tissue-type plasminogen activator (t-PA). Blood samples were taken before t-PA (time 0), 4-hourly for 24 h and daily up to 72 h. A continuous electrocardiogram was recorded in the first 24 h. Coronary arteriography was performed 90 min and 24 h after the start of t-PA. Patients with a patent infarct artery (n = 17), compared to those with occluded artery (n = 13), showed a fall in von Willebrand factor from 0 to 24 h (p = 0.001), a greater fall in plasminogen activator inhibitor from 24 to 48 h (p = 0.04) and a fall in C-reactive protein from 48 to 72 h (p = 0.002). The accuracy of these indices compared favourably with time to peak plasma MB creatine kinase and ≥ 50% resolution of maximal ST-deviation on the electrocardiogram.Thus, changes in plasma von Willebrand factor, plasminogen activator inhibitor and C-reactive protein during the first 3 days of myocardial infarction are indicative of thrombolytic efficacy. Their concordant behaviour may reflect a common regulatory mechanism.

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