Title
The influence of established genetic variation in the haemostatic system on clinical restenosis after percutaneous coronary interventions
Author
TNO Kwaliteit van Leven
Pons, D.
Monraats, P.S.
de Maat, M.P.M.
Pires, N.M.M.
Quax, P.H.A.
van Vlijmen, B.J.M.
Rosendaal, F.R.
Zwinderman, A.H.
Doevendans, P.A.F.M.
Waltenberger, J.
de Winter, R.J.
Tio, R.A.
Frants, R.R.
van der Laarse, A.
van der Wall, E.E.
Jukema, J.W.
Publication year
2007
Abstract
Since activation of the haemostatic system is an important feature of the wound healing response triggered by arterial injury, variations in genes involved in thrombus formation may play a role in restenosis after percutaneous coronary interventions (PCI). Therefore, our aim was to examine the relationship between polymorphisms that are known to play a role in the haemostatic system and the risk of clinical restenosis in the GENetic DEterminants of Restenosis (GENDER) studya multicenter prospective study design that enrolled 3,104 consecutive patients after successful PCI.Target vessel revascularization (TVR) was the primary endpoint.All patients were genotyped for six polymorphisms in the Factor II, Factor V, Factor VII and PAI-1 genes. The PAI-1 4G variant was associated with an increased risk ofTVR.When compared to 5G/5G homozygotes, heterozygous patients were at higher risk for TVR (HR: 1.46, 95%Cl: 1.05-2.03), whereas patients with the 4G/4G genotype had an even further increased risk (HR: 1.69, 95%Cl: 1.19-2.41). In contrast, the factor V 506GIn (factor V Leiden) amino acid substitution was associated with a decreased risk ofTVR (HR: 0.41, 95%Cl: 0.19-0.86). Our findings indicate that polymorphisms in the factor V and PAI-1 genes may play a role in the process of restenosis. © 2007 Schattauer GmbH, Stuttgart.
Subject
Biomedical Research
Coagulation factors
Polymorphisms
Restenosis
Aged
Angioplasty, Transluminal, Percutaneous Coronary
Coronary Restenosis
Coronary Stenosis
Diabetes Complications
Factor V
Factor VII
Female
Follow-Up Studies
Genetic Predisposition to Disease
Hemostasis
Heterozygote
Homozygote
Humans
Male
Middle Aged
Netherlands
Phenotype
Plasminogen Activator Inhibitor 1
Polymorphism, Genetic
Proportional Hazards Models
Prospective Studies
Prothrombin
Research Design
Risk Assessment
Risk Factors
Smoking
Time Factors
Treatment Outcome
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DOI
https://doi.org/10.1160/th07-04-0301
TNO identifier
240481
ISSN
0340-6245
Source
Thrombosis and Haemostasis, 98 (98), 1323-1328
Bibliographical note
PDF is de proefschrift variant
Document type
article