The influence of established genetic variation in the haemostatic system on clinical restenosis after percutaneous coronary interventions
Thrombosis and Haemostasis: international journal for vascular biology and medicine , Volume 98 - Issue 6 p. 1323- 1328
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.
|Coagulation factors, Polymorphisms, Restenosis|
|Thrombosis and Haemostasis: international journal for vascular biology and medicine|
|Organisation||Erasmus MC: University Medical Center Rotterdam|
Pons, D, Monraats, P.S, de Maat, M.P.M, Pires, N.M.M, Quax, P.H.A, van Vlijmen, B.J.M, … Jukema, J.W. (2007). The influence of established genetic variation in the haemostatic system on clinical restenosis after percutaneous coronary interventions. Thrombosis and Haemostasis: international journal for vascular biology and medicine, 98(6), 1323–1328. doi:10.1160/TH07-04-0301