A retrospective case control study on the role of hypercoagulability in late stent thrombosis
Abstract number: PP-TH-344
Winckers1 K., Poenitz2 V., van Oerle1 R., Spronk1 H., Hackeng3 T.M., Nilsen2 D.W.T., ten Cate1 H.
11Internal Medicine and Cardiovascular Research Institute Maastricht, Maastricht University Medical Center, Maastricht, The Netherlands 22Department of Medicine, Stavanger University Hospital, Stavanger, Norway 33Department of biochemistry, Maastricht University Medical Center, Maastricht, The Netherlands
How-to-cite Winckers K, Poenitz V, van Oerle R, Spronk H, Hackeng TM, Nilsen DWT, ten Cate H. A retrospective case control study on the role of hypercoagulability in late stent thrombosis. Journal of Thrombosis and Haemostasis 2009; Volume 7, Supplement 2: Abstract PP-TH-344
Background: Late stent thrombosis (LST) is a complex phenomenon of which the pathophysiologic basis remains largely unresolved. Premature cessation of dual antiplatelet therapy in combination with delayed endothelialization is a major risk factor. However, the majority of patients do not develop a LST subsequent to discontinuation of antiplatelet therapy. It seems that in patients with LST there is an additional factor triggering thrombus formation at the stent site. The aim of our study was to evaluate the role of hypercoagulability and some related markers in LST.
Methods: In this retrospective study we included 20 patients from the cardiology outpatient clinic of the Stavanger University Hospital who developed a LST between 2004 and 2008 and 32 control patients, matched for age, sex and stent type. Blood coagulation was determined using the Calibrated Automated Thrombogram by which thrombin generation (TG) was measured in the presence and absence of thrombomodulin (TM). von Willebrand factor, activated protein C -PCinhibitor complexes (APC-PCI), and full length tissue factor pathway inhibitor (fTFPI) antigen levels were determined by ELISA.
Results: Results indicated are mean ± SD. The normalized endogenous thrombin potential levels (116 ± 31 vs. 114 ± 32%), lag times (4.4 ± 0.9 vs. 4.4 ± 0.7 s) and normalized peak heights (148 ± 50 vs. 149 ± 51%) were comparable in patients and controls, respectively. Addition of TM to the assay did not reveal significant differences either. Additionally, there were no significant difference in APC-PCI (median 1.6 (range 0.4–68.8) vs. median 1.7 [range 0.4–132.1) Units], full length TFPI (132 ± 34.1 vs. 128 ± 39.5 Units) and von Willebrand factor level (149 ± 47.8 vs. 161 ± 49.3 pg/mL) between patients and controls, respectively.
Conclusion: According to this retrospective study, hypercoagulability assessed by means of TG and including markers of endothelial perturbation does not appear to play a role in LST.
Disclosure of interest: none declared.
