A history of late and very late stent thrombosis is not associated with increased activation of the contact system, a case control study

Activated factor XII (FXIIa), FXII zymogen (FXII), FXIIa-C1-esterase inhibitor (C1-inhibitor), Kallikrein-C1-inhibitor, FXIa-C1-inhibitor and FXIa-α1-antitrypsin (AT-inhibitor) complexes were measured by Enzyme-linked immunosorbent assy (ELISA) methodology.Cases and controls showed similar distributions in sex, age, baseline medications and stent type. Patients with a history of (V)LST had a significantly greater stent burden and a higher number of previous myocardial infarctions than the control patients.There were no significant between-group differences in the plasma levels of the components of the contact system.In a cohort of patients with a history of (V)LST, we did not observe differences in the activation state of the intrinsic coagulation system as compared to patients with a history of percutaneous coronary intervention without stent thrombosis.Coronary stents are routinely employed in percutaneous coronary revascularization procedures and have significantly decreased the rates of acute vessel closure and restenosis[1]. The rate of stent thrombosis (ST) after percutaneous coronary intervention (PCI) is estimated to be as low as <1% of the cases following implantation of bare-metal stents (BMS), of which approximately 50% occur within the first month following implantation [2,3]. However, the potential fatality due to acute vessel closure, still makes ST one of the most frightening complications after percutaneous coronary intervention (PCI) [4,5]. During the last years, concerns have been raised regarding later occurrence of ST in drug-eluting stents (DES), in particular beyond the traditional 1-month timeframe[6-8]. The actual incremental risk associated with DES has been an issue of controversy.Among others, discontinuation of antiplatelet therapy, increased intrinsic platelet activity, incomplete stent apposition, bifurcation stenting, renal insufficiency and diabetes have been discussed as possible risk factors for the development of late stent thrombo