Abstract W P82: Periprocedural Elevation of Von Willebrand Factor is Associated With Thromboembolic Events in Coil Embolization of Unruptured Intracranial Aneurysms Under Dual Antiplatelet Therapy

Abstract

Introduction and Objective: Although elevation of von Willebrand factor (vWF) is correlated with the outcome in patients with ischemic heart disease, there are no reports regarding the relevance of vWF and thromboembolism (TE) in coil embolization of unruptured intracranial aneurysms (UIAs). The aim of this study is to evaluate the impact of periprocedural elevation of vWF levels and preventive effect of antiplatelet drugs on TE in coiling of UIAs. Materials and methods: A total of 63 consecutive patients harboring wide-necked (>4mm) UIAs treated by coiling between February 2011 and July 2014 were prospectively included in this study. All patients received dual antiplatelet therapy (DAPT) starting 4 days prior to the procedure, continuing for at least three months. Patients’ characteristics, procedural profiles (procedure time, mode of technique used) were documented, and periprocedural hematological data including levels of vWF as well as platelet aggregation using light transmittance aggregometry (LTA) and VerifyNow system were measured. Their relevance with TE as defined by abnormalities in postprocedural diffusion weighted images were statistically assessed. Results: TE was observed in 30 cases (47.6 %). Elderly age (p=0.048), longer procedure time (p=0.004), low response to aspirin (collagen>21 by LTA, p=0.009), and elevation of vWF (p=0.009) were significantly associated with TE. In cases with longer procedure time (>238 minutes), low response to clopidogrel was also significantly correlated with TE (p=0.04). A weak, but significant correlation was observed between procedure time and elevated level of vWF (correlation coefficient=0.358, p=0.006). Conclusions: DAPT prevented the occurrence of TE in coiling of UIAs when their efficacy was confirmed by platelet aggregation studies. Longer procedure time seems to cause the elevation of vWF which reflects the vascular endothelial dysfunction, thus leading to TE.