Effect of Anticoagulation and Antiplatelet Therapy on Incidence of Endoleaks and Sac Size Expansions after Endovascular Aneurysm Repair John B. Wild, Nikesh Dattani, Phillip Stather, Matthew J. Bown, Robert D. Sayers, and Edward Choke, Leicester, United Kingdom Background: The effects of anticoagulation or antiplatelet therapy on the incidence of endoleak and aneurysm sac size after endovascular aneurysm repair (EVAR) are unclear. This study aims to determine whether these therapies affect the incidence of endoleaks or sac size expansions after EVAR. Methods: The case notes of 407 patients (367 men and 40 women, mean age 74.7 years) who underwent elective EVAR between January 2006 and November 2011 were reviewed for medi- cation history and EVAR-related outcomes. Results: The median follow-up period was 18 months. There were 45 (11.1%) patients on warfarin (WA), 292 (71.7%) on antiplatelet therapy (AT) (aspirin, clopidogrel, or dipyridamole modified release), and 70 (17.2%) on no anticoagulation or antiplatelet therapy (NA). During the study period, 51 (12.5%) endoleaks were documented, 8 type I (AT ¼ 6, NA ¼ 0, and WA ¼ 2) and 42 type II (AT ¼ 31, NA ¼ 9, and WA ¼ 2). Medication did not significantly affect the incidence of type I (P ¼ 0.24) (based on chi-squared analysis), type II (P ¼ 0.33), or type III (P ¼ 0.82) endoleaks, or sac expansions (P ¼ 0.95). Conclusions: Warfarin and antiplatelet therapies are not associated with increased inci- dence of postoperative endoleaks or aneurysm sac expansion after EVAR. The data in this study support safe use of anticoagulant and antiplatelet medications in patients under- going EVAR. INTRODUCTION Endovascular aneurysm repair (EVAR) compares favorably with open abdominal aortic aneurysm (AAA) repair in terms of 30-day mortality and dura- tion of intensive care stay. 1 In comparison to open AAA repair, The benefits of EVAR, such as reduced perioperative time, decreased pain, reduced number of blood transfusions, and decreased length of stay in intensive care units, are in contrast to an in- creased rate of postoperative intervention. 2 This increased intervention rate is, in part, due to endo- leak formation, which can result in significant patient morbidity and mortality. 3 Endoleaks repre- sent the persistence of blood flow within the aneu- rysm sac, which can lead to an increase in intrasac pressure and potentially result in aneurysm rupture, even after exclusion. 4 Endoleaks are subdivided by type: type I endoleaks arise from proximal graft leakage; type II endoleaks are from a retrograde accessory branch (lumbar, mesenteric, and testic- ular arteries); type III endoleaks are from bleeding between different portions of a graft; and type IV endoleaks occur through the graft. 3,5 Vascular Surgery Research Group, University of Leicester, Leicester Royal Infirmary, Leicester, UK. Correspondence to: John B. Wild, MBChB, Vascular Surgery Research Group, Robert Kilpatrick Clinical Sciences Building, Univer- sity of Leicester, Leicester Royal Infirmary, Leicester LE2 7LX, UK; E-mail: bw69@le.ac.uk Ann Vasc Surg 2014; 28: 554–559 http://dx.doi.org/10.1016/j.avsg.2013.03.013 Crown Copyright Ó 2014 Published by Elsevier Inc. All rights reserved. Manuscript received: September 5, 2012; manuscript accepted: March 4, 2013; published online: October 3, 2013. 554