Rates of Stent Thrombosis in Bare-Metal Versus Drug-Eluting Stents (from a Large Australian Multicenter Registry) Bryan P. Yan, MBBS a , Stephen J. Duffy, MBBS, PhD b , David J. Clark, MBBS c , Jeffery Lefkovits, MBBS d , Roderic Warren, MBBS, PhD d , Ronen Gurvitch, MBBS d , Robert Lew, MBBS, PhD e , Martin Sebastian, MBBS f , Angela Brennan, RN g , Nick Andrianopoulos, MBBS g , Christopher M. Reid, PhD g , and Andrew E. Ajani, MD d,g,h, *, for the Melbourne Interventional Group Recent reports suggest that drug-eluting stents (DESs) may increase the risk of stent thrombosis (ST) relative to bare-metal stents (BMSs). Therefore, the aim of this study was to compare DES and BMS outcomes with a specific focus on ST. We analyzed 30-day and 1-year outcomes of 2,919 patients who underwent percutaneous coronary intervention with stent implantation from the Melbourne Interventional Group registry. Academic Research Consortium definitions of ST were used: (1) definite ST (confirmed using angiography in patients with an acute coronary syndrome), (2) probable ST (unexplained death <30 days or target-vessel myocardial infarction without angiographic confirmation), and (3) possible ST (unexplained death >30 days). Multivariate analysis was performed to identify predic- tors of ST. The incidence of ST (early or late) was similar between BMSs and DESs (1.6% vs 1.4%; p  0.66), and DES use was not predictive of ST. Independent predictors of ST included the absence of clopidogrel therapy at 30 days (odds ratio [OR] 2.58, 95% confi- dence interval [CI] 1.29 to 5.29, p <0.01), renal failure (OR 3.30, 95% CI 1.43 to 7.59, p <0.01), index procedure presentation with an acute coronary syndrome (OR 2.59, 95% CI 1.14 to 5.87, p  0.02), diabetes mellitus (OR 2.25, 95% CI 1.19 to 4.23, p  0.01), and total stent length >20 mm (OR 1.85, 95% CI 1.00 to 3.42, p  0.04). In conclusion, DESs were not associated with increased risk of ST compared with BMSs at 12 months in this large Australian registry that selectively used DESs for patients at high risk of restenosis. © 2008 Elsevier Inc. All rights reserved. (Am J Cardiol 2008;xx:xxx) Given the concern about the long-term safety of drug- eluting stents (DESs) and the potential duration of incre- mental risk, indiscriminate use of DESs in all patients un- dergoing percutaneous coronary intervention may no longer be advisable. 1–4 In patients at low risk of restenosis, the clinical benefit of a decrease in restenosis derived from DESs may be offset by an increased risk of stent thrombosis (ST), which carries significant mortality and morbidity. A strategy that restricts use of DESs in patients at high risk of restenosis (such as those with diabetes mellitus, long le- sions, and small vessels) may shift the benefit-risk ratio in favor of DESs and avoid exposing patients at low risk of restenosis to the unnecessary risk of ST. 5 Nevertheless, it may be this group of patients who are at highest risk of late ST. The aim of this study was to examine the incidence and predictors of ST in a large real-world multicenter registry in which DES use was restricted to patients at high risk of restenosis. Methods The study population consisted of patients with 2,919 per- cutaneous coronary interventions with stent implantation in 3,583 lesions from the Melbourne Interventional Group registry (April 1, 2004, to October 10, 2006). The DES group had 1 DES used, and the bare-metal stent (BMS) group had only BMSs implanted. The registry is a voluntary collaborative venture of in- terventional cardiologists practicing at 7 Australian public (government-funded) hospitals designed to record data per- taining to percutaneous coronary intervention and perform long-term follow-up. The Melbourne Interventional Group registry was previously described (Monash University, Mel- bourne, Australia 6,7 ). Demographic, clinical, and procedural a Cardiology Division, Section of Vascular Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts; b Department of Cardiology, Alfred Hospital; c Department of Cardiology, Austin Hospital; d Department of Cardiology, Royal Melbourne Hospital; e Department of Cardiology, Frankston Hospital, Melbourne, Australia; f Department of Cardiology, Geelong Hospital, Geelong, Australia; g Na- tional Health and Medical Research Council Centre of Clinical Research Excellence in Therapeutics, Department of Epidemiology and Preventive Medicine, Monash University; and h University of Melbourne, Melbourne, Victoria, Australia. Manuscript received November 20, 2007; revised manuscript received and accepted February 13, 2008. The Melbourne Interventional Group was supported by Astra-Zeneca, Biotronik, Boston-Scientific, Johnson & Johnson, Medtronic, Pfizer, Schering-Plough, Sanofi-Aventis, Servier, St Jude, and Terumo. These companies do not have access to the data and do not have the right to review articles before publication. Dr. Duffy was supported by an NHMRC Centre of Clinical Research Excellence grant to the Alfred and Baker Medical Unit. *Corresponding author: Tel: +613-9347-0499; fax: +613-9347-6760. E-mail address: andrew.ajani@mh.org.au (A.E. Ajani). 0002-9149/08/$ – see front matter © 2008 Elsevier Inc. All rights reserved. www.AJConline.org doi:10.1016/j.amjcard.2008.02.058 ARTICLE IN PRESS