Relation Between White Blood Cell Count and Final Infarct Size in Patients With ST-Segment Elevation Acute Myocardial Infarction Undergoing Primary Percutaneous Coronary Intervention (from the INFUSE AMI Trial) Tullio Palmerini, MD a , Sorin J. Brener, MD b , Philippe Genereux, MD c,d , Akiko Maehara, MD c,d , Diego Della Riva, MD a , Andrea Mariani, MD a , Bernhard Witzenbichler, MD e , Jacek Godlewski, MD f , Helen Parise, ScD d , Jan-Henk E. Dambrink, MD g , Andrzej Ochala, MD h , Martin Fahy, MSc d , Ke Xu, MSc d , C. Michael Gibson, MD i , and Gregg W. Stone, MD c,d, * Although it has been shown that elevated white blood cell count (WBCc) on presentation is associated with an increased risk of cardiac mortality in patients with ST-segment elevation myocardial infarction (STEMI), the responsible mechanisms are unknown. We therefore sought to investigate whether elevated WBCc is associated with increased infarct size measured with cardiac magnetic resonance imaging 30 days after primary percutaneous coronary intervention in the Intracoronary Abciximab and Aspiration Thrombectomy in Patients With Large Anterior Myocardial Infarction trial. INFUSE AMI randomized patients with STEMI and proximal or mideleft anterior descending coronary artery occlusion to bolus intracoronary abciximab versus no abciximab and to manual aspiration versus no aspiration. WBCc at hospital admission was available in 407 of 452 randomized patients. Patients were stratified according to tertiles of WBCc. At 30 days, a significant stepwise increase in infarct size (percentage of total left ventricular mass) was apparent across tertiles of increasing WBCc (median [interquartile range] for tertiles I vs II vs III [ 11.2% [3.8% to 19.6%] vs 17.5% [0.5% to 22.9%] vs 19.1% [13.7 to 26.0], respectively, p <0.0001). Absolute infarct mass in grams and abnormal wall motion score were also significantly increased across tertiles of WBC. By multivariate linear regression analysis, WBCc was an independent predictor of infarct size along with intracoronary abciximab randomization, age, time from symptom onset to first device, proximal left anterior descending location, and baseline TIMI flow of 0/1. In conclusion, in patients with anterior wall STEMI, an elevated admission WBCc is a powerful independent predictor of infarct size measured with cardiac magnetic resonance imaging 30 days after primary percutaneous coronary intervention. Ó 2013 Elsevier Inc. All rights reserved. (Am J Cardiol 2013;112:1860e1866) Cardiac magnetic resonance imaging (cMRI) has emerged as the gold standard technique to evaluate infarct size and global and regional left ventricular functions in patients with ST-segment elevation myocardial infarction (STEMI). 1 cMRI has high spatial resolution and can detect subtle regional wall abnormalities that may be missed by other noninvasive techniques. By exploiting differences in tissue clearance of intravenously injected gadolinium that rapidly extravasates into the interstitium, cMRI is able to identify areas of myocardial necrosis that appear as hyperenhanced regions compared with normal myocardium on delayed imaging. As there are no data addressing the relation between white blood cell count (WBCc) and the extent of infarct size measured with cMRI in patients with STEMI undergoing primary percutaneous coronary intervention (PCI) and treated with contemporary antithrombotic therapies, we sought to investigate the impact of admission WBCc on infarct size determined by cMRI 30 days after primary PCI in patients with anterior STEMI enrolled in the Intracoronary Abciximab and Aspiration Thrombectomy in Patients With Large Anterior Myocardial Infarction (INFUSE AMI) trial. 2 Methods The study design and primary results of the INFUSE AMI trial have previously been reported in detail. 2,3 Briefly, INFUSE AMI was a prospective, 2  2 factorial, multi- center, single-blinded randomized trial evaluating the impact a Dipartimento Cardiovascolare, Policlinico S. Orsola, Bologna, Italy; b Weill Cornell Medical College, New York Methodist Hospital, New York, New York; c Columbia University Medical Center, New York, New York; d Cardiovascular Research Foundation, New York, New York; e Charite University Medicine Campus Benjamin Franklin, Berlin, Germany; f The Cardiovascular Intervention Center, Jagiellonian University, Krakow, Poland; g Department of cardiology, Isala Klinieken, Zwolle, The Netherlands; h Silesian Medical Academy, Katowice, Poland; and i Cardio- vascular Division, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts. Manuscript received July 4, 2013; revised manuscript received and accepted August 14, 2013. The INFUSE AMI trial was sponsored and funded by Atrium Medical (Hudson, New Hampshire). See page 1865 for disclosure information. *Corresponding author: Tel: (646) 434-4131; fax: (646) 434-4715. E-mail address: gstone@crf.org (G.W. Stone). 0002-9149/13/$ - see front matter Ó 2013 Elsevier Inc. All rights reserved. www.ajconline.org http://dx.doi.org/10.1016/j.amjcard.2013.08.010