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Study endpoints assessment Angiographic analysis Coronary angiograms were obtained with the aim of facilitating angiographic analyses (long acquisition without magnification). The core laboratory for centralized, blind analyses was the Casilino Hospital (a non enrolling center) where all coronary angiograms were reviewed off-line by an expert interventional cardiologist (E.R.). For each patient, coronary angiograms were analyzed to assess the following: (1) antegrade coronary flow according to the standard TIMI criteria flow (1), (2) corrected TIMI frame count according to Gibson et al. (2), (3) MBG according to van’t Hof et al. (3), (4) thrombus score according to TIMI study group (4). As previously reported (5), we defined angiographic MVO as a final TIMI flow ≤2 or final TIMI flow 3 with an MBG <2 [modified from Gibson et al. (6)]. ECG analysis A 12-lead ECG was acquired at presentation and at 90 min after PPCI aiming at evaluate STR on multiple leads showing ST-elevation at baseline. The sum of ST-segment elevation was measured 20 ms after the end of the QRS complex from leads 1, aVL and V1 to V6 for anterior and leads II, III, aVF and V5 to V6 for inferior myocardial infarction. In case of rescue PCI, baseline STsegment elevation was considered that observed at the admission in the PCI hospital. Lack of STR was defined as an STR <30%. Partial resolution was defined as an STR <70% but >30%. Complete STR was defined as an STR >70%. The detailed analysis of ECG resolution has been described elsewhere (7). Moreover, baseline mean ST-segment elevation, residual mean STsegment elevation at 90 minutes after PCI, along with mean time between the last contrast injection and second ECG, were reported. Finally, STR analysis was performed by visual assessment. The core laboratory for ECG blind analysis was the "Istituto Scienze della Vita, Scuola Superiore Sant’Anna, Pisa, Italy" (a non enrolling center) where an expert cardiologist performed the ECG analysis (A.R.D.C.). Biomarker of myocardial necrosis analysis Serum CK-MB and TnT measurements were obtained in all patients during hospitalization. The first measurement was performed before PPCI and then at 6, 12, 24 and 48 hours. The infarct size was based on CK-MB or TnT peak level. Cardiac troponin T was assessed by Elecsys® 2010, Roche Diagnostics. Roche Diagnostics reports for the Elecsys® 2010 troponin T assay a lower detection limit 0.01 μg/l, with a total precision range from 2.8–6.2%. Of note, TnT assay was performed at individual site. Clinical outcome assessment The incidence of cardiac death, myocardial infarction, target lesion revascularization and heart failure requiring hospitalization was assessed at 1 month by interview and clinical check. Cardiac death included sudden death or death preceded by typical chest pain; nonfatal myocardial reinfarction was defined as typical chest pain with electrocardiographic changes and more than three-fold elevation of CK-MB isoform levels above upper normal limit; clinically driven target lesion revascularization was defined as a second PCI of the original lesion, due to angina, with either a positive stress test or electrocardiographic evidence of new ST-depression or T-wave inversion, or due to a positive stress test without angina, attributable to the target vessel and the presence of luminal stenosis of >70% of the reference luminal diameter by visual estimate; while heart failure requiring hospitalization was considered as a congestive heart failure secondary to left ventricular systolic dysfunction, diagnosed by history, physical examination and echocardiographic evaluation. In line with protocol, interviewers and examiners did not know which drug was administrated at the time of procedure. The accumulation of such end-points was defined as MACE. Enrolling centers: Institute of Cardiology, Catholic University of the Sacred Heart, Rome, Italy: 90 patients U.O. Dipartimentale di Emodinamica e Cardiologia Interventistica, S. Pertini Hospital, Rome, Italy: 30 patients U.O. Cardiologia, G. B. Morgagni – L. Pierantoni Hospital, Forlı`, Italy: 30 patients Cardiology, Arcispedale S. Anna, Ferrara, Italy: 30 patients Department of Cardiovascular Sciences, European Hospital, Rome, Italy: 30 patients U. O. Cardiologia Interventistica, Cardiologic Center Monzino, Milan, Italy: 30 patients References 1. TIMI Study Group. The thrombolysis in myocardial infarction (TIMI) trial. Phase I findings. TIMI Study Group. N Engl J Med 1985;312:932–36. 2. Gibson CM, Cannon CP, Daley WL, et al. TIMI frame count: a quantitative method of assessing coronary artery flow. Circulation 1996;93:879–88. 3. van’t Hof AW, Liem A, Suryapranata H, Hoorntje JC, de Boer MJ, Zijlstra F. Angiographic assessment of myocardial reperfusion in patients treated with primary angioplasty for acute myocardial infarction: myocardial blush grade Zwolle Myocardial Infarction Study Group. Circulation 1998;97:2302–06. 4. Gibson CM, deLemos JA, Murphy SA, et al. Combination therapy with abciximab reduces angiographically evident thrombus in acute myocardial infarction: a TIMI 14 substudy. Circulation 2001;103:2550–54. 5. Niccoli G, Lanza GA, Shaw S, et al. Endothelin-1 and acute myocardial infarction: a no- reflow mediator after successful percutaneous myocardial revascularization. Eur Heart J 2006;27:1793-98. 6. Gibson CM, Murphy SA, Morrow DA, et al. Angiographic perfusion score: an angiographic variable that integrates both epicardial and tissue level perfusion before and after facilitated percutaneous coronary intervention in acute myocardial infarction. Am Heart J 2004;148:336–40. 7. Schroder R, Dissmann R, Bruggemann T, et al. Extent of early ST-segment elevation resolution: a simple but strong predictor of outcome in patients with acute myocardial infarction. J Am Coll Cardiol 1994;24:384–91.