Results: NSE levels signicantly increased after coronary angiography and inter- vention compared to baseline levels (22.0327.70, 10.083.15 consecutively). Baseline characteristics were similar between groups (Table-1). Left ventricular ejection fraction in the SNI+ group was signicantly lower than SNI- group (43.7112.51%, 50.849.34%, p¼0.002). Maximal CK-MB, Troponin-I, Syntax Score (SS), of SNI+ group were signicantly higher than SNI- group (103.8399.22, 51.9278.33, p¼0.006; 50.0466.18, 19.1830.50, p¼0.002; 103.8399.22, 51.9278.33, p¼0.006 and 50.0466.18, 19.1830.50, p¼0.002 successively). SS and performing PCI were the independent predictors of SNI (p¼0.009, OR¼1.06, 95%CI¼1.014-1.107, p¼0.036, OR¼4.262, 95%CI¼1.097-16.56). Conclusions: PCI and coronary artery lesion complexity may increase the risk of SNI in patients with acute coronary syndrome. OP-012 Treatment of Coronary No-Reow With Intracoronary Vasodilators Added to Intravenous Tiroban _ Ibrahim Faruk Aktürk 1 , Ahmet Arif Yalçın 1 , Çetin Sarıkamıs ¸ 1 , Nihan Turhan Çaglar 2 , _ Ismail Bıyık 1 , Mehmet Ertürk 1 , Ömer Çelik 1 , Fatih Uzun 1 , _ Ilker Murat Çaglar 3 , Ender Öner 1 1 Department of Cardiology _ Istanbul Mehmet Akif Ersoy Thoracic and Cardiovascular Surgery Training and Research Hospital, _ Istanbul, 2 Department of Cardiology _ Istanbul Training and Research Hospital, _ Istanbul, 3 Department of Cardiology Bakırköy Sadi Konuk Training and Research Hospital, _ Istanbul Objective: We prospectively assessed the management and short term prognosis of no-reow phenomenon in a tertiary referral hospital. Methods: We included 46 patients with ST-segment elevation acute myocardial infarction (STEMI) and occurrence of no-reow phenomenon after primary percuta- neous coronary intervention. They were all received intravenous tiroban and then randomized into one of the 3 groups: intracoronary adenosine (n¼16), intracoronary verapamil (n¼15) or serum physiologic as placebo (n¼15). Intracoronary drugs were administered after stent implantation. Thrombolysis In Myocardial Infarction (TIMI) frame counts were used to assess coronary ow. Results: Groups were similar in terms of age, sex, STEMI localisation, diabetes, hypertension, mean reperfusion time. Hemotologic and biochemical blood param- eters and procedural properties were also similar between groups (stent size and length, diameter and number of balloon(s) and stent(s) used). Verapamil plus tir- oban therapy had signicant effect in restoring impaired coronary blood ow, decreasing TIMI frame count from 7344 to 5248 (p¼0.024). However, adeno- sine and serum physiologic administration were not found to be so effective in decreasing TIMI frame count (from 8135 to 7146, p¼ 0.084; from 7432 to 7137, p¼0.612; respectively). In-hospital and 6-month survival rates were similar among groups. Conclusion: Tiroban plus verapamil restored the impaired coronary blood ow more effectively than tiroban plus adenosine and tiroban only. Although both verapamil and adenosine have multiple effects on coronary circulation and even on platelet aggregation, verapamil as a calcium channel blocker, not only relieves microvascular spasm but also reduces calcium inux into ischemic cells, relieves cellular edema and restores calcium homeostasis. It may be hypothesized that these additional features put verapamil ahead of other drugs and may explain the better results we obtained with verapamil in comparison to adenosine. OP-013 A Simple Index to Predict Adverse Clinical Outcome Associated with Acute Myocardial Infarction in Primary PCI Era Mustafa TarıkAgaç 1 , Suret Agaç 4 , Levent Korkmaz 1 , Turhan Turan 2 , Hüseyin Bektas ¸ 1 , Ali Rıza Akyüz 2 , Mustafa Çetin 1 , Hakan Erkan 1 , Bülent Vatan 3 , S ¸ükrü Çelik 1 1 Ahi Evren Cardiovascular and Thoracic Surgery Training and Research Hospital, Department of Cardiology, Trabzon, 2 Akcaabat Hackali Baba State Hospital, Department of Cardiology, Trabzon, 3 Sakarya University Medical Faculty Hospital, Department of Cardiology, Sakarya, 4 Karadeniz Technical University Medical Faculty Hospital, Department of Biochemisty, Trabzon Background: The major determinant of nal infarct size for a given coronary occlusion is the size of myocardium that the artery perfuses. Dening the initial area- at-risk (AAR) for infarction has major clinical implications since it permits an accurate estimate of myocardial salvage provided by reperfusion therapies. We proposed a new index 'Relative Importance Index (RII)' to predict potential infarct size in patients with anterior MI. Aim: The aim of the study is to assess the predictive role of RII for reduction in systolic function and its relation to adverse clinical outcomes. Methods: One Hundred twenty-three acute anterior MI patients with their rst acute coronary syndrome incident were consecutively and prospectively enrolled to the study. Patients with a clinical history of congestive heart failure, valvular heart disease, and previous coronary revascularization were excluded. All patients under- went primary percutaneous coronary intervention (PCI) for revascularization. Angiographic exclusion criteria were 1) pre-procedural TIMI ow 2 in the infarct related artery, 2) chronic total occlusion of other arterial territory 3) any visible collateral ow to infarct related artery 4) diffuse disease at proximal segments of coronary arteries that precludes dening reference segment. Coronary diameters were measured with quantitative coronary analysis program. RII was calculated by dividing culprit segment diameter to the sum of diameters of LAD, Cx, and RCA at their proximal segments (Figure 1). Troponin I (TnI) concentration at 72 hour was chosen as a serological estimate of infarct size. We evaluated 1-month follow up rates of major clinical endpoints (MCE), which is dened as death, non fatal MI, stroke, and new congestive heart failure. Left ventricular EF (LVEF) at 1st month was chosen as an index for systolic function. Results: RII was signicantly and negatively correlation LVEF (r¼-0.65, p<0.001) (Figure 2). As RII of culprit lesion increased there was tendency to end up with lower EF. Likewise, RII was signicantly correlated with 72 h TnI (r¼0.48, p<0.001). Patients were dichotomized according to median value of RII (median RII¼0.30) (Table 1). Supra-median RII was associated with lower EF and higher incidence of composite MACE. The mortality (12.9% vs. 6.6%), non-fatal MI (6.5% vs. 3.3%), and new CHF (12.9% vs. 3.3%) rate in supra-median RII group trend higher but they did not reach statistical signicance. An RII >0.30 had a 88% sensitivity and 60% specicity (ROC area 0.82, p<0.001, CI [0.73-0.90]) for predicting severe LV dysfunction (LVEF <30%) (Figure 3). Conclusion: A Simple index derived from coronary angiography at time of primary PCI can predict LV systolic function loss and adverse clinical outcome in patients with acute anterior myocardial infarction. Table-1 Variable SNI+ SNI- p value Age, year 62.689.33 64.0111.27 0.566 Male n(%) 26 (83.8%) 49 (73.1%) 0.243 Body Mass Index, kg/m2 28.064.03 28.014.85 0.515 Hypertension, n(%) 10 (32.3%) 25 (37.3%) 0.627 Diabetes, n(%) 10 (32.3%) 24 (35.8) 0.730 Hyperlipidemia, n(%) 9 (28.1%) 22 (32.8%) 0.782 Smoking, n(%) 11 (35.5%) 20 (29.9%9 0.752 Atrial brillation, n(%) 2 (6.5%) 8 (11.9%) 0.404 Mean Arterial Pressure, mmHg 100.7113.80 98.2612.14 0.374 Percutaneous Coronary Intervention, n(%) 21 (67.7%) 30 (44.8%) 0.034 SYNTAX score 28.1314.68 18.7113.23 0.002 Fluoroscopy Time, min 6.374.23 4.704.16 0.069 estimated Creatinine Clearance, ml/min 103.6530.51 99.1034.47 0.530 Glucose, mg/dl 127.7160.40 133.0767.80 0.707 LDL, mg/dl 141.3242.59 135.1947.74 0.733 Total Cholesterol, mg/dl 201.2166.84 205.8555.17 0.718 Hemoglobin, g/dl 14.421.59 13.971.70 0.210 Mean Platelet Volume, femtolitre 8.271.51 8.210.93 0.797 Red cell Distribution Width, % 13.550.91 13.361.42 0.498 CK-MB, ng/ml 103.8399.22 51.9278.33 0.006 Troponin-I, ng/ml 50.0466.18 19.1830.50 0.002 Left Atrial diameter, mm 38.294.09 38.515.85 0.853 Left Ventricular End Diastolic Diameter, mm 49.905.83 49.305.03 0.600 Left ventricular End Systolic Diameter, mm 36.105.76 33.396.00 0.037 Ejection Fraction, % 43.7112.51 50.849.34 0.002 Asendan Aorta diameter, mm 34.714.11 34.574.20 0.875 C4 JACC Vol 62/18/Suppl C j October 2629, 2013 j TSC Abstracts/ORALS ORALS