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      Intracoronary Eptifibatide During Primary Percutaneous Coronary Intervention in Early Versus Late Presenters with ST Segment Elevation Myocardial Infarction: A Randomized Trial

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          Abstract

          Introduction

          The role of intracoronary (IC) eptifibatide in primary percutaneous coronary intervention (PPCI) for ST segment elevation myocardial infarction (STEMI) and whether time of patient presentation affects this role are unclear. We sought to evaluate the benefit of IC eptifibatide use during primary PCI in early STEMI presenters compared to late STEMI presenters.

          Methods

          We included 70 patients who presented with STEMI and were eligible for PPCI. On the basis of symptom-to-door time, patients were classified into two arms: early (<3 h, n = 34) vs late (≥3 h, n = 36) presenters. They were then randomized to local IC eptifibatide infusion vs standard care (control group). The primary end point was post-PCI myocardial blush grade (MBG) in the culprit vessel. Other end points included corrected TIMI frame count (cTFC), ST segment resolution (STR) ≥70%, and peak CKMB.

          Results

          In the early presenters arm, no difference was observed in MBG results ≥2 in the IC eptifibatide and control groups (100% vs 82%; p = 0.23). In the late presenters arm, the eptifibatide subgroup was associated with improved MBG ≥2 (100% vs 50%; p = 0.001). IC eptifibatide in both early and late presenters was associated with less cTFC (early presenters 19 vs. 25.6, p = 0.001; late presenters 20 vs. 31.5, p < 0.001) and less peak CKMB (early presenters 210 vs 260 IU/L, p = 0.006; late presenters 228 vs 318 IU/L, p = 0.005) compared with the control group. No difference existed between both groups in STR index in early and late presenters.

          Conclusion

          IC eptifibatide might improve the reperfusion markers during PPCI for STEMI patients presenting after 3 h from onset of symptoms. A large randomized study is recommended to ascertain the benefits of IC eptifibatide in late presenters on clinical outcomes.

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          Most cited references 21

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          2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines.

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            Bivalirudin during primary PCI in acute myocardial infarction.

            Treatment with the direct thrombin inhibitor bivalirudin, as compared with heparin plus glycoprotein IIb/IIIa inhibitors, results in similar suppression of ischemia while reducing hemorrhagic complications in patients with stable angina and non-ST-segment elevation acute coronary syndromes who are undergoing percutaneous coronary intervention (PCI). The safety and efficacy of bivalirudin in high-risk patients are unknown. We randomly assigned 3602 patients with ST-segment elevation myocardial infarction who presented within 12 hours after the onset of symptoms and who were undergoing primary PCI to treatment with heparin plus a glycoprotein IIb/IIIa inhibitor or to treatment with bivalirudin alone. The two primary end points of the study were major bleeding and combined adverse clinical events, defined as the combination of major bleeding or major adverse cardiovascular events, including death, reinfarction, target-vessel revascularization for ischemia, and stroke (hereinafter referred to as net adverse clinical events) within 30 days. Anticoagulation with bivalirudin alone, as compared with heparin plus glycoprotein IIb/IIIa inhibitors, resulted in a reduced 30-day rate of net adverse clinical events (9.2% vs. 12.1%; relative risk, 0.76; 95% confidence interval [CI] 0.63 to 0.92; P=0.005), owing to a lower rate of major bleeding (4.9% vs. 8.3%; relative risk, 0.60; 95% CI, 0.46 to 0.77; P<0.001). There was an increased risk of acute stent thrombosis within 24 hours in the bivalirudin group, but no significant increase was present by 30 days. Treatment with bivalirudin alone, as compared with heparin plus glycoprotein IIb/IIIa inhibitors, resulted in significantly lower 30-day rates of death from cardiac causes (1.8% vs. 2.9%; relative risk, 0.62; 95% CI, 0.40 to 0.95; P=0.03) and death from all causes (2.1% vs. 3.1%; relative risk, 0.66; 95% CI, 0.44 to 1.00; P=0.047). In patients with ST-segment elevation myocardial infarction who are undergoing primary PCI, anticoagulation with bivalirudin alone, as compared with heparin plus glycoprotein IIb/IIIa inhibitors, results in significantly reduced 30-day rates of major bleeding and net adverse clinical events. (ClinicalTrials.gov number, NCT00433966 [ClinicalTrials.gov].). Copyright 2008 Massachusetts Medical Society.
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              TIMI frame count: a quantitative method of assessing coronary artery flow.

              Although the Thrombolysis in Myocardial Infarction (TIMI) flow grade is valuable and widely used qualitative measure in angiographic trials, it is limited by its subjective and categorical nature. In normal patients and patients with acute myocardial infarction (MI) (TIMI 4), the number of cineframes needed for dye to reach standardized distal landmarks was counted to objectively assess an index of coronary blood flow as a continuous variable. The TIMI frame-counting method was reproducible (mean absolute difference between two injections, 4.7 +/- 3.9 frames, n=85). In 78 consecutive normal arteries, the left anterior descending coronary artery (LAD) TIMI frame count (36.2 +/- 2.6 frames) was 1.7 times longer than the mean of the right coronary artery (20.4 +/- 3.0) and circumflex counts (22.2 +/- 4.1, P < .001 for either versus LAD). Therefore, the longer LAD frame counts were corrected by dividing by 1.7 to derive the corrected TIMI frame count (CTFC). The mean CTFC in culprit arteries 90 minutes after thrombolytic administration followed a continuous unimodal distribution (there were not subpopulations of slow and fast flow) with a mean value of 39.2 +/- 20.0 frames, which improved to 31.7 +/- 12.9 frames by 18 to 36 hours (P < .001). No correlation existed between improvements in CTFCs and changes in minimum lumen diameter (r=-.05, P=.59). The mean 90-minute CTFC among nonculprit arteries (25.5 +/- 9.8) was significantly higher (flow was slower) compared with arteries with normal flow in the absence of acute MI (21.0 +/- 3.1, P < .001) but improved to that of normal arteries by 1 day after thrombolysis (21.7 +/- 7.1, P=NS). The CTFC is a simple, reproducible, objective and quantitative index of coronary flow that allows standardization of TIMI flow grades and facilitates comparisons of angiographic end points between trials. Disordered resistance vessel function may account in part for reductions in flow in the early hours after thrombolysis.
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                Author and article information

                Contributors
                Islam.elgendy@medicine.ufl.edu
                Journal
                Cardiol Ther
                Cardiol Ther
                Cardiology and Therapy
                Springer Healthcare (Cheshire )
                2193-8261
                2193-6544
                14 November 2016
                14 November 2016
                December 2016
                : 5
                : 2
                : 203-213
                Affiliations
                [1 ]Department of Internal Medicine, Rochester General Hospital, Rochester, NY USA
                [2 ]Department of Cardiovascular Medicine, Ain Shams Medical School, Cairo, Egypt
                [3 ]Department of Cardiovascular Medicine, Rochester General Hospital, Rochester, NY USA
                [4 ]Division of Cardiovascular Medicine, University of Florida, Gainesville, FL USA
                [5 ]Division of Pulmonary, Critical Care and Sleep Medicine, Department of Medicine, Medical University of South Carolina, Charleston, SC USA
                [6 ]Department of Pharmaceutics and Pharmaceutical Technology, Faculty of Pharmaceutical Sciences and Pharmaceutical Industries, Future University in Egypt, Cairo, Egypt
                [7 ]Sidney Kimmel Medical College at Thomas Jefferson University/Christiana Care Health System, Newark, DE USA
                [8 ]Division of Cardiovascular Medicine, Department of Medicine, University of Arkansas for Medical Sciences, Little Rock, AR USA
                Article
                73
                10.1007/s40119-016-0073-3
                5125115
                27844422
                © The Author(s) 2016
                Categories
                Original Research
                Custom metadata
                © Springer Healthcare 2016

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