Relation of Level of Platelet Inhibition after Eptifibatide with Major Cardiovascular Events in ST-Segment Elevation Acute Myocardial Infarction Undergoing Primary Percutaneous Coronary Intervention
Abstract
Background: Eptifibatide, an inhibitor of glycoprotein IIb/IIIa administered as adjunctive therapy to reperfusion therapy Primary PCI in STEMI patients. Persistently high platelet reactivity was found in patients who experienced recurrent atherothrombotic events during antiplatelet therapy.Objective: To evaluate the level of platelet inhibition after eptifibatide therapy and to assess the relation between level of platelet inhibition and Major Cardiaovascular event (MACE).
Methods: Platelet function test by Multiplate analyzer was performed in STEMI Patients who undergone Primary-PCI, 10 minutes after a bolus of eptifibatide. MACE were prospectively monitored during hospitalization and the incidence of MACE correlated with the measured level of platelet inhibition.
Results: From 99 subjects, approximately 55% of the subjects were non-responders (high platelet reactivity). 18 patients experienced MACE, most were heart failure (8 people), malignant arrhythmias (3 people), recurrent angina (2 people), stroke (2 people) and reinfarction, infections and major bleeding each 1 person. 12 subjects experienced MACE was from the non-responder group and 8 subjects from the responder grup. The study was found that the level of platelet inhibition wasn’t an independent predictor for the risk of MACE.
Conclusion: Less achieved therapeutic effects of platelet Inhibition (non-responders) was found in the majority (55%) subjects. Different level of platelet inhibition wasn’t an independent predictor for the risk of MACE.
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References
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Clappers N, Brouwer M, Verheuget F. Antiplatelet treatment for Coronary Artery Disease. Heart 2007;93:258-65.
Cattaneo M. The clinical relevance of response variability to antiplatelet therapy. Hematology Am Soc Hematol Educ Program 2011;2011:70-5.
Bonello L, Tantry US, Marcucci R, et al. Consensus and future directions on the definition of high on-treatment platelet reactivity to adenosine diphosphate. J Am Coll Cardiol 2010;56:919-33.
Siller-Matula JM, Christ G, Lang IM, Delle-Karth G, Huber K, Jilma B. Multiple electrode aggregometry predicts stent thrombosis better than the vasodilator-stimulated phosphoprotein phosphorylation assay. J Thromb Haemost 2010;8:351-9.
Velik-Salchner C, Maier S, Innerhofer P, et al. Point-of-care whole blood impedance aggregometry versus classical light transmission aggregometry for detecting aspirin and clopidogrel: the results of a pilot study. Anesth Analg 2008;107:1798-806.
Chew DP, Moliterno DJ. A critical appraisal of platelet glycoprotein IIb/IIIa inhibition. J Am Coll Cardiol 2000;36:2028-35.
Ernst NM, Suryapranata H, Miedema K, et al. Achieved platelet aggregation inhibition after different antiplatelet regimens during percutaneous coronary intervention for ST-segment elevation myocardial infarction. J Am Coll Cardiol 2004;44:1187-93.
Harrington RA. Overview of clinical trials of glycoprotein IIb-IIIa inhibitors in acute coronary syndromes. Am Heart J 1999;138:276-86.
Danzi GB, Capuano C, Sesana M, Mauri L, Sozzi FB. Variability in extent of platelet function inhibition after administration of optimal dose of glycoprotein IIb/IIIa receptor blockers in patients undergoing a high-risk percutaneous coronary intervention. Am J Cardiol 2006;97:489-93.
Steinhubl SR, Talley JD, Braden GA, et al. Point-of-care measured platelet inhibition correlates with a reduced risk of an adverse cardiac event after percutaneous coronary intervention: results of the GOLD (AU-Assessing Ultegra) multicenter study. Circulation 2001;103:2572-8.
Piana RN, Paik GY, Moscucci M, et al. Incidence and treatment of ‘no-reflow’ after percutaneous coronary intervention. Circulation 1994;89:2514-8.
Abbo KM, Dooris M, Glazier S, et al. Features and outcome of no-reflow after percutaneous coronary intervention. Am J Cardiol 1995;75:778-82.
Niccoli G, Burzotta F, Galiuto L, Crea F. Myocardial no-reflow in humans. J Am Coll Cardiol 2009;54:281-92.
Ellis SG, Tendera M, de Belder MA, et al. Facilitated PCI in patients with ST-elevation myocardial infarction. N Engl J Med 2008;358:2205-17.
Sten Berg JM, van ‘t Hof AW, Dill T, et al. Effect of early, pre-hospital initiation of high bolus dose tirofiban in patients with ST-segment elevation myocardial infarction on short- and long-term clinical outcome. J Am Coll Cardiol 2010;55:2446-55.
Steg PG, James SK, Atar D, et al. ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation: The Task Force on the management of ST-segment elevation acute myocardial infarction of the European Society of Cardiology (ESC). Eur Heart J 2012.
Published
2015-03-31
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How to Cite
Pakpahan, E., Soerianata, S., & Haryono, N. (2015). Relation of Level of Platelet Inhibition after Eptifibatide with Major Cardiovascular Events in ST-Segment Elevation Acute Myocardial Infarction Undergoing Primary Percutaneous Coronary Intervention. Indonesian Journal of Cardiology, 35(1), 22-33. https://doi.org/10.30701/ijc.v35i1.372
Section
Clinical Research
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