P-23/CO-03 : Impact of Gene Polymorphisms, Platelet Reactivity, and the SYNTAX Score on 1-Year Clinical Outcomes in Patients with Acute Coronary Syndrome Undergoing Percutaneous Coronary Intervention

posted Jan 26, 2017, 8:36 AM by sourav ghosh   [ updated Jan 26, 2017, 8:36 AM ]
Rama kumari
Nizam's Institute of Medical Sciences, Hyderabad, India

Background: High on-treatment platelet reactivity (HPR) has emerged as risk factor for stent thrombosis and major adverse cardiovascular events (MACE) in patients who receive Clopidogrel after percutaneous coronary intervention (PCI). the SYNTAX score (SS) has been shown to be associated with an increased risk of mortality, myocardial infarction MI, and the stent thrombosis in patients with ST-segment elevation acute coronary syndromes (ACS) undergoing PCI. We studied 1) the association between platelet reactivity and the SS for the risk of MACE in patients with ACS undergoing PCI treated with Clopidogrel; 2) the association between genetic variants involved in Clopidogrel-mediated platelet effects and the risk of MACE; 3) the incremental prognostic value of the platelet reactivity measured at several time points Methods Eighty four in-patients with ACS were enrolled .HPR was determined before PCI, at hospital discharge, and at1 month. The risk of MACE (cardiac mortality, MI, and stent thrombosis) with 1-month HPR and the SS in the period between 1 month and 1 year was investigated. The determination of platelet aggregation was done by using a platelet aggregometer > 46 AU and <19 AU HPR and LPR in the setting of PCI have been defined by the (ROC) curve analyses. Genetic analysis of CYP2C19 was done by PCR-RFLP technique.
Results: The relative impact of HPR, SS and genetic variants modulating Clopidogrel effects and the risk of MACE in patients with ACS undergoing PCI was studied. CYP2C19*2 was associated with HPR but was not independently associated with the risk of MACE at any point. Patients with HPR and a high SS displayed a higher risk of MACE compared with patients with HPR and a low SS. By cox regression analysis for MACE, it was found that there was 3 fold more hazard of developing MACE though statistically not significant with increase in platelet reactivity at 1 month. 
Conclusion: HPR is associated with increased rates of ischemic events in patients with high SS suggesting a possibility that platelet function testing could be implemented to optimise antiplatelet therapy.

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