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Aim: To evaluate the usefulness of copeptin as a rapid and reliable marker for discarding non-ST elevation acute myocardial infarction (NSTEMI) in patients attended in an Emergency Care Department due to acute chest pain with a normal or non-diagnostic electrocardiogram and a negative first troponin I result., Design: A prospective observational study was carried out., Setting: The Emergency Care Department of a university hospital., Patients: The study comprised a total of 97 patients attended in the Emergency Care Department due to chest pain suggestive of acute coronary syndrome with an evolution of under 12h, a non-diagnostic electrocardiogram and a negative first troponin I result., Interventions: None., Variables of Interest: Patient demographic data and baseline characteristics, copeptin upon admission, troponin I upon admission and after 6h, and final diagnosis., Results: The final diagnosis was NSTEMI in 14 patients (14.4%) -no significant differences in copeptin concentration being observed between the 2 groups, though a tendency towards higher values was recorded in the NSTEMI group (median: 24.6pmol/l [interquartile range: 42.0] vs. 12.0pmol/l [16.1]; P=.06). The AUC ROC for copeptin upon admission was 0.657 (95%CI: 0.504-0.810), with a negative predictive value of 92% for a cutoff point of 14pmol/l., Conclusions: Copeptin determination upon admission to the Emergency Care Department in patients with chest pain for ≤12h, suggestive of acute coronary syndrome, with a non-diagnostic electrocardiogram and a negative first troponin I determination does not allow rapid and reliable exclusion of the presence of NSTEMI. Serial troponin I measurements are needed in this respect., (Copyright © 2014 Elsevier España, S.L.U. and SEMICYUC. All rights reserved.)

Background and Objective: Previous studies have shown that the metabolism of P2Y12 receptor blockers is influenced not only by CYP2C19 2 but also by PON1-Q192R alelles. We aimed to evaluate the impact of CYP2C19 2 and PON1-Q192R polymorphisms carriage in platelet reactivity and clinical outcome in patients with ischemic heart disease undergoing cardiac catheterization., Patients and Method: We recruited prospectively patients with acute coronary syndrome undergoing cardiac catheterization (n=247). We evaluated the genotype (CYP2C19 2, CYP2C19 17, PON1-Q192R) with TaqMan(®) assay and platelet aggregometry in all patients. We assessed both in and out-of-hospital events (unstable angina, periprocedural and spontaneous myocardial infarction, myocardial infarction, all-cause death, stent thrombosis and stroke) during follow-up., Results: Carriers of CYP2C19 2 alleles showed a significant higher residual platelet reactivity (PRU, mean [SD], 252 [76] vs. 287 [74], P=.002). Carriers of PON1-Q192R CT(RQ) and TT(QQ) alleles and CYP2C19 17 did not present a different response to clopidogrel. In a multivariable setting for the prediction of platelet reactivity, the contribution of CYP2C19 2 was modest (Wald=7.5; odds ratio [OR] for ≥ 1 alelle 2=2,786, 95% confidence interval [95% CI] 1,337-5,808). Independent predictors were baseline hemoglobin levels (g/dL, OR .666, 95% CI .555-.801) and the use of statins (OR .376, 95% CI .162-.873). Body mass index was a risk factor (OR 1,074, CI 95% 1,005-1,148). Studied polymorphisms did not predict an adverse outcome., Conclusions: CYP2C19 2 polymorphism influenced moderately platelet reactivity but did not show an impact on clinical outcome in patients with acute coronary syndrome. Neither CYP2C19 17 nor PON1-Q192R polymorphisms showed an impact upon platelet reactivity or outcome., (Copyright © 2013 Elsevier España, S.L. All rights reserved.)