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RESUMEN Introducción: La resistencia a antiagregantes y el volumen plaquetario medio (VPM) son predictores de eventos en el síndrome coronario agudo (SCA). La asociación entre ambos ha sido poco estudiada. Objetivos: Evaluar si existe asociación entre la resistencia a la aspirina (AAS) e inhibidores del receptor P2Y12 (iP2Y12) y el VPM en pacientes mayores de 65 años con SCA. Material y métodos: Se incluyeron pacientes mayores de 65 años con diagnóstico de SCA. Se dividieron en: grupo 1 (resistencia a ambos antiagregantes), grupo 2 (a uno de los antiagregantes) y grupo 3 (a ningún antiagregante). Se midió la agregación plaquetaria entre las 12 y 24 horas poscarga (por light transmission aggregometry). Se consideró resistencia a iP2Y12 a un porcentaje máximo de agregación (PMA) con ADP > 60% y a la AAS a un PMA con ARA > 20%. En el seguimiento se consi-deró el punto final combinado de muerte global y reinternación cardiovascular. Resultados: Se incluyeron 195 pacientes que recibieron AAS e iP2y12 (120 recibieron clopidogrel y 75 ticagrelor); grupo 1 (19%), grupo 2 (34,4%) y grupo 3 (46,6%). El VPM se asoció a la resistencia a ambos antiagregantes (OR 1,02 (IC 95% 1,01-1,05), p = 0,03. A su vez, el VPM y el GRACE fueron predictores independientes del punto combinado (HR 1,03 (IC 95% 1,01-1,07), p = 0,04 y HR 1,02 (IC 95% 1,01-1,04), p = 0,02), respectivamente. Conclusiones: El VPM se asoció a la presencia de resistencia a ambos antiagregantes. En el seguimiento el VPM y el score GRACE fueron predictores del punto combinado.
ABSTRACT Background: Antiplatelet resistance and mean platelet volume (MPV) are event predictors in acute coronary syndrome (ACS). However, the association between both has been poorly studied. Objective: The aim of this study was to evaluate the association between MPV and resistance to aspirin (ASA) and P2Y12 receptor inhibitors (P2Y12i) in elderly patients with ACS. Methods: Patients over 65 years old with diagnosis of ACS were included in the study. They were divided into group 1 (re-sistance to both antiplatelet agents), group 2 (resistance to one antiplatelet agent) and group 3 (no resistance to antiplatelet agents). Platelet aggregation was measured between 12 and 24 hours postload (by light transmission aggregometry). Resis-tance to P2Y12i was considered as maximum percentage of aggregation (MPA) with adenosine diphosphate (ADP) >60% and resistance to ASA as MPA with arachidonic acid (ARA) >20%. The composite endpoint of global death and cardiovascular re-hospitalization was considered during follow-up. Results: One hundred and ninety five patients included in the study received ASA and P2Y12i (120 received clopidogrel and 75 ticagrelor). Nineteen percent of patients belonged to group 1, 34.4% to group 2 and 46.6% to group 3. Mean platelet volume was associated with resistance to both antiplatelet agents [OR 1.02 (95% CI 1.01-1.05), p=0.03], while MPV and the GRACE score were independent predictors of the composite endpoint [HR 1.03 (95% CI 1.01-1.07), p=0.04] and [HR 1.02 (95% CI 1.01-1.04), p=0.02], respectively. Conclusions: Mean platelet volume was associated with the presence of resistance to both antiplatelet agents. During follow-up, MPV and the GRACE score were predictors of the composite endpoint.
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Objective To investigate the correlations of P2Y12 gene polymorphisms with clopidogrel resistance and long-term outcome in patients with acute ischemic stroke. Methods From June 2015 to June 2017, consecutive patients with acute ischemic stroke admitted to the Department of Neurology, Nanjing Jiangbei People's Hospital were enrolled. Thromboelastography was used to measure platelet inhibition rate and assess clopidogrel resistance. Polymerase chain reaction was used to assay C34T and G52T polymorphisms of P2Y12 gene. The patients were followed up at 12 months after discharge. The primary outcome was combined outcome of stroke recurrence, myocardial infarction, and death due to cardiocerebrovascular events. Results A total of 214 patients were enrolled, 51 (23.8%) had clopidogrel re-sistance and 29 (13.4%) had major outcome events. One hundred twenty-eight (59.8%) patients were C34T CC genotype and 86 (40.2%) were CT+TT genotype. The proportion of clopidogrel resistance in patients with CT+TT genotype was significantly higher than that with CC genotype ( 76.5% vs.28.8%;χ2=25.672, P=0.001). There were 131 patients (61.2%) with G52T GG genotype and 83 (38.8%) with GT+TT genotype. There was no significant difference in the proportion of clopidogrel resistance between the GT+TT genotype and the GG genotype (43.1% vs.37.4%; χ2=0.534, P=0.465). Multiple logistic regression analysis indicated that age (odds ratio [OR] 1.064, 95%confidence interval [CI] 1.009-1.115;P=0.021), diabetes ( OR 3.773, 95%CI 1.672-8.475; P=0.004), and C34T CT+TT genotype ( OR 9.087, 95%CI 4.416-22.665; P=0.002) were the independent risk factors fot clopidogrel resistance. Cox proportional hazards model analysis showed that age (Hazard ratio [HR] 1.058, 95%CI 1.001-1.121; P=0.049), hypertension ( HR 3.105, 95%CI 1.149-9.523; P=0.028), homocysteine ( HR 1.101, 95%CI 1.020-1.190; P=0.014), and C34T CT+TT genotype ( HR 2.588, 95%CI 1.121-5.967; P=0.026) were independent risk factors for the composite outcome. Conclusion C34T polymorphism of P2Y12 gene in patients with acute ischemic stroke may be a risk factor for clopidogrel resistance and is independently associated with the risk of long-term recurrence of vascular events.
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BACKGROUND AND OBJECTIVES: Ticagrelor is considered a potent antiplatelet agent compared to clopidogrel. However, there are no studies regarding the effect of ticagrelor loading on infarct size in patients with ST-segment elevation myocardial infarction (STEMI) in a primary percutaneous coronary intervention (PCI) setting. SUBJECTS AND METHODS: In this single-center, randomized, open-label study, 188 patients who underwent primary PCI for STEMI were enrolled (92 patients in the clopidogrel group and 96 in the ticagrelor group) and compared the infarct size by technetium-99m (Tc-99m) tetrofosmin single-photon emission computed tomography (SPECT) and serial cardiac biomarker levels between the groups. SPECT was performed at a median of 2 days after PCI. RESULTS: Baseline clinical and procedural characteristics were similar between the groups. Infarct size on SPECT, was similar between the 2 groups (28.1%±34.5% vs. 32.8%±29.2%; p=0.169). At all time-points after PCI (8, 24, and 48 hours), the peak levels of creatine kinase-myocardial band (CK-MB) and troponin T were lower in the clopidogrel group. The clopidogrel group showed lower cumulative troponin T levels than the ticagrelor group (12.59±10.66 vs. 17.67±19.51 ng/mL; p=0.029). CONCLUSION: Ticagrelor loading before primary PCI was not associated with reduced myocardial infarct size during the first 48 hours, compared to clopidogrel loading.
Subject(s)
Humans , Angioplasty , Blood Platelets , Creatine , Myocardial Infarction , Percutaneous Coronary Intervention , Receptors, Purinergic P2Y12 , Tomography, Emission-Computed , Tomography, Emission-Computed, Single-Photon , Troponin TABSTRACT
Clopidogrel is an antiplatelet drug widely used in clinical practice now.It has been used as the secondary prevention medication for myocardial infarction,ischemic stroke,and peripheral vascular disease.However,the anti-platelet aggregation effect of clopidogrel has significant individual differences.A large part of patients have clopidogrel resistance phenomenon.The mechanism of clopidogrel resistance is not fully understood.The genetic polymorphism is an important cause of clopidogrel resistance,including ABCB1,CYP2C19,CYP3A4,CYP3A5,P2Y12,and ITGB3.