RESUMEN
The addition of clopidogrel to aspirin for patients undergoing percutaneous coronary intervention (PCI) had significantly reduced cardiovascular events. However, despite dual antiplatelet therapy ischaemic events still occur, especially stent thrombosis, which is associated with a high mortality rate. Inter-individual response to clopidogrel is highly variable. It was shown that 4-46% could be considered as high on treatment platelet reactivity (HTPR). Recent studies had demonstrated a relationship between HTPR and ischaemic events in the setting of PCI. Actually the assessment of platelet reactivity in routine practice and its interpretation to make a decision is a debatable issue.
Asunto(s)
Angioplastia Coronaria con Balón/métodos , Aspirina , Isquemia Miocárdica , Activación Plaquetaria/efectos de los fármacos , Trombosis/prevención & control , Ticlopidina/análogos & derivados , Aspirina/administración & dosificación , Aspirina/efectos adversos , Aspirina/farmacocinética , Clopidogrel , Terapia Combinada , Inhibidores de la Ciclooxigenasa/administración & dosificación , Inhibidores de la Ciclooxigenasa/efectos adversos , Inhibidores de la Ciclooxigenasa/farmacocinética , Interacciones Farmacológicas , Resistencia a Medicamentos , Humanos , Isquemia Miocárdica/sangre , Isquemia Miocárdica/complicaciones , Isquemia Miocárdica/terapia , Pruebas de Función Plaquetaria/métodos , Antagonistas del Receptor Purinérgico P2Y/administración & dosificación , Antagonistas del Receptor Purinérgico P2Y/efectos adversos , Antagonistas del Receptor Purinérgico P2Y/farmacocinética , Stents , Trombosis/sangre , Trombosis/etiología , Ticlopidina/administración & dosificación , Ticlopidina/efectos adversos , Ticlopidina/farmacocinética , Resultado del TratamientoRESUMEN
BACKGROUND: High P2Y12 platelet reactivity (PR) level after primary percutaneous coronary intervention (PPCI) for ST-segment elevation myocardial infarction (STEMI) affects prognosis and may induce the no-reflow phenomenon. AIM: To investigate the role of PR in the genesis of microvascular obstruction. METHODS: Patients with STEMI undergoing PPCI within 12hours of symptoms onset were included prospectively. All patients received a 600mg clopidogrel-loading dose before PPCI and 250mg aspirin. PR was measured thereafter during PPCI while wiring the culprit lesion and before coronary dilatation, using the P2Y12 VerifyNow® assay. No-reflow was defined as ST-segment regression<50% observed 90minutes after PPCI. RESULTS: Between January 2014 and November 2015, 140 STEMI patients were included, and divided into two groups: a low PR group (LPR) defined as PR<209P2Y12 reaction units (PRU); and a high PR group (HPR) defined as PR≥209PRU. There were no differences in baseline characteristics between LPR and HPR groups, including age (57.8±11.9 vs. 59.4±13.2 years, respectively; P=0.44) and weight (76.1±15.1 vs. 74.8±10.9kg, respectively; P=0.55). Delay to revascularization was 270.1±175.5 vs. 295.6±206.2minutes (P=0.49) and time between clopidogrel-loading and PR measurement was 53±37 vs 65±54minutes (P=0.29) in the LPR and HPR groups, respectively. No-reflow was more frequent in the HPR group (44 [47.3%] vs. 9 [19.1%]; P=0.0012). Mean PR was higher in patients with no-reflow: 268.3±53 vs. 223.8±50.1 PRU (P=0.002). In multivariable analysis, HPR was an independent predictor of no-reflow. Area under the receiver operating characteristic curve was 0.745 (0.654, 0.835); the cut-off value predicting no-reflow was 254PRU. CONCLUSION: High PR level measured at PPCI is independently associated with no-reflow.