Division of Cardiology, Yokohama City University Medical Center.
Advanced Critical Care and Emergency Center, Yokohama City University Medical Center.
Circ J. 2020 May 25;84(6):975-984. doi: 10.1253/circj.CJ-19-1043. Epub 2020 Mar 19.
Prompt and potent antiplatelet effects are important aspects of management of ST-elevation myocardial infarction (STEMI) patients undergoing primary percutaneous coronary intervention (PPCI). We evaluated the association between platelet-derived thrombogenicity during PPCI and enzymatic infarct size in STEMI patients.
Platelet-derived thrombogenicity was assessed in 127 STEMI patients undergoing PPCI by: (1) the area under the flow-pressure curve for the PL-chip (PL-AUC) using the total thrombus-formation analysis system (T-TAS); and (2) P2Yreaction units (PRU) using the VerifyNow system. Patients were divided into 2 groups (High and Low) based on median PL-AUCduring PPCI. PRU levels during PPCI were suboptimal in both the High and Low PL-AUCgroups (median [interquartile range] 266 [231-311] vs. 272 [217-317], respectively; P=0.95). The percentage of final Thrombolysis in Myocardial Infarction (TIMI) 3 flow was lower in the High PL-AUCgroup (75% vs. 90%; P=0.021), whereas corrected TIMI frame count (31.3±2.5 vs. 21.0±2.6; P=0.005) and the incidence of slow-flow/no-reflow phenomenon (31% vs. 11%, P=0.0055) were higher. The area under the curve for creatine kinase (AUC) was greater in the High PL-AUCgroup (95,231±7,275 IU/L h vs. 62,239±7,333 IU/L h; P=0.0018). Multivariate regression analysis identified high PL-AUCduring PPCI (β=0.29, P=0.0006) and poor initial TIMI flow (β=0.37, P<0.0001) as independent determinants of AUC.
T-TAS-based high platelet-derived thrombogenicity during PPCI was associated with enzymatic infarct size in patients with STEMI.
ST 段抬高型心肌梗死(STEMI)患者行直接经皮冠状动脉介入治疗(PPCI)时,迅速且强效的抗血小板作用非常重要。我们评估了 PPCI 期间血小板源性血栓形成与 STEMI 患者酶性梗死面积之间的关系。
通过:(1)使用血栓形成总分析系统(T-TAS)评估 PL 芯片的压力-面积曲线下面积(PL-AUC);(2)使用 VerifyNow 系统评估 P2Y 反应单位(PRU),对 127 例接受 PPCI 的 STEMI 患者的血小板源性血栓形成进行评估。根据 PPCI 期间 PL-AUC 的中位数,将患者分为 2 组(高和低)。在高和低 PL-AUC 组中,PPCI 期间的 PRU 水平均不理想(中位数[四分位间距]分别为 266[231-311]和 272[217-317];P=0.95)。高 PL-AUC 组的最终心肌梗死溶栓治疗(TIMI)3 级血流比例较低(75%比 90%;P=0.021),校正 TIMI 帧数(31.3±2.5 比 21.0±2.6;P=0.005)和慢血流/无复流现象的发生率(31%比 11%;P=0.0055)较高。高 PL-AUC 组的肌酸激酶曲线下面积(AUC)较大(95,231±7,275IU/L h 比 62,239±7,333IU/L h;P=0.0018)。多变量回归分析确定 PPCI 期间的高 PL-AUC(β=0.29,P=0.0006)和初始 TIMI 血流不良(β=0.37,P<0.0001)是 AUC 的独立决定因素。
PPCI 期间 T-TAS 检测到的高血小板源性血栓形成与 STEMI 患者的酶性梗死面积相关。