Division of Cardiology, Yokohama City University Medical Center.
Division of Cardiology, Fujisawa City Hospital.
J Atheroscler Thromb. 2024 Sep 1;31(9):1277-1292. doi: 10.5551/jat.64395. Epub 2024 Mar 6.
High platelet-derived thrombogenicity during the acute phase of ST-segment elevation myocardial infarction (STEMI) is associated with poor outcomes; however, the associated factors remain unclear. This study aimed to examine whether acute inflammatory response after STEMI affects platelet-derived thrombogenicity.
This retrospective observational single-center study included 150 patients with STEMI who were assessed for platelet-derived thrombogenicity during the acute phase. Platelet-derived thrombogenicity was assessed using the area under the flow-pressure curve for platelet chip (PL-AUC), which was measured using the total thrombus-formation analysis system (T-TAS). The peak leukocyte count was evaluated as an acute inflammatory response after STEMI. The patients were divided into two groups: the highest quartile of the peak leukocyte count and the other three quartiles combined.
Patients with a high peak leukocyte count (>15,222/mm; n=37) had a higher PL-AUC upon admission (420 [386-457] vs. 385 [292-428], p=0.0018), higher PL-AUC during primary percutaneous coronary intervention (PPCI) (155 [76-229] vs. 96 [29-170], p=0.0065), a higher peak creatine kinase level (4200±2486 vs. 2373±1997, p<0.0001), and higher PL-AUC 2 weeks after STEMI (119 [61-197] vs. 88 [46-122], p=0.048) than those with a low peak leukocyte count (≤ 15,222/mm; n=113). The peak leukocyte count after STEMI positively correlated with PL-AUC during primary PPCI (r=0.37, p<0.0001). A multivariable regression analysis showed the peak leukocyte count to be an independent factor for PL-AUC during PPCI (β=0.26, p=0.0065).
An elevated leukocyte count is associated with high T-TAS-based platelet-derived thrombogenicity during the acute phase of STEMI.
ST 段抬高型心肌梗死(STEMI)急性期血小板源性血栓形成活性升高与不良预后相关,但相关因素尚不清楚。本研究旨在探讨 STEMI 后急性炎症反应是否影响血小板源性血栓形成活性。
本回顾性观察性单中心研究纳入了 150 例 STEMI 患者,在急性期评估血小板源性血栓形成活性。使用血栓形成总分析系统(T-TAS)测定血小板芯片的流压曲线下面积(PL-AUC)来评估血小板源性血栓形成活性。将 STEMI 后白细胞计数的峰值作为急性炎症反应的评估指标。患者被分为两组:白细胞计数峰值最高四分位数组(>15222/mm³;n=37)和其他三分位组合并组。
白细胞计数峰值较高组(>15222/mm³;n=37)入院时 PL-AUC 更高(420[386-457] vs. 385[292-428],p=0.0018),行直接经皮冠状动脉介入治疗(PPCI)时 PL-AUC 更高(155[76-229] vs. 96[29-170],p=0.0065),峰值肌酸激酶水平更高(4200±2486 vs. 2373±1997,p<0.0001),STEMI 后 2 周 PL-AUC 更高(119[61-197] vs. 88[46-122],p=0.048)。STEMI 后白细胞计数峰值较高组与白细胞计数较低组(≤15222/mm³;n=113)相比。PPCI 时的 PL-AUC 与 STEMI 后白细胞计数峰值呈正相关(r=0.37,p<0.0001)。多变量回归分析显示,PPCI 时白细胞计数峰值是 PL-AUC 的独立影响因素(β=0.26,p=0.0065)。
STEMI 急性期白细胞计数升高与 T-TAS 血小板源性血栓形成活性升高相关。