{"title":"使用血栓形成总分析系统测量 ST 段抬高型心肌梗死患者白细胞计数升高和血小板衍生血栓形成率","authors":"Shinnosuke Kikuchi, Kengo Tsukahara, Shinya Ichikawa, Takeru Abe, Hidefumi Nakahashi, Yugo Minamimoto, Yuichiro Kimura, Eiichi Akiyama, Kozo Okada, Yasushi Matsuzawa, Masaaki Konishi, Nobuhiko Maejima, Noriaki Iwahashi, Masami Kosuge, Toshiaki Ebina, Kouichi Tamura, Kazuo Kimura, Kiyoshi Hibi","doi":"10.5551/jat.64395","DOIUrl":null,"url":null,"abstract":"<p><strong>Aims: </strong>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.</p><p><strong>Methods: </strong>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.</p><p><strong>Results: </strong>Patients with a high peak leukocyte count (＞15,222/mm<sup>3</sup>; 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<sup>3</sup>; 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).</p><p><strong>Conclusions: </strong>An elevated leukocyte count is associated with high T-TAS-based platelet-derived thrombogenicity during the acute phase of STEMI.</p>","PeriodicalId":15128,"journal":{"name":"Journal of atherosclerosis and thrombosis","volume":" ","pages":"1277-1292"},"PeriodicalIF":3.0000,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11374560/pdf/","citationCount":"0","resultStr":"{\"title\":\"Elevated Leukocyte Count and Platelet-Derived Thrombogenicity Measured Using the Total Thrombus-Formation Analysis System in Patients with ST-Segment Elevation Myocardial Infarction.\",\"authors\":\"Shinnosuke Kikuchi, Kengo Tsukahara, Shinya Ichikawa, Takeru Abe, Hidefumi Nakahashi, Yugo Minamimoto, Yuichiro Kimura, Eiichi Akiyama, Kozo Okada, Yasushi Matsuzawa, Masaaki Konishi, Nobuhiko Maejima, Noriaki Iwahashi, Masami Kosuge, Toshiaki Ebina, Kouichi Tamura, Kazuo Kimura, Kiyoshi Hibi\",\"doi\":\"10.5551/jat.64395\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Aims: </strong>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.</p><p><strong>Methods: </strong>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.</p><p><strong>Results: </strong>Patients with a high peak leukocyte count (＞15,222/mm<sup>3</sup>; 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<sup>3</sup>; 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).</p><p><strong>Conclusions: </strong>An elevated leukocyte count is associated with high T-TAS-based platelet-derived thrombogenicity during the acute phase of STEMI.</p>\",\"PeriodicalId\":15128,\"journal\":{\"name\":\"Journal of atherosclerosis and thrombosis\",\"volume\":\" \",\"pages\":\"1277-1292\"},\"PeriodicalIF\":3.0000,\"publicationDate\":\"2024-09-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11374560/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of atherosclerosis and thrombosis\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.5551/jat.64395\",\"RegionNum\":2,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2024/3/6 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"Q2\",\"JCRName\":\"PERIPHERAL VASCULAR DISEASE\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of atherosclerosis and thrombosis","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.5551/jat.64395","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/3/6 0:00:00","PubModel":"Epub","JCR":"Q2","JCRName":"PERIPHERAL VASCULAR DISEASE","Score":null,"Total":0}
引用次数: 0
摘要
目的：ST段抬高型心肌梗死（STEMI）急性期血小板源性血栓形成率高与预后不良有关，但相关因素仍不清楚。本研究旨在探讨 STEMI 后的急性炎症反应是否会影响血小板源性血栓形成：这项回顾性观察性单中心研究纳入了 150 名 STEMI 患者，对他们在急性期的血小板衍生血栓形成性进行了评估。血小板源性血栓形成性是通过血小板芯片流压曲线下面积（PL-AUC）进行评估的，而血小板芯片流压曲线下面积是通过总血栓形成分析系统（T-TAS）测量的。白细胞计数峰值被评估为 STEMI 后的急性炎症反应。患者被分为两组：白细胞计数峰值的最高四分位数和其他三个四分位数的总和：结果：白细胞计数峰值较高（＞15222/mm3；n=37）的患者入院时的 PL-AUC 较高（420 [386-457] vs. 385 [292-428]，p=0.0018），在经皮冠状动脉介入治疗（PPCI）期间的 PL-AUC 较高（155 [76-229] vs. 96 [29-170]，p=0.0018）。与白细胞计数峰值较低（≤ 15,222/mm3; n=113）的患者相比，白细胞计数峰值较高（4200±2486 vs. 2373±1997，p＜0.0001）的患者在 STEMI 后 2 周的 PL-AUC 较高（119 [61-197] vs. 88 [46-122]，p=0.048），肌酸激酶峰值较高（4200±2486 vs. 2373±1997，p＜0.0001）。STEMI 后的白细胞计数峰值与初级 PPCI 期间的 PL-AUC 呈正相关（r=0.37，p＜0.0001）。多变量回归分析显示，白细胞计数峰值是影响 PPCI 期间 PL-AUC 的独立因素（β=0.26，p=0.0065）：结论：在 STEMI 急性期，白细胞计数升高与基于 T-TAS 的血小板源性血栓形成相关。
Elevated Leukocyte Count and Platelet-Derived Thrombogenicity Measured Using the Total Thrombus-Formation Analysis System in Patients with ST-Segment Elevation Myocardial Infarction.
Aims: 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.
Methods: 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.
Results: Patients with a high peak leukocyte count (＞15,222/mm3; 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/mm3; 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).
Conclusions: An elevated leukocyte count is associated with high T-TAS-based platelet-derived thrombogenicity during the acute phase of STEMI.
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