Elevated Leukocyte Count and Platelet-Derived Thrombogenicity Measured Using the Total Thrombus-Formation Analysis System in Patients with ST-Segment Elevation Myocardial Infarction

被引:0
作者
Kikuchi, Shinnosuke [1 ]
Tsukahara, Kengo [1 ,2 ,6 ]
Ichikawa, Shinya [1 ]
Abe, Takeru [3 ]
Nakahashi, Hidefumi [1 ]
Minamimoto, Yugo [1 ]
Kimura, Yuichiro [1 ]
Akiyama, Eiichi [1 ]
Okada, Kozo [1 ]
Matsuzawa, Yasushi [1 ]
Konishi, Masaaki [1 ]
Maejima, Nobuhiko [1 ]
Iwahashi, Noriaki [1 ]
Kosuge, Masami [1 ]
Ebina, Toshiaki [1 ]
Tamura, Kouichi [4 ]
Kimura, Kazuo [1 ]
Hibi, Kiyoshi [1 ,5 ]
机构
[1] Yokohama City Univ, Div Cardiol, Med Ctr, Yokohama, Japan
[2] Fujisawa City Hosp, Div Cardiol, Fujisawa, Japan
[3] Yokohama City Univ, Med Ctr, Adv Crit Care & Emergency Ctr, Yokohama, Japan
[4] Yokohama City Univ, Grad Sch Med, Dept Med Sci & Cardiorenal Med, Yokohama, Japan
[5] Yokohama City Univ, Grad Sch Med, Dept Cardiol, Yokohama, Kanagawa, Japan
[6] Yokohama City Univ, Div Cardiol, Med Ctr, 4-57 Urafune-cho,Minami Ku, Yokohama 2320024, Japan
关键词
ST-segment elevation myocardial infarction; Primary percutaneous coronary intervention; Platelet-derived thrombogenicity; Leukocyte count; Inflammation; FLOW-CHAMBER SYSTEM; BLOOD-FLOW; ASSOCIATION; MORTALITY; THERAPY; AGGREGATION; PERFUSION; PREDICTS; OUTCOMES; DISEASE;
D O I
10.5551/jat.64395
中图分类号
R6 [外科学];
学科分类号
1002 ; 100210 ;
摘要
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/mm(3); 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(3); 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 (beta=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.
引用
收藏
页码:1277 / 1292
页数:16
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