Park Yongwhi, Tantry Udaya S, Koh Jin-Sin, Ahn Jong-Hwa, Kang Min Gyu, Kim Kye Hwan, Jang Jeong Yoon, Park Hyun Woong, Park Jeong-Rang, Hwang Seok-Jae, Park Ki-Soo, Kwak Choong Hwan, Hwang Jin-Yong, Gurbel Paul A, Jeong Young-Hoon
Dr. Young-Hoon Jeong, Cardiovascular Center, Gyeongsang National University Changwon Hospital, 11 Samjeongja-ro, Seongsan-gu, Changwon-si, Gyeongsangnam-do, 51472 Republic of Korea, Tel.: +82 55 214 3721, Fax: +82 55 214 3721, E-mail:
Thromb Haemost. 2017 May 3;117(5):911-922. doi: 10.1160/TH16-10-0744. Epub 2017 Feb 2.
The role of platelet-leukocyte interaction in the infarct myocardium still remains unveiled. We aimed to determine the linkage of platelet activation to post-infarct left ventricular remodelling (LVR) process. REMODELING was a prospective, observational, cohort trial including patients (n = 150) with ST-segment elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention. Patients were given aspirin plus clopidogrel therapy (600 mg loading and 75 mg daily). Platelet reactivity (PRU: P2Y12 Reaction Units) was assessed with VerifyNow P2Y12 assay on admission. Transthoracic echocardiography was performed on admission and at one-month follow-up. The primary endpoint was the incidence of LVR according to PRU-based quartile distribution. LVR was defined as a relative ≥ 20 % increase in LV end-diastolic volume (LVEDV) between measurements. Adverse LVR was observed in 36 patients (24.0 %). According to PRU quartile, LVR rate was 10.8 % in the first, 23.1 % in the second, 27.0 % in the third, and 35.1 % in the fourth (p = 0.015): the optimal cut-off of PRU was ≥ 248 (area under curve: 0.643; 95 % confidence interval: 0.543 to 0.744; p = 0.010). LVR rate also increased proportionally according to the level of high sensitivity-C reactive protein (hs-CRP) (p = 0.012). In multivariate analysis, the combination of PRU (≥ 248) and hs-CRP (≥ 1.4 mg/l) significantly increased the predictive value for LVR occurrence by about 21-fold. In conclusion, enhanced levels of platelet activation and inflammation determined the incidence of adverse LVR after STEMI. Combining the measurements of these risk factors increased risk discrimination of LVR. The role of intensified antiplatelet or anti-inflammatory therapy in post-infarct LVR process deserves further study.
血小板与白细胞相互作用在梗死心肌中的作用仍未明确。我们旨在确定血小板活化与梗死后左心室重构（LVR）过程之间的联系。REMODELING是一项前瞻性、观察性队列试验，纳入了150例接受直接经皮冠状动脉介入治疗的ST段抬高型心肌梗死（STEMI）患者。患者接受阿司匹林加氯吡格雷治疗（负荷剂量600 mg，每日75 mg）。入院时采用VerifyNow P2Y12检测法评估血小板反应性（PRU：P2Y12反应单位）。入院时及随访1个月时进行经胸超声心动图检查。主要终点是根据基于PRU的四分位数分布的LVR发生率。LVR定义为两次测量之间左心室舒张末期容积（LVEDV）相对增加≥20%。36例患者（24.0%）观察到不良LVR。根据PRU四分位数，LVR发生率在第一四分位数为10.8%，第二四分位数为23.1%，第三四分位数为27.0%，第四四分位数为35.1%（p = 0.015）：PRU的最佳截断值为≥248（曲线下面积：0.643；95%置信区间：0.543至0.744；p = 0.010）。LVR发生率也根据高敏C反应蛋白（hs-CRP）水平成比例增加（p = 0.012）。在多变量分析中，PRU（≥248）和hs-CRP（≥1.4 mg/l）的组合使LVR发生的预测价值显著增加约21倍。总之，血小板活化和炎症水平升高决定了STEMI后不良LVR的发生率。联合测量这些危险因素可提高LVR的风险辨别能力。强化抗血小板或抗炎治疗在梗死后LVR过程中的作用值得进一步研究。
