Platelet Activation Is Associated With Myocardial Infarction in Patients With Pneumonia

Platelet Activation Is Associated With Myocardial Infarction in Patients With Pneumonia
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DOI:
10.1016/j.jacc.2014.07.985
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发表时间:
2014-11-04
影响因子:
24
通讯作者:
Violi, Francesco
Violi, Francesco
中科院分区:
医学1区
文献类型:
--
作者:
Cangemi, Roberto;Casciaro, Marco;Violi, Francesco

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背景:肺炎患者肌钙蛋白可能升高,但与心肌梗死(MI)和血小板活化的关系尚不明确。目的:本研究旨在探讨社区获得性肺炎患者住院早期肌钙蛋白升高与体内血小板活化标志物的关系。方法纳入278例连续住院的社区获得性肺炎患者,随访至出院。入院时,检测血小板活化标志物,如血浆可溶性p选择素、可溶性CD40配体和血清血栓素B-2 (TxB(2))。分别每隔12 h和24 h检测血清高敏心肌肌钙蛋白T水平和心电图。结果在144例高敏感性心肌肌钙蛋白T升高的患者中,31例有心肌梗死的体征,113例没有。出现心肌梗死体征的患者血浆可溶性p -选择素、可溶性CD40配体和血清TxB(2)的基线水平均显著升高。Logistic回归分析显示,血浆可溶性CD40配体(p < 0.001)、可溶性p -选择素(p < 0.001)、血清TxB(2) (p = 0.030)、平均血小板体积(p = 0.037)、肺炎严重程度指数评分(p = 0.030)、和射血分数(p = 0.001)是心肌梗死的独立预测因子。123例(45%)服用阿司匹林(100 mg/天)和未服用阿司匹林的患者心肌梗死发生率无显著差异(12% vs. 10%; p = 0.649)。阿司匹林治疗的MIs患者血清TxB(2)高于非MIs患者(p = 0.005)。结论:心肌梗死是肺炎的早期并发症,与体内血小板活化和血清TxB(2)过量产生有关;阿司匹林100毫克/天似乎不足以抑制血栓素的生物合成。(MACCE在社区获得性肺炎住院患者中的应用;NCT01773863) (C) 2014由美国心脏病学会基金会发布。
BACKGROUND Troponins may be elevated in patients with pneumonia, but associations with myocardial infarction (MI) and with platelet activation are still undefined.OBJECTIVES The aim of this study was to investigate the relationship between troponin elevation and in vivo markers of platelet activation in the early phase of hospitalization of patients affected by community-acquired pneumonia.METHODS A total of 278 consecutive patients hospitalized for community-acquired pneumonia, who were followed up until discharge, were included. At admission, platelet activation markers such as plasma soluble P-selectin, soluble CD40 ligand, and serum thromboxane B-2 (TxB(2)) were measured. Serum high-sensitivity cardiac troponin T levels and electrocardiograms were obtained every 12 and 24 h, respectively.RESULTS Among 144 patients with elevated high-sensitivity cardiac troponin T, 31 had signs of MI and 113 did not. Baseline plasma levels of soluble P-selectin and soluble CD40 ligand and serum TxB(2) were significantly higher in patients who developed signs of MI. Logistic regression analysis showed plasma soluble CD40 ligand (p < 0.001) and soluble P-selectin (p < 0.001), serum TxB(2) (p = 0.030), mean platelet volume (p = 0.037), Pneumonia Severity Index score (p = 0.030), and ejection fraction (p = 0.001) to be independent predictors of MI. There were no significant differences in MI rate between the 123 patients (45%) taking aspirin (100 mg/day) and those who were not aspirin treated (12% vs. 10%; p = 0.649). Aspirin-treated patients with MIs had higher serum TxB(2) compared with those without MIs (p = 0.005).CONCLUSIONS MI is an early complication of pneumonia and is associated with in vivo platelet activation and serum TxB(2) overproduction; aspirin 100 mg/day seems insufficient to inhibit thromboxane biosynthesis. (MACCE in Hospitalized Patients With Community-acquired Pneumonia; NCT01773863) (C) 2014 by the American College of Cardiology Foundation.