Centre for Trauma Sciences, Barts and the London School of Medicine & Dentistry, Queen Mary, UK.
Shock. 2013 May;39(5):415-20. doi: 10.1097/SHK.0b013e31828ded41.
Clinical evidence supports the existence of a trauma-induced secondary cardiac injury. Experimental research suggests inflammation as a possible mechanism. The study aimed to determine if there was an early association between inflammation and secondary cardiac injury in trauma patients.
A cohort study of critically injured patients between January 2008 and January 2010 was undertaken. Levels of the cardiac biomarkers troponin I and heart-specific fatty acid-binding protein and the cytokines tumor necrosis factor α (TNF-α), interleukin (IL)-6, IL-1β, and IL-8 were measured on admission to hospital, and again at 24 and 72 h. Participants were reviewed for adverse cardiac events (ACEs) and in-hospital mortality.
Of 135 patients recruited, 18 (13%) had an ACE. Patients with ACEs had higher admission plasma levels of TNF-α (5.4 vs. 3.8 pg/mL; P = 0.03), IL-6 (140 vs. 58.9 pg/mL, P = 0.009), and IL-8 (19.3 vs. 9.1 pg/mL, P = 0.03) compared with those without events. Hour 24 cytokines were not associated with events, but IL-8 (14.5 vs. 5.8 pg/mL; P = 0.01) and IL-1β (0.55 vs. 0.19 pg/mL; P = 0.04) were higher in patients with ACEs at 72 hours. Admission IL-6 was independently associated with heart-specific fatty acid-binding protein increase (P < 0.05). Patients who presented with an elevated troponin I combined with either an elevated TNF-α (relative risk [RR], 11.0; 95% confidence interval [CI], 1.8-66.9; P = 0.015), elevated IL-6 (RR, 17.3; 95% CI, 2.9-101.4; P = 0.001), or elevated IL-8 (RR, 15.0; 95% CI, 3.1-72.9; P = 0.008) were at the highest risk of in-hospital death when compared with individuals with normal biomarker and cytokine values.
There is an association between hyperacute elevations in inflammatory cytokines with cardiac injury and ACEs in critically injured patients. Biomarker evidence of cardiac injury and inflammation on admission is associated with a higher risk of in-hospital death.
临床证据支持创伤后存在继发性心脏损伤。实验研究表明炎症可能是一种潜在机制。本研究旨在确定创伤患者中炎症与继发性心脏损伤之间是否存在早期关联。
对 2008 年 1 月至 2010 年 1 月期间危重症患者进行了队列研究。入院时测量心肌肌钙蛋白 I 和心脏特异性脂肪酸结合蛋白以及细胞因子肿瘤坏死因子-α（TNF-α）、白细胞介素（IL）-6、IL-1β和 IL-8 的水平，并在 24 小时和 72 小时再次测量。对参与者进行不良心脏事件（ACE）和院内死亡率的回顾性分析。
在纳入的 135 名患者中，有 18 名（13%）发生 ACE。发生 ACE 的患者入院时血浆 TNF-α（5.4 比 3.8 pg/mL；P = 0.03）、IL-6（140 比 58.9 pg/mL，P = 0.009）和 IL-8（19.3 比 9.1 pg/mL，P = 0.03）水平较高。与无事件患者相比。24 小时细胞因子与事件无关，但 ACE 患者的 IL-8（14.5 比 5.8 pg/mL；P = 0.01）和 IL-1β（0.55 比 0.19 pg/mL；P = 0.04）在 72 小时时更高。入院时的 IL-6 与心脏特异性脂肪酸结合蛋白的增加独立相关（P < 0.05）。入院时 TNF-α升高（相对风险 [RR]，11.0；95%置信区间 [CI]，1.8-66.9；P = 0.015）、IL-6 升高（RR，17.3；95% CI，2.9-101.4；P = 0.001）或 IL-8 升高（RR，15.0；95% CI，3.1-72.9；P = 0.008）与正常生物标志物和细胞因子值的个体相比，发生 ACE 的风险最高。
在危重症患者中，急性炎症细胞因子升高与心脏损伤和 ACE 之间存在关联。入院时心脏损伤和炎症的生物标志物证据与更高的院内死亡风险相关。
