Université de Lorraine, CHRU de Nancy, Médecine Intensive et Réanimation Brabois, INSERM U942 and U1116, F-CRIN-INIC RCT, Vandœuvre-lès-Nancy, France.
Université de Lorraine, CHRU de Nancy, INSERM CIC-P 1433, INSERM, F-CRIN-INI CRCT, Vandœuvre-lès-Nancy, France.
Clin Res Cardiol. 2022 Jun;111(6):604-613. doi: 10.1007/s00392-021-01823-0. Epub 2021 Mar 7.
Optimal outcome after cardiogenic shock (CS) depends on a coordinated healing response in which both debris removal and extracellular matrix tissue repair play a crucial role. Excessive inflammation can perpetuate a vicious circle, positioning leucocytes as central protagonists and potential therapeutic targets. High levels of circulating Triggering Receptor Expressed on Myeloid cells-1 (TREM-1), were associated with death in acute myocardial infarction confirming excessive inflammation as determinant of bad outcome. The present study aims to describe the association of soluble TREM-1 with 90-day mortality and with various organ injuries in patients with CS.
This is a post-hoc study of CardShock, a prospective, multicenter study assessing the clinical presentation and management in patients with CS. At the time of this study, 87 patients had available plasma samples at either baseline, and/or 48 h and/or 96-120 h for soluble TREM-1 (sTREM-1) measurements. Plasma concentration of sTREM-1 was higher in 90-day non-survivors than survivors at baseline [median: 1392 IQR: (724-2128) vs. 621 (525-1233) pg/mL, p = 0.008), 48 h (p = 0.019) and 96-120 h (p = 0.029). The highest tertile of sTREM-1 at baseline (threshold: 1347 pg/mL) was associated with 90-day mortality with an unadjusted HR 3.08 CI 95% (1.48-6.42). sTREM-1 at baseline was not associated to hemodynamic parameters (heart rate, blood pressure, use of vasopressors or inotropes) but rather with organ injury markers: renal (estimated glomerular filtration rate, p = 0.0002), endothelial (bio-adrenomedullin, p = 0.018), myocardial (Suppression of Tumourigenicity 2, p = 0.002) or hepatic (bilirubin, p = 0.008).
In CS patients TREM-1 pathway is highly activated and gives an early prediction of vital organ injuries and outcome.
心源休克（CS）后的最佳预后取决于协调的愈合反应，其中清除碎片和细胞外基质组织修复都起着关键作用。过度的炎症可能会导致恶性循环，使白细胞成为主要的主角和潜在的治疗靶点。循环中触发受体表达在髓样细胞-1（TREM-1）的高水平与急性心肌梗死患者的死亡相关，证实过度炎症是不良预后的决定因素。本研究旨在描述可溶性 TREM-1 与 CS 患者 90 天死亡率和各种器官损伤的相关性。
这是一项 CardShock 的事后研究，这是一项前瞻性、多中心研究，评估了 CS 患者的临床表现和管理。在本研究时，87 名患者有可用的血浆样本，可在基线时，和/或 48 小时和/或 96-120 小时进行可溶性 TREM-1（sTREM-1）测量。90 天幸存者的基线、48 小时和 96-120 小时的 sTREM-1 浓度均高于非幸存者[中位数：1392 IQR：（724-2128）比 621（525-1233）pg/ml，p=0.008）、48 小时（p=0.019）和 96-120 小时（p=0.029）。基线时 sTREM-1 的最高三分位数（阈值：1347 pg/ml）与 90 天死亡率相关，未调整的 HR 95%CI 为 3.08（1.48-6.42）。基线时 sTREM-1 与血流动力学参数（心率、血压、血管加压素或正性肌力药物的使用）无关，但与器官损伤标志物有关：肾脏（估计肾小球滤过率，p=0.0002）、内皮（生物肾上腺髓质素，p=0.018）、心肌（肿瘤抑制因子 2，p=0.002）或肝（胆红素，p=0.008）。
CS 患者的 TREM-1 途径高度激活，并能早期预测重要器官损伤和预后。
