Cheng Wenke, Fuernau Georg, Desch Steffen, Freund Anne, Feistritzer Hans-Josef, Pöss Janine, Buettner Petra, Thiele Holger
Department of Internal Medicine/Cardiology, Heart Center Leipzig at University of Leipzig, 04289 Leipzig, Germany.
Medical Faculty, University of Leipzig, 04103 Leipzig, Germany.
J Cardiovasc Dev Dis. 2022 Aug 20;9(8):280. doi: 10.3390/jcdd9080280.
There is evidence that monocyte chemoattractant protein-1 (MCP-1) levels reflect the intensity of the inflammatory response in patients with cardiogenic shock (CS) complicating acute myocardial infarction (AMI) and have a predictive value for clinical outcomes. However, little is known about the effect of mild therapeutic hypothermia (MTH) on the inflammatory response in patients with CS complicating AMI. Therefore, we conducted a biomarker study to investigate the effect of MTH on MCP-1 levels in patients with CS complicating AMI.
In the randomized mild hypothermia in cardiogenic shock (SHOCK-COOL) trial, 40 patients with CS complicating AMI were enrolled and assigned to MTH (33 °C) for 24 h or normothermia at a 1:1 ratio. Blood samples were collected at predefined time points at the day of admission/day 1, day 2 and day 3. Differences in MCP-1 levels between and within the MTH and normothermia groups were assessed. Additionally, the association of MCP-1 levels with the risk of all-cause mortality at 30 days was analyzed. Missing data were accounted for by multiple imputation as sensitivity analyses.
There were differences in MCP-1 levels over time between patients in MTH and normothermia groups ( for interaction = 0.013). MCP-1 levels on day 3 were higher than on day 1 in the MTH group (day 1 vs day 3: 21.2 [interquartile range, 0.25-79.9] vs. 125.7 [interquartile range, 87.3-165.4] pg/mL; = 0.006) and higher than in the normothermia group at day 3 (MTH 125.7 [interquartile range, 87.3-165.4] vs. normothermia 12.3 [interquartile range, 0-63.9] pg/mL; 0.011). Irrespective of therapy, patients with higher levels of MCP-1 at hospitalization tended to have a decreased risk of all-cause mortality at 30 days (HR, 2.61; 95% CI 0.997-6.83; = 0.051).
The cooling phase of MTH had no significant effect on MCP-1 levels in patients with CS complicating AMI compared to normothermic control, whereas MCP-1 levels significantly increased after rewarming.
NCT01890317.
有证据表明，单核细胞趋化蛋白-1（MCP-1）水平反映了并发急性心肌梗死（AMI）的心源性休克（CS）患者炎症反应的强度，并且对临床结局具有预测价值。然而，关于轻度治疗性低温（MTH）对并发AMI的CS患者炎症反应的影响知之甚少。因此，我们开展了一项生物标志物研究，以调查MTH对并发AMI的CS患者MCP-1水平的影响。
在“心源性休克低温治疗（SHOCK-COOL）”试验中，纳入40例并发AMI的CS患者，并按1:1的比例将其分配至MTH组（33℃）持续24小时或常温组。在入院当天/第1天、第2天和第3天的预定时间点采集血样。评估MTH组和常温组之间以及组内MCP-1水平的差异。此外，分析MCP-1水平与30天全因死亡风险的关联。作为敏感性分析，采用多重填补法处理缺失数据。
MTH组和常温组患者的MCP-1水平随时间存在差异（交互作用P = 0.013）。MTH组第3天的MCP-1水平高于第1天（第1天 vs 第3天：21.2[四分位间距，0.25 - 79.9] vs. 125.7[四分位间距，87.3 - 165.4] pg/mL；P = 0.006），且第3天高于常温组（MTH组125.7[四分位间距，87.3 - 165.4] vs. 常温组12.3[四分位间距，0 - 63.9] pg/mL；P = 0.011）。无论采用何种治疗方法，住院期间MCP-1水平较高的患者30天全因死亡风险往往降低（HR，2.61；95%CI 0.997 - 6.83；P = 0.051）。
与常温对照组相比，MTH的降温阶段对并发AMI的CS患者的MCP-1水平无显著影响，而复温后MCP-1水平显著升高。
NCT01890317。
