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Background <p>Patients with cardiogenic shock (CS) following acute myocardial infarction (AMI) are challenged by pro-inflammatory and pro-apoptotic cellular processes. Little is known about the effect of mild therapeutic hypothermia (MTH) on these alterations.</p> Methods <p>Blood plasma from 40 patients included in the randomized SHOCK-COOL trial, which compared MTH (33&#xa0;°C) versus no hypothermia in AMI-CS without cardiac arrest, from the first 3&#xa0;days of hospitalization was used to determine interleukins (IL)-6 and IL-1β, tumor necrosis factor-alpha (TNF-α), intercellular and vascular soluble adhesion molecules (ICAM1 and VCAM1), TNF-receptor 1 (TNF-R1), TNF-related apoptosis-inducing ligand receptor 2 (TRAIL-R2), soluble FAS-ligand (sFASL), and soluble FAS (sFAS). These markers were also determined in 11 healthy controls.</p> Results <p>All markers except for TNF-R1 and sFASL reached their highest levels on day two or day three in both CS groups. IL-1β and sFAS reached higher maximum levels in the MTH group. IL-1β was higher in the MTH group on day 2 (+ 38%, <i>p</i> = 0.014) and on day 3 (+ 9%, <i>p</i> = 0.047), but the averaged group-wise individual maxima were comparable (24 [17–30] versus 20 [12–25], <i>p</i> = 0.138). The pro-apoptotic marker sFAS was also higher in the MTH group on day 2 (+ 85%, <i>p</i> = 0.004) and day 3 (+ 170%, <i>p</i> &lt; 0.001); the averaged individual maxima were significantly higher in the MTH group (25 [15–38] versus 15 [10–21] ng/ml, <i>p</i> = 0.008).</p> Conclusions <p>Hypothermia in AMI-CS without cardiac arrest has no moderating effect on the assessed pro-inflammatory cytokines. However, sFAS showed significantly higher individual peak maxima in the MTH group indicating enhancement of pro-apoptotic mechanisms via the soluble FAS/FASL pathway.</p> Graphical Abstract <p>The graphical abstract was designed using illustrations from Servier Medical Art (<a href="https://creativecommons.org/licenses/by/4.0/">https://creativecommons.org/licenses/by/4.0/</a>). Abbreviations: AMI-CS, acute myocardial infarction complicated by cardiogenic shock; IL, interleukin; ICAM1, intercellular adhesion molecule 1; MTH, mild therapeutic hypothermia; sFAS, soluble FAS; sFASL, soluble FAS-ligand; TNF-α, tumor necrosis factor alpha; TNF-R1, TNF-receptor 1; TRAIL-R2, TNF-related apoptosis-inducing ligand receptor 2; VCAM 1, vascular cell adhesion molecule 1</p> <p></p>

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Impact of mild therapeutic hypothermia on plasma markers of inflammation and apoptosis in non-resuscitated patients with acute myocardial infarction and cardiogenic shock

  • 期刊论文

  • 发表日期：

    2025年9月3日

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  • Anne Freund,
  • Petra Büttner,
  • Maria Buske,
  • Janine Pöss,
  • Hans-Josef Feistritzer,
  • Steffen Desch,
  • Georg Fuernau,
  • Holger Thiele

摘要

Background

Patients with cardiogenic shock (CS) following acute myocardial infarction (AMI) are challenged by pro-inflammatory and pro-apoptotic cellular processes. Little is known about the effect of mild therapeutic hypothermia (MTH) on these alterations.

Methods

Blood plasma from 40 patients included in the randomized SHOCK-COOL trial, which compared MTH (33 °C) versus no hypothermia in AMI-CS without cardiac arrest, from the first 3 days of hospitalization was used to determine interleukins (IL)-6 and IL-1β, tumor necrosis factor-alpha (TNF-α), intercellular and vascular soluble adhesion molecules (ICAM1 and VCAM1), TNF-receptor 1 (TNF-R1), TNF-related apoptosis-inducing ligand receptor 2 (TRAIL-R2), soluble FAS-ligand (sFASL), and soluble FAS (sFAS). These markers were also determined in 11 healthy controls.

Results

All markers except for TNF-R1 and sFASL reached their highest levels on day two or day three in both CS groups. IL-1β and sFAS reached higher maximum levels in the MTH group. IL-1β was higher in the MTH group on day 2 (+ 38%, p = 0.014) and on day 3 (+ 9%, p = 0.047), but the averaged group-wise individual maxima were comparable (24 [17–30] versus 20 [12–25], p = 0.138). The pro-apoptotic marker sFAS was also higher in the MTH group on day 2 (+ 85%, p = 0.004) and day 3 (+ 170%, p < 0.001); the averaged individual maxima were significantly higher in the MTH group (25 [15–38] versus 15 [10–21] ng/ml, p = 0.008).

Conclusions

Hypothermia in AMI-CS without cardiac arrest has no moderating effect on the assessed pro-inflammatory cytokines. However, sFAS showed significantly higher individual peak maxima in the MTH group indicating enhancement of pro-apoptotic mechanisms via the soluble FAS/FASL pathway.

Graphical Abstract

The graphical abstract was designed using illustrations from Servier Medical Art (https://creativecommons.org/licenses/by/4.0/). Abbreviations: AMI-CS, acute myocardial infarction complicated by cardiogenic shock; IL, interleukin; ICAM1, intercellular adhesion molecule 1; MTH, mild therapeutic hypothermia; sFAS, soluble FAS; sFASL, soluble FAS-ligand; TNF-α, tumor necrosis factor alpha; TNF-R1, TNF-receptor 1; TRAIL-R2, TNF-related apoptosis-inducing ligand receptor 2; VCAM 1, vascular cell adhesion molecule 1