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April 8, 2026Perfusion0 citationsOpen Access

Exploring weaning-related shock: Cardiac injury and overload, platelet-endothelial cell activation, and inflammatory response markers following ECMO decannulation

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LPLara CA PladetCKCarlos V. Elzo KraemerSNStefan Nierkens

Key Points

  • This research aims to understand the causes of weaning-related shock (WRS) following ECMO decannulation by analyzing plasma biomarker profiles.
  • Analyzed a prospective cohort of patients weaned from veno-arterial (V-A) or veno-venous (V-V) ECMO from 2011 to 2022.
  • Defined WRS based on a rise in vasoactive inotropic score and other clinical markers.
  • Assessed key plasma biomarkers before and after decannulation, stratifying by WRS occurrence and ECMO mode.
  • 24 out of 88 analyzed patients developed WRS after V-A ECMO.
  • Significant increases in NT-proBNP levels were observed in WRS patients post-decannulation compared to those without WRS.
  • No significant differences were noted in inflammation or platelet-endothelial cell activation markers over time.

Abstract

IntroductionMortality in patients receiving Extracorporeal Membrane Oxygenation (ECMO) is partly attributable to unanticipated hemodynamic instability after elective decannulation, termed weaning-related shock (WRS). This study explored the etiology of WRS by analyzing sequential plasma biomarker profiles.MethodsWe analyzed a prospective cohort (2011-2022) of consecutive patients weaned from veno-arterial (V-A) or veno-venous (V-V) ECMO to evaluate WRS occurrence. WRS was defined as a rise in Vasoactive Inotropic Score ≥15 points for >6 h with a positive fluid balance and lactate >2 mmol/L within 72 h post-decannulation. Shock etiology was adjudicated as hemorrhagic, cardiogenic, septic, or unclassifiable. Subsequently, key plasma biomarkers reflecting inflammation, platelet-endothelial cell activation, and cardiac injury and overload were assessed pre- and post-decannulation, stratified on WRS occurrence, apparent etiology, and ECMO mode.ResultsOut of 97 eligible individuals, 88 (91%) were analyzed (70 V-A and 18 V-V). Among them, 24 (27%) patients developed WRS, all of whom had received V-A ECMO. WRS was attributed to hemorrhagic, cardiogenic, septic, or unclassifiable causes in 0, 8, 8 and 8 cases, respectively. No differences were observed between groups in markers of inflammation or platelet-endothelial cell activation, nor in their trajectories over time. Conversely, NT-proBNP levels, but not HsTnI, increased significantly after decannulation in WRS patients compared to V-V or V-A ECMO patients without WRS (p = 0.003 and p = 0.02, respectively). NT-proBNP was also higher in these subjects prior to decannulation (all p < 0.001).ConclusionBiomarker responses following ECMO decannulation suggest cardiac overload as the primary driver of WRS, irrespective of clinical shock diagnosis.

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Cite This Study

Pladet et al. (2026) studied this question.

synapsesocial.com/papers/69d5f13674eaea4b11a7abd0https://doi.org/10.1177/02676591261439583
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