Immunoinflammatory Response in Post Cardiac Arrest Syndrome (PCAS)
NCT ID: NCT02664831
Last Updated: 2025-07-18
Study Results
The study team has not published outcome measurements, participant flow, or safety data for this trial yet. Check back later for updates.
Basic Information
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RECRUITING
400 participants
OBSERVATIONAL
2016-01-31
2028-01-31
Brief Summary
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Detailed Description
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Comparative analysis showed that cardiac arrest survivors have more CD73+ lymphocytes compared to non-survivors. CD73 is the key enzyme in the generation of anti-inflammatory and immunosuppressive adenosine. We have also identified novel populations of neutrophils (CD14posCD16low and DEspR+) that had amplified response to inflammatory stimuli. The investigators hypothesize that individual variability in the expression and signaling profiles of white blood cells (lymphocytes, neutrophils, monocytes and macrophages) following resuscitation affects inflammation and is independently associated with neurological outcome. To test this hypothesis, investigators will determine levels of various immune cell populations at different time points in peripheral blood of patients. Characterization of blood circulating factors, clinical phenotypes, and neurological outcomes after cardiac arrest is a second aim of this project, with a focus on understanding the heterogeneity of cellular and humoral immune responses and how they relate to different clinical phenotypes of post-resuscitation syndrome.
PCAS metabolism:
IT is known that hyperglycemia is an independent risk factor for poor outcome after cardiac arrest, but it is not known if modification of hyperglycemia reduces this risk. Published studies have not demonstrated benefit with intensive insulin therapy. Our preliminary data suggest correlation between brown adipose tissue activity and good outcome. We have postulated that BAT may be activated by therapeutic hypothermia and may act as a glucose sink reducing the oxidative stress caused by hyperglycemia, and secondarily reducing injury to the brain, heart, and other organs.
In these studies we will also investigate other actionable targets for new therapies.
Conditions
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Study Design
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COHORT
PROSPECTIVE
Eligibility Criteria
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Inclusion Criteria
* Admitted to the intensive care unit after cardiac arrest episode
* Unresponsive after resuscitation
Exclusion Criteria
* Informed consent cannot be obtained within 24 hours of resuscitation
* Hemoglobin less than 7.0 g/dL, active high-volume bleeding, or requiring a transfusion
18 Years
ALL
Yes
Sponsors
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National Institute of General Medical Sciences (NIGMS)
NIH
National Heart, Lung, and Blood Institute (NHLBI)
NIH
MaineHealth
OTHER
Responsible Party
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David B. Seder MD
Chair, Department of Critical Care Services
Principal Investigators
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Sergey Ryzhov, MD, PhD
Role: PRINCIPAL_INVESTIGATOR
MaineHealth Institute for Research
David B Seder, MD
Role: PRINCIPAL_INVESTIGATOR
MaineHealth
Locations
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Maine Medical Center
Portland, Maine, United States
Countries
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Central Contacts
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Facility Contacts
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References
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deKay JT, Chepurko E, Chepurko V, Knudsen L, Lord C, Searight M, Tsibulnikov S, Robich MP, Sawyer DB, Gagnon DJ, May T, Riker R, Seder DB, Ryzhov S. Delayed CCL23 response is associated with poor outcomes after cardiac arrest. Cytokine. 2024 Apr;176:156536. doi: 10.1016/j.cyto.2024.156536. Epub 2024 Feb 6.
Ryzhov S, May T, Dziodzio J, Emery IF, Lucas FL, Leclerc A, McCrum B, Lord C, Eldridge A, Robich MP, Ichinose F, Sawyer DB, Riker R, Seder DB. Number of Circulating CD 73-Expressing Lymphocytes Correlates With Survival After Cardiac Arrest. J Am Heart Assoc. 2019 Jul 2;8(13):e010874. doi: 10.1161/JAHA.118.010874. Epub 2019 Jun 25.
Other Identifiers
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DBS1
Identifier Type: -
Identifier Source: org_study_id
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