[{"data":1,"prerenderedAt":-1},["ShallowReactive",2],{"trial:NCT02664831":3,"trial-entities:NCT02664831":124,"trial-summary:NCT02664831":128},{"id":4,"nct_id":4,"org_study_id":5,"brief_title":6,"official_title":7,"overall_status":8,"completion_date":9,"status_verified_date":10,"last_update_date":11,"start_date":12,"sponsor_name":13,"lead_sponsor_class":14,"has_dmc":15,"brief_summary":16,"detailed_description":17,"conditions":18,"keywords":23,"study_type":32,"primary_purpose":33,"phases":34,"enrollment_info":35,"interventions":38,"primary_outcomes":39,"secondary_outcomes":46,"sex":53,"minimum_age":54,"maximum_age":33,"healthy_volunteers":55,"eligibility_criteria":56,"std_ages":66,"locations":69,"central_contacts":106,"overall_officials":111,"references":115,"see_also_links":123},"NCT02664831","DBS1","Immunoinflammatory Response in Post Cardiac Arrest Syndrome (PCAS)","Immunoinflammatory and Metabolic Responses in Post Cardiac Arrest Syndrome (PCAS)","RECRUITING","2028-01","2025-07","2025-07-18","2016-01","MaineHealth","OTHER",false,"This is a prospective, observational study to investigate molecular mechanisms mediating the systemic inflammatory process, and changes to metabolism, and their impact on brain injury, survival, and functional outcomes after cardiac arrest. Investigators have shown that cardiac arrest induces changes in the numbers and properties of circulating immune cells, shifting the balance towards a pro-inflammatory phenotype and there is increased interest in the inflammatory pathways and the signaling mechanisms through which they are modulated. Participants will undergo blood sampling during 7 days following cardiac arrest, and analyses performed. Patient characteristics, clinical circumstances, and outcomes will be recorded and their associations with these inflammatory pathways characterized.","Preliminary evidence indicates that inter-individual variables such as immune cell activity and the production of pro-inflammatory factors may differentiate patients with the highest risk of poor neurological outcome, and may reveal novel therapeutic approaches based on promoting molecular pathways of inflammation-resolution and recovery to reduce the severity of hypoxic ischemic encephalopathy (HIE). Additionally, there are intrinsic, modifiable metabolic factors, such as the presence and metabolic activity of brown adipose tissue (BAT) that may modulate injury and recovery.\n\nComparative 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.\n\nPCAS metabolism:\n\nIT 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.\n\nIn these studies we will also investigate other actionable targets for new therapies.",[19,20,21,22],"Cardiac Arrest","Inflammation","Obesity","Hypoxic Ischemic Encephalopathy (HIE)",[24,25,26,27,28,29,30,31],"cardiac arrest","inflammation","immune","neuregulin","lymphocyte","neutrophil","brown adipose","HIE","OBSERVATIONAL",null,[],{"count":36,"type":37},400,"ESTIMATED",[],[40,43],{"measure":41,"description":41,"timeFrame":42},"Correlations between inflammatory markers and clinical outcomes","14 days",{"measure":44,"description":44,"timeFrame":45},"Correlations between inflammatory markers and biomarkers of neurological and cardiac injury","7 days",[47,49],{"measure":48,"description":48,"timeFrame":45},"Characterization of post-resuscitation inflammatory mechanisms and their regulators",{"measure":50,"description":51,"timeFrame":52},"Brown Fat activity","Correlations between 12,13 diHOME, blood glucose, and outcome","2 weeks","ALL","18 Years",true,{"inclusion":57,"exclusion":61,"raw_text":65},[58,59,60],"Aged 18 years or older","Admitted to the intensive care unit after cardiac arrest episode","Unresponsive after resuscitation",[62,63,64],"Moribund \u002F actively dying at the time of evaluation","Informed consent cannot be obtained within 24 hours of resuscitation","Hemoglobin less than 7.0 g\u002FdL, active high-volume bleeding, or requiring a transfusion","Inclusion Criteria:\n\n* Aged 18 years or older\n* Admitted to the intensive care unit after cardiac arrest episode\n* Unresponsive after resuscitation\n\nExclusion Criteria:\n\n* Moribund \u002F actively dying at the time of evaluation\n* Informed consent cannot be obtained within 24 hours of resuscitation\n* Hemoglobin less than 7.0 g\u002FdL, active high-volume bleeding, or requiring a transfusion",[67,68],"ADULT","OLDER_ADULT",[70],{"facility":71,"status":8,"city":72,"state":73,"zip":74,"country":75,"contacts":76,"geoPoint":103},"Maine Medical Center","Portland","Maine","04102","United States",[77,82,85,88,90,91,93,95,97,99,101],{"name":78,"role":79,"phone":80,"email":81},"David B Seder, MD","CONTACT","207-662-2179","david.seder@mainehealth.org",{"name":83,"role":79,"email":84},"Sergey Ryzhov, MD, PhD","Sergey.ryzhov@mainehealth.org",{"name":86,"role":87},"David J Gagnon, PharmD","SUB_INVESTIGATOR",{"name":78,"role":89},"PRINCIPAL_INVESTIGATOR",{"name":83,"role":89},{"name":92,"role":87},"Teresa May, DO",{"name":94,"role":87},"Richard Riker, MD",{"name":96,"role":87},"Angela M Leclerc, PA-C",{"name":98,"role":87},"Brittany Lachance, DO",{"name":100,"role":87},"Patrick T Mailloux, DO",{"name":102,"role":87},"Matthew Lynes, PhD",{"lat":104,"lon":105},43.65737,-70.2589,[107,108],{"name":78,"role":79,"phone":80,"email":81},{"name":109,"role":79,"email":110},"Sergey Ryzhov, PhD","sergey.ryzhov@mainehealth.org",[112,114],{"name":83,"affiliation":113,"role":89},"MaineHealth Institute for Research",{"name":78,"affiliation":13,"role":89},[116,120],{"pmid":117,"type":118,"citation":119},"38325139","RESULT","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\u002Fj.cyto.2024.156536. Epub 2024 Feb 6.",{"pmid":121,"type":118,"citation":122},"31237169","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\u002FJAHA.118.010874. Epub 2019 Jun 25.",[],{"nct_id":4,"conditions":125,"biomarkers":127},[19,126,20,21],"Hypoxic Ischemic Encephalopathy",[],{"nct_id":4,"found":55,"summary":129,"prompt_version":139},{"design":130,"status":131,"heading":132,"summary":133,"follow_up":134,"word_count":135,"commitments":136,"compensation":137,"drugs_mentioned":138},"This is an observational study planning to include 400 participants. It is not testing a specific treatment but rather observing how the body responds after cardiac arrest.","completed","Understanding Inflammation After Cardiac Arrest","This observational study is looking at how your body's immune system responds after a cardiac arrest. Researchers want to understand how inflammation (your body's response to injury or infection) and changes in metabolism (how your body uses energy) affect brain injury, survival, and recovery. They are particularly interested in how different types of white blood cells, like lymphocytes and neutrophils, behave. By studying blood samples taken over 7 days after cardiac arrest, they hope to find connections between these inflammatory responses and your clinical outcomes, including neurological (brain) and cardiac (heart) injury. This study is for adults aged 18 and older who have been admitted to the intensive care unit after a cardiac arrest and are unresponsive after resuscitation. The study is currently unclear on its recruitment status.","The study will look at correlations between inflammatory markers and clinical outcomes at 14 days, and neurological and cardiac injury biomarkers at 7 days.",128,"You would have blood samples taken during the 7 days following cardiac arrest. Your patient characteristics, clinical circumstances, and outcomes will also be recorded.","Not stated in the trial record.",[],"v2"]