Mechanisms of Ultra-acute Hyperglycemia After Successful Resuscitation From Out-of-hospital Cardiac Arrest
Recruitment status was: Recruiting
The aim of the study is to describe the mechanisms of ultra-acute hyperglycemic response after return of spontaneous circulation (ROSC) in patients suffering out-of-hospital cardiac arrest. The investigators hypothesize that ischemia and reperfusion injury leads decreased secretion of insulin and glucose-like peptide 1 (GLP-1).
Two blood samples will be drawn: (1.) Immediately after ROSC and (2.) 60 minutes after first sample. Concentrations of glucose, insulin, glucagon and GLP-1 will be compared between the samples.
Metabolic profile will be compared between: (1.) diabetic and non-diabetic patients and (2.) survivors and non-survivors.
|Heart Arrest Cardiac Arrest|
|Study Design:||Observational Model: Cohort
Time Perspective: Prospective
- Change in level of insulin [ Time Frame: 60 minutes ]
- Change in level of glucagon [ Time Frame: 60 minutes ]
- Blood cortisol level [ Time Frame: 60 minutes after ROSC ]
- Blood interleukin-6 level [ Time Frame: 60 minutes after ROSC ]
- Change in blood glucose level [ Time Frame: 60 minutes ]
- Change in level of GLP-1 [ Time Frame: 60 minutes ]
Biospecimen Retention: Samples Without DNA
|Study Start Date:||November 2013|
|Estimated Primary Completion Date:||October 2015 (Final data collection date for primary outcome measure)|
Please refer to this study by its ClinicalTrials.gov identifier: NCT01968148
|Contact: Jouni Nurmi, MD, PhDemail@example.com|
|Helsinki Emergency Medical Services||Recruiting|
|Contact: Ari Salo, MD +35894711 firstname.lastname@example.org|
|Helsinki Area Helicopter Emergency Medical Services||Recruiting|
|Contact: Susanne Ångerman-Haasmaa, MD +358 50 5818015 email@example.com|
|Principal Investigator:||Jouni Nurmi, MD, PhD||Helsinki University Central Hospital|