Determination of the Role of Oxygen in Suspected Acute Myocardial Infarction by Biomarkers (DETO2X-bio)
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|ClinicalTrials.gov Identifier: NCT02290080|
Recruitment Status : Completed
First Posted : November 13, 2014
Last Update Posted : December 11, 2017
Oxygen treatment is widely used in acutely ill patients, both pre-hospital and in hospital. The indication for oxygen is sometimes unquestionable, such as in many hypoxic patients, but in other situations its use is more of a practise and much less based on scientific evidence. In particular, oxygen treatment is routinely used in patients with a suspected heart attack and variably recommended in guidelines, despite very limited data supporting a beneficial effect. Indeed, a few studies even indicate that oxygen treatment might be harmful.
Immediate re-opening of the acutely blocked artery to the heart muscle is the treatment of choice to limit permanent injury. However, the sudden re-initiation of blood flow achieved with primary percutaneous coronary intervention (PCI), the reopening and stenting of the blocked vessel, can give rise to further endothelial and myocardial damage, so-called reperfusion injury. Ischemia and reperfusion associated myocardial injury (IR-injury) involves a wide range of pathological processes. Vascular leakage, activation of cell death programs, thrombocytes and white blood cells leading to extended inflammation and formation of clots are examples of those effects.
The role of oxygen treatment on these pathological processes, on the extent of IR-injury and the final infarct size in patients with acute myocardial infarctions (AMI) has not previously been studied.
In an ongoing national multicentre, randomized, registry based clinical trial, the DETO2X-AMI trial (NCT01787110), the effect of oxygen on morbidity and mortality in ACS patients is being investigated.
The present DETO2X-biomarkers study is a substudy of the DETO2X-AMI trial, evaluating the effect of oxygen treatment on biological systems involved in the pathogenesis of reversible and irreversible myocardial damage and cell death in ACS.
|Condition or disease||Intervention/treatment||Phase|
|Acute Myocardial Infarction (AMI) Acute Coronary Syndrome (ACS) ST Elevation (STEMI) Myocardial Infarction Ischemic Reperfusion Injury Non-ST Elevation (NSTEMI) Myocardial Infarction Angina, Unstable||Drug: Oxygen||Phase 3|
|Study Type :||Interventional (Clinical Trial)|
|Actual Enrollment :||175 participants|
|Intervention Model:||Parallel Assignment|
|Masking:||Single (Outcomes Assessor)|
|Official Title:||Determination of the Role of Oxygen on Mechanisms Involved in Ischemia-reperfusion Injury in Suspected Acute Myocardial Infarction by Biomarkers. A Sub Study to the DETO2X-AMI Trial.|
|Actual Study Start Date :||October 2014|
|Actual Primary Completion Date :||December 2015|
|Actual Study Completion Date :||December 2015|
For patients randomized to oxygen therapy:
see arm description
No Intervention: No oxygen
For patients randomized to withholding oxygen treatment
- Plasma concentration levels over time of biomarkers of oxidative stress, apoptosis, inflammation and platelet aggregation [ Time Frame: Within 8hours from baseline ]
Venous blood samples will be collected at baseline and 5-7 hours after baseline. Plasma concentration levels will be analyzed for Interleukin (IL)-6 [pg/mL], CRP [mg/L], Isoprostane [pg/mL], Soluble TNF receptor 1 [pg/mL], Soluble TNF receptor 2 [pg/mL], Soluble Fas [pg/mL], Soluble Fas ligand (pg/mL], MMP-2 [ng/mL], TIMP-2 [ng/mL], Soluble P-selectin [ng/mL], Platelet factor (PF)-4 [ng/mL], Beta-thromboglobulin [ng/mL].
Optional, flow cytometry will be used to analyse neutrophil integrin receptors (CD11b/CD18) and platelet-leukocyte aggregates (CD41a/CD11b/CD45) in whole blood. Whole blood will be fixated and red blood cells lysed before analysis.
To learn more about this study, you or your doctor may contact the study research staff using the contact information provided by the sponsor.
Please refer to this study by its ClinicalTrials.gov identifier (NCT number): NCT02290080
|Linköping University Hospital|
|Linköping, Sweden, 58191|
|Stockholm, Sweden, 11883|
|Principal Investigator:||Lennart Lennart, MD, PHD||Department of Medical and Health Sciences, Linköping University, and Department of Cardiology, University Hospital, 58185 Linköping, Sweden|