Acute Myocardial Infarction (AMI)Phase 3DETO2X-bioNCT02290080
Determination of the Role of Oxygen in Suspected Acute Myocardial Infarction by Biomarkers
A Phase 3 study testing Oxygen in people with Acute Myocardial Infarction (AMI) and Acute Coronary Syndrome (ACS), run by Karolinska Institutet at 2 sites in Sweden.
Trial summary
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. Read more about this study
- Who is it for?
- Ages 30 years and older
- Conditions the study is for
- Acute Myocardial Infarction (AMI), Acute Coronary Syndrome (ACS), ST Elevation (STEMI) Myocardial Infarction
- What is being tested?
- Oxygen
- Could I receive a placebo?
- No, everyone receives an active treatment
- How many people
- 175 participants
- Where
- 2 sitesSweden
- Study dates
- Oct 2014to Dec 2015
- Phase
- Phase 3
- Are there results?
- None posted in the registry
Key requirements
Who can take part, as listed by the sponsor. Only the study team can confirm whether you are eligible, so take this list to your doctor.
- Ages 30 years and older
- All sexes
- No healthy volunteers
- Adult, Older adult
Who may be able to join
- symptoms (chest pain, dyspnea) indicating acute myocardial ischemia within the last 6 hours
- ECG changes (ST-segment elevation ≥ 2 mm V1-V4, or ≥ 1 mm in other leads, ST-segment depression >1 mm in any lead, negative T-wave in leads V2-V6, pathological Q-wave in at least 2 adjacent leads), left bundle branch block
- and/or elevated levels of cardiac troponin levels in the emergency department indicating acute myocardial ischemia
- oxygen saturation ≥90% (pulse oximeter)
- age ≥30
Who cannot join
- unwillingness to participate
- inability to comprehend given information
- continuous oxygen delivery at home prior to inclusion
- cardiac arrest prior to inclusion
Trial locations and contacts
2 sites in 1 country.
Sweden2 sites
Linköping University Hospital
Linköping, 58191
Södersjukhuset
Stockholm, 11883
About this study
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.
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.
Read more
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.
Read the detailed description
The DETermination of the role of OXygen i suspected Acute Myocardial Infarction (DETO2X-AMI) trial (NCT01787110), an ongoing multicentre, randomized, registry based clinical trial, is investigating the effect of oxygen on morbidity and mortality in ACS patients.
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.
AIMS
To evaluate the effect of oxygen treatment on markers of oxidative stress in ACS patients. To assess the effect of oxygen treatment on soluble markers of apoptosis, MMPs and TIMPs in ACS patients.
To study the effect of oxygen treatment on systemic inflammatory activity and leukocyte activation.
To evaluate the effect of oxygen treatment on platelet activation in ACS patients.
HYPOTHESIS
The main hypothesis is that oxygen treatment enhances oxidative stress, systemic inflammation, and markers of apoptosis and MMPs in ACS patients, thereby potentially increasing myocardial damage and cell death, and worsening the prognosis.
STUDY DESIGN and POPULATION
The present study is a biomarker substudy of the DETO2X-AMI trial. The design and population of the DETO2X-AMI trial has previously been described in detail (NCT01787110). All patients included in the DETO2X-AMI trial at Södersjukhuset Stockholm and University Hospital Linköping during the study period specified below are also eligible to be included in the DETO2X-biomarkers study. We intend to include 150 patients with suspected AMI.
STUDY PLAN
All study participants in the DETO2X-biomarkers study have been allocated to receive oxygen (6L/min) or no oxygen treatment as part of the DETO2X-AMI trial. To a variable degree, the participants have already started this treatment when entering the biomarker substudy. Baseline blood samples will be collected as soon as possible after inclusion in the DETO2X-AMI trial, preferably prior to initiation of oxygen treatment. Study subjects will then continue to receive their allocated DETO2X-AMI study treatment. A second set of blood samples will be collected 5-7 hours after randomisation in the DETO2X-AMI trial, and always prior to discontinuation of oxygen treatment.
ANALYSIS of blood samples
As a marker of oxidative stress, plasma-isoprostane will be measured using gas chromatography combined with a massspectrometric detector. Soluble markers of apoptosis, MMP-2 and TIMP-2 will be analyzed by Luminex. Plasma inflammatory markers (C-reactive protein (CRP) and interleukin (IL)-6), myeloperoxidase, and markers of platelet activation will be analysed by ELISA. Flow cytometry will be used to analyse neutrophil integrin receptors and platelet-leukocyte aggregates in whole blood. Whole blood will be fixated and red blood cells lysed before analysis.
EFFICACY OUTCOME
To determine the effect of oxygen treatment on biomarkers of oxidative stress, apoptosis, matrix metalloproteinases, markers of inflammation, and leukocyte and platelet activation in patients admitted to hospital due to suspected AMI.
SUMMARY
The DETO2X-AMI trial will address the effects of oxygen on morbidity and mortality in ACS patients. The present DETO2X-biomarkers substudy is evaluating effects of oxygen treatment on biological systems involved in the pathogenesis of reversible and irreversible myocardial damage and cell death in ACS and may add essential new knowledge to the mechanistics of ischaemic myocardial injury.
- Conditions
- Acute Myocardial Infarction (AMI), Acute Coronary Syndrome (ACS), ST Elevation (STEMI) Myocardial Infarction, Ischemic Reperfusion Injury, Non-ST Elevation (NSTEMI) Myocardial Infarction, Angina, Unstable
- Being tested
- Oxygen
- Keywords
- acute myocardial infarction (AMI), acute coronary syndrome (ACS), ST-segment elevation myocardial infarction (STEMI), Non ST-segment elevation myocardial infarction (NSTEMI), Ischemic Reperfusion injury (IR-injury), Biomarkers, Oxygen, Apoptosis, Fluorescence-activated cell sorting (FACS), Flow cytometry, Matrix metalloproteinase (MMP)
- Medical subject headings
- Acute Coronary Syndrome, ST Elevation Myocardial Infarction, Myocardial Infarction, Non-ST Elevated Myocardial Infarction, Angina, Unstable
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
OxygenDrug
see arm description
| Study group | Role | What they receive |
|---|---|---|
| Oxygen | Experimental | For patients randomized to oxygen therapy:
* 6 L/min of oxygen delivered by oxymask® started immediately after inclusion of the ambulance service or in the emergency department given continuously for 6-12 hours (at least 6 hours)
* all patients receive standard acute coronary syndrome treatment including reperfusion strategies Receives: Drug: Oxygen |
| No oxygen | No intervention | For patients randomized to withholding oxygen treatment * no oxygen is administered at any time as long as the oxygen saturation is ≥90% on pulse oximeter (repetitive checks are performed) * all patients receive standard acute coronary syndrome treatment including reperfusion strategies * observation duration 12 hours |
What is being measured
The primary outcome is the main question the study is designed to answer.
Plasma concentration levels over time of biomarkers of oxidative stress, apoptosis, inflammation and platelet aggregation
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.
Measured: Within 8hours from baseline
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted13 Nov 2014 (estimated)
- Study startOct 2014
- Primary completionDec 2015
- Study completionDec 2015
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (9)Papers the sponsor has linked to this study.
- Other trials for Acute Myocardial Infarction (AMI)Studies of the same condition, open and under way.
- More trials run by Karolinska InstitutetThe sponsor's other registered studies.
- What the trial phases meanHow a treatment moves from first tests in people to approval.
More details
For doctors and researchers: how the study is designed, who runs it, and its registry IDs.
Study design
- Study type
- Interventional
- Phase
- Phase 3
- Primary purpose
- Treatment
- Allocation
- Randomised
- Intervention model
- Parallel groups
- Masking
- Single blind
- Who is masked
- Outcomes assessor
- Enrolment
- 175 participants (actual)
Sponsor and investigators
- Lead sponsor
- Karolinska Institutet
- Sponsor type
- University, hospital or other
- Collaborators
- University Hospital, Linkoeping
- Responsible party
- Principal investigator, Leif Svensson, Karolinska Institutet
- Investigators
- Lennart Lennart, MD, PHD, Principal investigator, Department of Medical and Health Sciences, Linköping University, and Department of Cardiology, University Hospital, 58185 Linköping, Sweden
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT02290080
- Sponsor's protocol ID
- DETO2X-biomarkers 2012/287-12
- Acronym
- DETO2X-bio
- Status last verified
- Dec 2017
- First submitted
- 8 Nov 2014
- Last updated
- 11 Dec 2017
- Results posted
- No
- Data monitoring committee
- No
- FDA-regulated drug
- No
- FDA-regulated device
- No
Publications
Cabello JB, Burls A, Emparanza JI, Bayliss S, Quinn T. Oxygen therapy for acute myocardial infarction. Cochrane Database Syst Rev. 2013 Aug 21;(8):CD007160. doi: 10.1002/14651858.CD007160.pub3.
PubMed 23963794Yellon DM, Hausenloy DJ. Myocardial reperfusion injury. N Engl J Med. 2007 Sep 13;357(11):1121-35. doi: 10.1056/NEJMra071667. No abstract available.
PubMed 17855673Ekstrom M, Eriksson P, Tornvall P. Vaccination, a human model of inflammation, activates systemic inflammation but does not trigger proinflammatory gene expression in adipose tissue. J Intern Med. 2008 Dec;264(6):613-7. doi: 10.1111/j.1365-2796.2008.01998.x. No abstract available.
PubMed 19017180Eltzschig HK, Eckle T. Ischemia and reperfusion--from mechanism to translation. Nat Med. 2011 Nov 7;17(11):1391-401. doi: 10.1038/nm.2507.
PubMed 22064429Shuvy M, Atar D, Gabriel Steg P, Halvorsen S, Jolly S, Yusuf S, Lotan C. Oxygen therapy in acute coronary syndrome: are the benefits worth the risk? Eur Heart J. 2013 Jun;34(22):1630-5. doi: 10.1093/eurheartj/eht110. Epub 2013 Apr 3.
PubMed 23554440Piper HM, Meuter K, Schafer C. Cellular mechanisms of ischemia-reperfusion injury. Ann Thorac Surg. 2003 Feb;75(2):S644-8. doi: 10.1016/s0003-4975(02)04686-6.
PubMed 12607706Hofmann R, James SK, Svensson L, Witt N, Frick M, Lindahl B, Ostlund O, Ekelund U, Erlinge D, Herlitz J, Jernberg T. DETermination of the role of OXygen in suspected Acute Myocardial Infarction trial. Am Heart J. 2014 Mar;167(3):322-8. doi: 10.1016/j.ahj.2013.09.022. Epub 2013 Dec 19.
PubMed 24576515Andell P, James S, Ostlund O, Yndigegn T, Sparv D, Pernow J, Jernberg T, Lindahl B, Herlitz J, Erlinge D, Hofmann R. Oxygen therapy in suspected acute myocardial infarction and concurrent normoxemic chronic obstructive pulmonary disease: a prespecified subgroup analysis from the DETO2X-AMI trial. Eur Heart J Acute Cardiovasc Care. 2020 Dec;9(8):984-992. doi: 10.1177/2048872619848978. Epub 2019 May 13.
PubMed 31081342Hofmann R, Tornvall P, Witt N, Alfredsson J, Svensson L, Jonasson L, Nilsson L. Supplemental oxygen therapy does not affect the systemic inflammatory response to acute myocardial infarction. J Intern Med. 2018 Apr;283(4):334-345. doi: 10.1111/joim.12716. Epub 2017 Dec 11.
PubMed 29226465
Study at a glance
From the registry record, last updated by the sponsor on 11 Dec 2017. Recruitment status is as the sponsor reported it: confirm with the study team.
- 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.
- ClinicalTrials.gov ID
- NCT02290080
- Acronym / sponsor ID
- DETO2X-bio / DETO2X-biomarkers 2012/287-12
- Conditions
- Acute Myocardial Infarction (AMI), Acute Coronary Syndrome (ACS), ST Elevation (STEMI) Myocardial Infarction, Ischemic Reperfusion Injury, Non-ST Elevation (NSTEMI) Myocardial Infarction, Angina, Unstable
- Keywords
- acute myocardial infarction (AMI), acute coronary syndrome (ACS), ST-segment elevation myocardial infarction (STEMI), Non ST-segment elevation myocardial infarction (NSTEMI), Ischemic Reperfusion injury (IR-injury), Biomarkers, Oxygen, Apoptosis
- Phase
- Phase 3
- Study type
- Interventional
- Recruitment status
- Completed
- Enrolment
- 175 participants (actual)
- Lead sponsor
- Karolinska InstitutetUniversity, hospital or other
- Collaborators
- University Hospital, Linkoeping
- Study start
- Oct 2014 (actual)
- Primary completion
- Dec 2015 (actual)
- Study completion
- Dec 2015 (actual)
- First posted
- 13 Nov 2014 (estimated)
- Results
- Not posted in the source record
Clinical summary
The research question as the sponsor registered it. This describes what the study plans to test, not what it found.
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.
Detailed description
The DETermination of the role of OXygen i suspected Acute Myocardial Infarction (DETO2X-AMI) trial (NCT01787110), an ongoing multicentre, randomized, registry based clinical trial, is investigating the effect of oxygen on morbidity and mortality in ACS patients.
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.
AIMS
To evaluate the effect of oxygen treatment on markers of oxidative stress in ACS patients. To assess the effect of oxygen treatment on soluble markers of apoptosis, MMPs and TIMPs in ACS patients.
To study the effect of oxygen treatment on systemic inflammatory activity and leukocyte activation.
To evaluate the effect of oxygen treatment on platelet activation in ACS patients.
HYPOTHESIS
The main hypothesis is that oxygen treatment enhances oxidative stress, systemic inflammation, and markers of apoptosis and MMPs in ACS patients, thereby potentially increasing myocardial damage and cell death, and worsening the prognosis.
STUDY DESIGN and POPULATION
The present study is a biomarker substudy of the DETO2X-AMI trial. The design and population of the DETO2X-AMI trial has previously been described in detail (NCT01787110). All patients included in the DETO2X-AMI trial at Södersjukhuset Stockholm and University Hospital Linköping during the study period specified below are also eligible to be included in the DETO2X-biomarkers study. We intend to include 150 patients with suspected AMI.
STUDY PLAN
All study participants in the DETO2X-biomarkers study have been allocated to receive oxygen (6L/min) or no oxygen treatment as part of the DETO2X-AMI trial. To a variable degree, the participants have already started this treatment when entering the biomarker substudy. Baseline blood samples will be collected as soon as possible after inclusion in the DETO2X-AMI trial, preferably prior to initiation of oxygen treatment. Study subjects will then continue to receive their allocated DETO2X-AMI study treatment. A second set of blood samples will be collected 5-7 hours after randomisation in the DETO2X-AMI trial, and always prior to discontinuation of oxygen treatment.
ANALYSIS of blood samples
As a marker of oxidative stress, plasma-isoprostane will be measured using gas chromatography combined with a massspectrometric detector. Soluble markers of apoptosis, MMP-2 and TIMP-2 will be analyzed by Luminex. Plasma inflammatory markers (C-reactive protein (CRP) and interleukin (IL)-6), myeloperoxidase, and markers of platelet activation will be analysed by ELISA. Flow cytometry will be used to analyse neutrophil integrin receptors and platelet-leukocyte aggregates in whole blood. Whole blood will be fixated and red blood cells lysed before analysis.
EFFICACY OUTCOME
To determine the effect of oxygen treatment on biomarkers of oxidative stress, apoptosis, matrix metalloproteinases, markers of inflammation, and leukocyte and platelet activation in patients admitted to hospital due to suspected AMI.
SUMMARY
The DETO2X-AMI trial will address the effects of oxygen on morbidity and mortality in ACS patients. The present DETO2X-biomarkers substudy is evaluating effects of oxygen treatment on biological systems involved in the pathogenesis of reversible and irreversible myocardial damage and cell death in ACS and may add essential new knowledge to the mechanistics of ischaemic myocardial injury.
Study design
- Primary purpose
- Treatment
- Allocation
- Randomised
- Intervention model
- Parallel groups
- Masking
- Single blind (outcomes assessor)
- Number of arms
- 2
| Arm | Type | Receives |
|---|---|---|
| Oxygen | Experimental | Drug: OxygenFor patients randomized to oxygen therapy: * 6 L/min of oxygen delivered by oxymask® started immediately after inclusion of the ambulance service or in the emergency department given continuously for 6-12 hours (at least 6 hours) * all patients receive standard acute coronary syndrome treatment including reperfusion strategies |
| No oxygen | No intervention | –For patients randomized to withholding oxygen treatment * no oxygen is administered at any time as long as the oxygen saturation is ≥90% on pulse oximeter (repetitive checks are performed) * all patients receive standard acute coronary syndrome treatment including reperfusion strategies * observation duration 12 hours |
Who may qualify
- Ages
- 30 years and older
- Sex
- All
- Healthy volunteers
- Not accepted
- Age groups
- Adult, Older adult
Key inclusion criteria (5 listed)
- symptoms (chest pain, dyspnea) indicating acute myocardial ischemia within the last 6 hours
- ECG changes (ST-segment elevation ≥ 2 mm V1-V4, or ≥ 1 mm in other leads, ST-segment depression >1 mm in any lead, negative T-wave in leads V2-V6, pathological Q-wave in at least 2 adjacent leads), left bundle branch block
- and/or elevated levels of cardiac troponin levels in the emergency department indicating acute myocardial ischemia
- oxygen saturation ≥90% (pulse oximeter)
- age ≥30
Key exclusion criteria (4 listed)
- unwillingness to participate
- inability to comprehend given information
- continuous oxygen delivery at home prior to inclusion
- cardiac arrest prior to inclusion
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Interventions
| Intervention | Type | Arms |
|---|---|---|
| Oxygensee arm description | Drug | Oxygen |
Primary outcome
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.
Results and safety
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 11 Dec 2017.
- Background: PubMed 23963794Cabello JB, Burls A, Emparanza JI, Bayliss S, Quinn T. Oxygen therapy for acute myocardial infarction. Cochrane Database Syst Rev. 2013 Aug 21;(8):CD007160. doi: 10.1002/14651858.CD007160.pub3.
- Background: PubMed 17855673Yellon DM, Hausenloy DJ. Myocardial reperfusion injury. N Engl J Med. 2007 Sep 13;357(11):1121-35. doi: 10.1056/NEJMra071667. No abstract available.
- Background: PubMed 19017180Ekstrom M, Eriksson P, Tornvall P. Vaccination, a human model of inflammation, activates systemic inflammation but does not trigger proinflammatory gene expression in adipose tissue. J Intern Med. 2008 Dec;264(6):613-7. doi: 10.1111/j.1365-2796.2008.01998.x. No abstract available.
- Background: PubMed 22064429Eltzschig HK, Eckle T. Ischemia and reperfusion--from mechanism to translation. Nat Med. 2011 Nov 7;17(11):1391-401. doi: 10.1038/nm.2507.
- Background: PubMed 23554440Shuvy M, Atar D, Gabriel Steg P, Halvorsen S, Jolly S, Yusuf S, Lotan C. Oxygen therapy in acute coronary syndrome: are the benefits worth the risk? Eur Heart J. 2013 Jun;34(22):1630-5. doi: 10.1093/eurheartj/eht110. Epub 2013 Apr 3.
- Background: PubMed 12607706Piper HM, Meuter K, Schafer C. Cellular mechanisms of ischemia-reperfusion injury. Ann Thorac Surg. 2003 Feb;75(2):S644-8. doi: 10.1016/s0003-4975(02)04686-6.
- Results publication: PubMed 24576515Hofmann R, James SK, Svensson L, Witt N, Frick M, Lindahl B, Ostlund O, Ekelund U, Erlinge D, Herlitz J, Jernberg T. DETermination of the role of OXygen in suspected Acute Myocardial Infarction trial. Am Heart J. 2014 Mar;167(3):322-8. doi: 10.1016/j.ahj.2013.09.022. Epub 2013 Dec 19.
- Derived from this study: PubMed 31081342Andell P, James S, Ostlund O, Yndigegn T, Sparv D, Pernow J, Jernberg T, Lindahl B, Herlitz J, Erlinge D, Hofmann R. Oxygen therapy in suspected acute myocardial infarction and concurrent normoxemic chronic obstructive pulmonary disease: a prespecified subgroup analysis from the DETO2X-AMI trial. Eur Heart J Acute Cardiovasc Care. 2020 Dec;9(8):984-992. doi: 10.1177/2048872619848978. Epub 2019 May 13.
- Derived from this study: PubMed 29226465Hofmann R, Tornvall P, Witt N, Alfredsson J, Svensson L, Jonasson L, Nilsson L. Supplemental oxygen therapy does not affect the systemic inflammatory response to acute myocardial infarction. J Intern Med. 2018 Apr;283(4):334-345. doi: 10.1111/joim.12716. Epub 2017 Dec 11.
- Homepage of the DETO2X trialLink provided by the sponsor.
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Referral and contact
AzTrials does not enrol participants or take referrals. Contact the study team or a site listed below; they decide who can take part. This study is not recruiting at the moment.
Lennart Lennart, MD, PHD principal investigator
Department of Medical and Health Sciences, Linköping University, and Department of Cardiology, University Hospital, 58185 Linköping, Sweden
2 sites in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
A Phase 3 study testing Oxygen in people with Acute Myocardial Infarction (AMI) and Acute Coronary Syndrome (ACS), run by Karolinska Institutet at 2 sites in Sweden.
The full registered description is in the About this study section and the official record.
Who may be eligible to take part?
The sponsor lists 5 inclusion and 4 exclusion criteria. Eligibility is decided by the study team after screening, so read the full criteria and contact a listed site.
Is this clinical trial currently recruiting?
The record says: finished, as of the sponsor's last update on 11 Dec 2017. Status can change between updates, so confirm with the study contact before making plans.
Where is the study taking place?
The record lists 2 sites in Sweden. Whether a site is taking part right now should be confirmed with that site. See every site.
What are the possible benefits and risks?
They depend on the study and the treatment, and no study can promise a benefit. The study team explains the known risks during informed consent, before anyone joins; the record itself does not list them.
What does this phase mean?
Phase 3 studies compare the treatment with the current standard treatment or a placebo in a large group, to confirm how well it works and watch for side effects.
Not every study follows the same path, and some studies (observational studies, device studies) have no phase.
Are results available for this study?
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
How can a doctor refer a patient or contact the research team?
The record lists no contact. The official record names the sponsor, who can be asked directly. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
Plasma concentration levels over time of biomarkers of oxidative stress, apoptosis, inflammation and platelet aggregation (time frame: Within 8hours from baseline). It is what the study was designed to measure, not a finding.
Where can I read the original study information?
On the ClinicalTrials.gov record for NCT02290080, which also lists 9 linked publications.
Does a listing mean the treatment is approved or proven to work?
No. A listing means the study is registered. It does not show that the treatment is safe, works, or is approved by a regulator.
How often is this information updated?
AzTrials copies changed records from ClinicalTrials.gov every night and reloads the whole registry every week. The sponsor last updated this record on 11 Dec 2017; AzTrials last refreshed its copy on 8 Nov 2026.