Acute Myocardial InfarctionPhase 2NCT01172171
The Effect of Melatonin on Ischemia-reperfusion Injury Following Acute Myocardial Infarction
A Phase 2 study testing Melatonin, N-acetyl-5-methoxytryptamine and Isotonic saline, Natrium chloride in people with Acute Myocardial Infarction and Ischemia-reperfusion Injury, run by Herlev Hospital at 2 sites in Denmark.
Trial summary
In Denmark, 12.000 people a year, is struck by acute myocardial infarction. A third of these cannot be saved before treatment is possible. Despite quick and effective reperfusion of the coronary arteries using PCI (Percutaneous Coronary Intervention) after an acute ST-elevation myocardial infarction, substantial… Read more about this study
- Who is it for?
- Ages 18 years and older
- Conditions the study is for
- Acute Myocardial Infarction, Ischemia-reperfusion Injury
- What is being tested?
- Melatonin, N-acetyl-5-methoxytryptamine and Isotonic saline, Natrium chloride
- Type of treatment
- Injection or infusion
- Could I receive a placebo?
- Yes, some participants may receive a placebo
- How many people
- 41 participants
- Where
- 2 sitesDenmark
- Study dates
- Jun 2013to Dec 2016
- Phase
- Phase 2
- 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 18 years and older
- All sexes
- No healthy volunteers
- Adult, Older adult
Who may be able to join
- Adults who are able to give informed consent
- 1 significant coronary occlusion (>2mm) with TIMI 0-1 expected to undergo PCI.
- The occlusion must be ECG-verified with new ST-elevations ≥ 0.2 mV in V2-V3 and/or ≥ 0.1 in the other leads or a new onset left bundle branch block.
- Having onset of symptoms of qualifying AMI and undergo PCI within 6 hours.
- If the patients do not fulfill the ECG inclusion criteria they can still be included if the primary PCI reveals an acute coronary occlusion (>2mm) with TIMI 0-1.
Who cannot join
- Patients with prior myocardial infarction
- more than one significant occlusion
- prehospital thrombolysis
- known history of renal failure
- history of autoimmune diseases
- pregnancy, fertile women or breastfeeding
Show all 13Show fewer
- severe concurrent illness with reduced short-term prognosis
- pacemaker
- claustrophobia
- cardiogenic shock
- metals in the body
- atrial fibrillation
- BMI ≥ 40.
Trial locations and contacts
2 sites in 1 country.
Denmark2 sites
Aalborg University Hospital
Aalborg, Aalborg, 9000
Odense University Hospital
Odense, Odense, 5000
About this study
Official title: Intracoronary Injection of Melatonin for Patients With ST-elevation Myocardial Infarction: a Placebo Controlled Randomized Study
In Denmark, 12.000 people a year, is struck by acute myocardial infarction. A third of these cannot be saved before treatment is possible.
Despite quick and effective reperfusion of the coronary arteries using PCI (Percutaneous Coronary Intervention) after an acute ST-elevation myocardial infarction, substantial morbidity and mortality remain. Infarct size is an important determinant of the short-and long-term outcome after acute myocardial infarction. The most widely used and most effective proven therapy to limit infarct size is the early reperfusion induced by or PCI.
Read more
Although beneficial in terms of myocardial salvage, reperfusion itself may contribute to additional damage of the myocardium; the damage due to the combined processes is known as "ischemia-reperfusion injury". The pathogenesis of myocardial ischemia-reperfusion injury is a multifactorial process involving the interaction of multiple mechanisms. Numerous studies indicate that there are three pivotal factors in the pathogenesis of ischemia-reperfusion injury: elevated oxidative damage, depressed energy metabolism, and altered calcium homeostasis.
Partially reduced species of oxygen, including the superoxide anion radical, hydroxyl radical, and hydrogen peroxide, are generated intracellularly as by-product of oxygen metabolism. These reactive oxygen species cause peroxidation af membrane lipids, denaturation of proteins, and modification of DNA, all of which ultimately can lead to cell death. In mammals, cell damage induced by partially reduced oxygen species can also initiate local inflammatory responses, which then lead to further oxidant-mediated tissue injury.
Melatonin is mainly known for its role as an endogenously produced circadian hormone.
For the last twenty years, increasing evidence has proven melatonin to be a very potent direct and indirect antioxidant.
Recent experimental studies have documented the beneficial effects of melatonin in reducing tissue damage and limiting cardiac pathophysiology in models of experimental ischemia-reperfusion.
Primary hypothesis: Melatonin given to patients undergoing PCI can reduce the myocardial damage sustained by ischemia-reperfusion.
Read the detailed description
Purpose The purpose of this Ph.D study is to examine the antioxidative effect of melatonin in relation to ischemia-reperfusion injury.
The investigators wish to examine to which extend melatonin administered to patients undergoing primary PCI for acute myocardial infarction will reduce the damage of the myocardium caused by ischemia-reperfusion injury and thereby hopefully improve the clinical outcome.
Theory and hypotheses Because there is strong evidence that free radicals contribute to post-ischemic injury, antioxidant enzyme therapy could potentially be extremely effective in reducing the cellular damage. In reality, however, the usefulness of this therapy is limited by a number of factors, in particular the ability of the antioxidants to penetrate the cell membrane and to scavenge free radicals in situ. Fortunately, this limitation can, in part, be addressed with the use of melatonin, a potent indirect and direct free radical scavenger that easily diffuses through the cell membrane to exert its antioxidant effects in all compartments of the cell. Indeed, in contrast to the partial of distribution of other antioxidants, such as vitamin C or E, the melatonin distributes it readily in all subcellular compartments owing to its double-solubility in both, aqueous and in lipid environment. Several recent publications present evidence that the newly discovered antioxidant melatonin has significant protective actions against the cardiac damage such as occurs during ischemia-reperfusion injury.
Primary hypothesis: Melatonin given to patients undergoing PCI can reduce the myocardial damage sustained by ischemia-reperfusion.
Inclusion:
- Adults who are able to give informed consent
- 1 significant coronary occlusion (>2mm) with TIMI 0-1 expected to undergo PCI.
- ECG criteria: The occlusion must be ECG-verified with new ST-elevations ≥ 0.2 mV in V2-V3 and/or ≥ 0.1 in the other leads or with a new onset left bundle branch block.
- Having onset of symptoms of qualifying AMI and undergo PCI within 6 hours.
- If the patients do not fulfill the ECG inclusion criteria they can still be included if the primary PCI reveals an acute coronary occlusion (>2mm) with TIMI 0-1.
Exclusion: Patients with prior myocardial infarction, more than one significant occlusion, prehospital thrombolysis, known history of renal failure, history of autoimmune diseases, pregnancy, fertile women or breastfeeding, severe concurrent illness with reduced short-term prognosis, pacemaker, claustrophobia, cardiogenic shock, metals in the body, atrial fibrillation, BMI ≥ 40.
Intervention: The STEMI patient with 1 significant occlusion undergoing PCI less than 6 hours from onset of symptoms will be randomized to intracoronary injection of either melatonin or placebo(saline). The melatonin or placebo will be given as a bolus of 10 ml in relation to PCI, as soon as the occlusion is removed. Immediately after the bolus is given, a solution of 490 ml of either placebo (saline) or 0,1 mg/ml melatonin (49 mg melatonin)will be given intravenously over 6 hours (80 ml/hour).
Primary end point: MRI of the heart at day 4 (+/- 1 day) after the PCI procedure to determine myocardial salvage index.
Secondary end point:
- To determine whether melatonin treatment reduces infarct size as determined by the concentration of high sensitive TnT or high-sensitive TnI and Creatinin Kinase Myocardial Band (CK-MB)(area under the curve) in the blood, measured daily for the first 4 days after AMI.
- the concentration of plasma melatonin after PCI
- the concentration of oxidative markers 24 hours after PCI
Clinical events occurring within the first 90 days after surgery; death, sustained ventricular arrhythmias, resuscitation from cardiac arrest, cardiogenic shock, heart failure, major bleedings, stroke, need for revascularization, recurrent ischemia, re-infarctions and re-hospitalization.
Design: Randomized, double-blind, placebo-controlled interventional study.
Method: Patients who meet the criteria of inclusion will be randomized to intra-coronary injection plus intravenous infusion of melatonin or placebo. The bolus will be given just after the opening of the vessel (TIMI ≥ 2) . Hs-Troponin T/I and CK-MB will be measured in a blood sample taken 1 hour, 6 hours, 24 hours, 48 hours, 72 hours and 96 hours after the PCI procedure. At day 4 after PCI, the patients will undergo MRI of the heart focusing on infarct size and area at risk.
Patient number: Statistical power analysis shows that with a type 1 error of 5% and a type 2 error of 20%, mean at 9,63 and the SD with MRI of 0,16, one should be able to detect a difference in infarct size of 25% between the two groups, when including 2x17 patients in each group. The investigators are including 2x 20 patients.
Safety: The experiments are considered to be of no risk or discomfort for the patients. Both the intervention group and the placebo group are operated by current clinical guidelines.
- Being tested
- Melatonin, N-acetyl-5-methoxytryptamine, Isotonic saline, Natrium chloride
- Keywords
- Ischemia-reperfusion injury, Acute Myocardial Infarction, Intracoronary melatonin
- Medical subject headings
- Reperfusion Injury
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
Melatonin, N-acetyl-5-methoxytryptamineDrug
The investigators will give the randomized patients 10 ml of 0,1 mg/ml melatonin intracoronarily and 490 ml of 0,1 mg/ml (49 mg) melatonin.
Isotonic saline, Natrium chlorideDrug
The randomized patients will be given 10 ml of isotonic saline intracoronarily and 490 ml intravenously.
| Study group | Role | What they receive |
|---|---|---|
| Melatonin | Active comparator | The randomized patients will receive 10 ml 0,1 mg/ml melatonin intracoronarily and 49 mg intravenously. Receives: Drug: Melatonin, N-acetyl-5-methoxytryptamine |
| Isotonic saline | Placebo comparator | The randomized patients will receive 10 ml isotonic saline (NaCl)and 490 ml intravenously. Receives: Drug: Isotonic saline, Natrium chloride |
What is being measured
The primary outcome is the main question the study is designed to answer.
MRI of the heart
Focusing on quantification infarct size, area at risk and myocardial salvage index
Measured: day 4 after pci (+/- 1 day)
Secondary outcomes (5)
Creatinin Kinase Myocardial Band (CK-MB)
CK-MB is a cardiac enzyme, which is elevated when the myocardium is damaged.
Measured: 96 Hours after pci
Clinical events
Death, sustained ventricular arrhythmias, resuscitation from cardiac arrest, cardiogenic shock, heart failure, major bleedings, stroke, need for revascularization, recurrent ischemia, re-infarctions and re-hospitalization.
Measured: Within 90 days of pci
High-sensitive Troponin T (Hs-TnT) or High-sensitive TnI
Troponin T/I is a cardiac enzyme, which rises when the myocardium is damaged. To determine whether melatonin treatment reduces infarct size as determined by the concentration of Troponin T/I (area under the curve) in the blood, it will be measured daily for the first 4 days after infarction.
Measured: 96 hours after pci
plasma level of melatonin
An assessment of the endogenous level of plasma melatonin
Measured: after pci
Oxidative markers in plasma
Measured: 24 hours after pci
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted29 Jul 2010 (estimated)
- Study startJun 2013
- Primary completionJun 2016
- Study completionDec 2016
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (1)Papers the sponsor has linked to this study.
- Other trials for Acute Myocardial InfarctionStudies of the same condition, open and under way.
- 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 2
- Primary purpose
- Treatment
- Allocation
- Randomised
- Intervention model
- Parallel groups
- Masking
- Double blind
- Who is masked
- Participant, Investigator
- Enrolment
- 41 participants (actual)
Sponsor and investigators
- Lead sponsor
- Herlev Hospital
- Sponsor type
- University, hospital or other
- Responsible party
- Principal investigator, Ismail Gögenür, Herlev Hospital
- Investigators
- Ismail L. Gögenur, MD, DSMc, Principal investigator, Herlev Hospital
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT01172171
- Sponsor's protocol ID
- NLH-01
- Status last verified
- Jan 2017
- First submitted
- 28 Jul 2010
- Last updated
- 4 Jan 2017
- Results posted
- No
- Data monitoring committee
- Yes
Publications
Halladin NL, Busch SE, Jensen SE, Hansen HS, Zaremba T, Aaroe J, Rosenberg J, Gogenur I. Intracoronary and systemic melatonin to patients with acute myocardial infarction: protocol for the IMPACT trial. Dan Med J. 2014 Feb;61(2):A4773.
PubMed 24495883
Study at a glance
From the registry record, last updated by the sponsor on 4 Jan 2017. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Intracoronary Injection of Melatonin for Patients With ST-elevation Myocardial Infarction: a Placebo Controlled Randomized Study
- ClinicalTrials.gov ID
- NCT01172171
- Acronym / sponsor ID
- NLH-01
- Keywords
- Ischemia-reperfusion injury, Acute Myocardial Infarction, Intracoronary melatonin
- Phase
- Phase 2
- Study type
- Interventional
- Recruitment status
- Completed
- Enrolment
- 41 participants (actual)
- Lead sponsor
- Herlev HospitalUniversity, hospital or other
- Study start
- Jun 2013
- Primary completion
- Jun 2016 (actual)
- Study completion
- Dec 2016 (actual)
- First posted
- 29 Jul 2010 (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.
In Denmark, 12.000 people a year, is struck by acute myocardial infarction. A third of these cannot be saved before treatment is possible.
Despite quick and effective reperfusion of the coronary arteries using PCI (Percutaneous Coronary Intervention) after an acute ST-elevation myocardial infarction, substantial morbidity and mortality remain. Infarct size is an important determinant of the short-and long-term outcome after acute myocardial infarction. The most widely used and most effective proven therapy to limit infarct size is the early reperfusion induced by or PCI.
Although beneficial in terms of myocardial salvage, reperfusion itself may contribute to additional damage of the myocardium; the damage due to the combined processes is known as "ischemia-reperfusion injury". The pathogenesis of myocardial ischemia-reperfusion injury is a multifactorial process involving the interaction of multiple mechanisms. Numerous studies indicate that there are three pivotal factors in the pathogenesis of ischemia-reperfusion injury: elevated oxidative damage, depressed energy metabolism, and altered calcium homeostasis.
Partially reduced species of oxygen, including the superoxide anion radical, hydroxyl radical, and hydrogen peroxide, are generated intracellularly as by-product of oxygen metabolism. These reactive oxygen species cause peroxidation af membrane lipids, denaturation of proteins, and modification of DNA, all of which ultimately can lead to cell death. In mammals, cell damage induced by partially reduced oxygen species can also initiate local inflammatory responses, which then lead to further oxidant-mediated tissue injury.
Melatonin is mainly known for its role as an endogenously produced circadian hormone.
For the last twenty years, increasing evidence has proven melatonin to be a very potent direct and indirect antioxidant.
Recent experimental studies have documented the beneficial effects of melatonin in reducing tissue damage and limiting cardiac pathophysiology in models of experimental ischemia-reperfusion.
Primary hypothesis: Melatonin given to patients undergoing PCI can reduce the myocardial damage sustained by ischemia-reperfusion.
Detailed description
Purpose The purpose of this Ph.D study is to examine the antioxidative effect of melatonin in relation to ischemia-reperfusion injury.
The investigators wish to examine to which extend melatonin administered to patients undergoing primary PCI for acute myocardial infarction will reduce the damage of the myocardium caused by ischemia-reperfusion injury and thereby hopefully improve the clinical outcome.
Theory and hypotheses Because there is strong evidence that free radicals contribute to post-ischemic injury, antioxidant enzyme therapy could potentially be extremely effective in reducing the cellular damage. In reality, however, the usefulness of this therapy is limited by a number of factors, in particular the ability of the antioxidants to penetrate the cell membrane and to scavenge free radicals in situ. Fortunately, this limitation can, in part, be addressed with the use of melatonin, a potent indirect and direct free radical scavenger that easily diffuses through the cell membrane to exert its antioxidant effects in all compartments of the cell. Indeed, in contrast to the partial of distribution of other antioxidants, such as vitamin C or E, the melatonin distributes it readily in all subcellular compartments owing to its double-solubility in both, aqueous and in lipid environment. Several recent publications present evidence that the newly discovered antioxidant melatonin has significant protective actions against the cardiac damage such as occurs during ischemia-reperfusion injury.
Primary hypothesis: Melatonin given to patients undergoing PCI can reduce the myocardial damage sustained by ischemia-reperfusion.
Inclusion:
- Adults who are able to give informed consent
- 1 significant coronary occlusion (>2mm) with TIMI 0-1 expected to undergo PCI.
- ECG criteria: The occlusion must be ECG-verified with new ST-elevations ≥ 0.2 mV in V2-V3 and/or ≥ 0.1 in the other leads or with a new onset left bundle branch block.
- Having onset of symptoms of qualifying AMI and undergo PCI within 6 hours.
- If the patients do not fulfill the ECG inclusion criteria they can still be included if the primary PCI reveals an acute coronary occlusion (>2mm) with TIMI 0-1.
Exclusion: Patients with prior myocardial infarction, more than one significant occlusion, prehospital thrombolysis, known history of renal failure, history of autoimmune diseases, pregnancy, fertile women or breastfeeding, severe concurrent illness with reduced short-term prognosis, pacemaker, claustrophobia, cardiogenic shock, metals in the body, atrial fibrillation, BMI ≥ 40.
Intervention: The STEMI patient with 1 significant occlusion undergoing PCI less than 6 hours from onset of symptoms will be randomized to intracoronary injection of either melatonin or placebo(saline). The melatonin or placebo will be given as a bolus of 10 ml in relation to PCI, as soon as the occlusion is removed. Immediately after the bolus is given, a solution of 490 ml of either placebo (saline) or 0,1 mg/ml melatonin (49 mg melatonin)will be given intravenously over 6 hours (80 ml/hour).
Primary end point: MRI of the heart at day 4 (+/- 1 day) after the PCI procedure to determine myocardial salvage index.
Secondary end point:
- To determine whether melatonin treatment reduces infarct size as determined by the concentration of high sensitive TnT or high-sensitive TnI and Creatinin Kinase Myocardial Band (CK-MB)(area under the curve) in the blood, measured daily for the first 4 days after AMI.
- the concentration of plasma melatonin after PCI
- the concentration of oxidative markers 24 hours after PCI
Clinical events occurring within the first 90 days after surgery; death, sustained ventricular arrhythmias, resuscitation from cardiac arrest, cardiogenic shock, heart failure, major bleedings, stroke, need for revascularization, recurrent ischemia, re-infarctions and re-hospitalization.
Design: Randomized, double-blind, placebo-controlled interventional study.
Method: Patients who meet the criteria of inclusion will be randomized to intra-coronary injection plus intravenous infusion of melatonin or placebo. The bolus will be given just after the opening of the vessel (TIMI ≥ 2) . Hs-Troponin T/I and CK-MB will be measured in a blood sample taken 1 hour, 6 hours, 24 hours, 48 hours, 72 hours and 96 hours after the PCI procedure. At day 4 after PCI, the patients will undergo MRI of the heart focusing on infarct size and area at risk.
Patient number: Statistical power analysis shows that with a type 1 error of 5% and a type 2 error of 20%, mean at 9,63 and the SD with MRI of 0,16, one should be able to detect a difference in infarct size of 25% between the two groups, when including 2x17 patients in each group. The investigators are including 2x 20 patients.
Safety: The experiments are considered to be of no risk or discomfort for the patients. Both the intervention group and the placebo group are operated by current clinical guidelines.
Study design
- Primary purpose
- Treatment
- Allocation
- Randomised
- Intervention model
- Parallel groups
- Masking
- Double blind (participant, investigator)
- Number of arms
- 2
| Arm | Type | Receives |
|---|---|---|
| Melatonin | Active comparator | Drug: Melatonin, N-acetyl-5-methoxytryptamineThe randomized patients will receive 10 ml 0,1 mg/ml melatonin intracoronarily and 49 mg intravenously. |
| Isotonic saline | Placebo comparator | Drug: Isotonic saline, Natrium chlorideThe randomized patients will receive 10 ml isotonic saline (NaCl)and 490 ml intravenously. |
Who may qualify
- Ages
- 18 years and older
- Sex
- All
- Healthy volunteers
- Not accepted
- Age groups
- Adult, Older adult
Key inclusion criteria (5 listed)
- Adults who are able to give informed consent
- 1 significant coronary occlusion (>2mm) with TIMI 0-1 expected to undergo PCI.
- The occlusion must be ECG-verified with new ST-elevations ≥ 0.2 mV in V2-V3 and/or ≥ 0.1 in the other leads or a new onset left bundle branch block.
- Having onset of symptoms of qualifying AMI and undergo PCI within 6 hours.
- If the patients do not fulfill the ECG inclusion criteria they can still be included if the primary PCI reveals an acute coronary occlusion (>2mm) with TIMI 0-1.
Key exclusion criteria (13 listed)
- Patients with prior myocardial infarction
- more than one significant occlusion
- prehospital thrombolysis
- known history of renal failure
- history of autoimmune diseases
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 |
|---|---|---|
| Melatonin, N-acetyl-5-methoxytryptamineThe investigators will give the randomized patients 10 ml of 0,1 mg/ml melatonin intracoronarily and 490 ml of 0,1 mg/ml (49 mg) melatonin. | Drug | Melatonin |
| Isotonic saline, Natrium chlorideThe randomized patients will be given 10 ml of isotonic saline intracoronarily and 490 ml intravenously. | Drug | Isotonic saline |
Primary outcome
MRI of the heart
Time frame: day 4 after pci (+/- 1 day)
Focusing on quantification infarct size, area at risk and myocardial salvage index
5 secondary outcomes
Creatinin Kinase Myocardial Band (CK-MB)
Time frame: 96 Hours after pci
Clinical events
Time frame: Within 90 days of pci
High-sensitive Troponin T (Hs-TnT) or High-sensitive TnI
Time frame: 96 hours after pci
plasma level of melatonin
Time frame: after pci
Oxidative markers in plasma
Time frame: 24 hours after pci
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 4 Jan 2017.
- Derived from this study: PubMed 24495883Halladin NL, Busch SE, Jensen SE, Hansen HS, Zaremba T, Aaroe J, Rosenberg J, Gogenur I. Intracoronary and systemic melatonin to patients with acute myocardial infarction: protocol for the IMPACT trial. Dan Med J. 2014 Feb;61(2):A4773.
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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.
Ismail L. Gögenur, MD, DSMc principal investigator
Herlev Hospital
2 sites in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
A Phase 2 study testing Melatonin, N-acetyl-5-methoxytryptamine and Isotonic saline, Natrium chloride in people with Acute Myocardial Infarction and Ischemia-reperfusion Injury, run by Herlev Hospital at 2 sites in Denmark.
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 13 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 4 Jan 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 Denmark. 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. Some participants in this study may receive a placebo. 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 2 studies give the treatment to a larger group to see whether it has the intended effect and to keep checking safety.
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?
MRI of the heart (time frame: day 4 after pci (+/- 1 day)). 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 NCT01172171, which also lists 1 linked publication.
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 4 Jan 2017.