Carbon Monoxide PoisoningNCT04419298
Cardiac Magnetic Resonance Image (CMR) in Acute Carbon Monoxide (CO) Poisoning
An observational study of Carbon Monoxide Poisoning and Myocardial Injury, run by Wonju Severance Christian Hospital at 1 site in South Korea.
Trial summary
Previous report showed that 37% of patients with moderate to severe carbon monoxide (CO) poisoning experienced a myocardial injury, defined as elevated cardiac enzyme [creatine kinase, CK-MB, and cardiac troponin I (TnI)] or ischemic electrocardiogram (ECG) change. Read more about this study
- Who is it for?
- Ages 19 years and older
- Conditions the study is for
- Carbon Monoxide Poisoning, Myocardial Injury, Image, Body
- What is being tested?
- Cardiac MRI
- How many people
- 104 participants
- Where
- 1 siteSouth Korea
- Study dates
- 1 Aug 2017to 25 May 2020
- Phase
- Observational
- 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 19 years and older
- All sexes
- No healthy volunteers
- Adult, Older adult
Study population: Acute CO poisoning with myocardial injury, which was defined as elevated TnI (reference range < 0.045 ng/mL), within 24 hours after ED arrival.
Who may be able to join
- Acute CO poisoning with myocardial injury, which was defined as elevated TnI (reference range < 0.045 ng/mL), within 24 hours after ED arrival.
Who cannot join
- Age <19 years
- No elevated TnI within 24 hours after ED arrival
- Cardiac arrest upon ED arrival or before taking a CMR
- Co-ingestion of cardiac toxic drugs
- Transferred patients without admission
- Declined to enrollment in the study
Show all 12Show fewer
- Impossible CMR due to artificial device
- Calculated creatinine clearance (Ccr) < 30 mL/min
- Previous known history of hypersensitivity of gadolinium
- History of acute coronary syndrome, heart failure, or cardiomyopathy
- Patients who refuse CMR or fail to take a CMR although written informed consent was obtained
- Impossible of interpretation of CMR although CMR was taken
Trial locations and contacts
1 site in 1 country.
South Korea1 site
Wonju Severance Christian Hospital
Wŏnju, Gangwon-do, 26426
About this study
Official title: Evaluation for Acute and Chronic Features of Cardiac Injury by CMR in Acute CO Poisoned Patients With Elevated Troponin I (TnI)
Previous report showed that 37% of patients with moderate to severe carbon monoxide (CO) poisoning experienced a myocardial injury, defined as elevated cardiac enzyme [creatine kinase, CK-MB, and cardiac troponin I (TnI)] or ischemic electrocardiogram (ECG) change. In other study, 24% of the patients with the myocardial injury after CO poisoning died during a median follow-up of 7.6 years. The myocardial injury was the major predictor of mortality. In addition, in the Taiwanese nationwide population-based cohort study, CO poisoning itself reported as a higher risk of a major adverse cardiovascular event.
According to the previous study of investigators, among CO poisoned patients with myocardial injury, 74.4% of patients experienced CO-induced cardiomyopathy. All CO-induced cardiomyopathy recovered to normal status. In this situation, there is no definite approved reason why more cardiovascular events are occurred in CO poisoned patients with myocardial injury during long term follow-up period despite normalization of CO-induced elevated TnI and cardiac dysfunction.
Read more
Two image cases related to cardiac magnetic resonance imaging (CMR) in acute CO poisoning previously reported. One image case reported that patient had mildly depressed left ventricular (LV) systolic function with hypokinesis of the anterior wall and regional akinesis of the inferior wall on the transthoracic echocardiography performed during hospitalization and late gadolinium-enhancement (LGE) images of CMR demonstrated multiple focal areas of high signal consistent with myocardial necrosis or fibrosis. Another image case reported an image case that in CMR, inferolateral mid-wall myocardial fibrosis, which was defined as LGE, was present despite the setting of a completely normal echocardiogram at 4-month follow-up in CO poisoned patients.
Therefore, the investigators evaluate prevalence (frequency of LGE positive) and patterns (involved LV wall and range of LGE positive) of myocardial fibrosis (LGE positive) in acute CO-poisoned patients during acute (within seven days after CO exposure) and chronic phase (at 4-5 months after CO exposure) and whether LGE positive developed in acute phase have been changed through cardiac MRI performed at chronic phase. The investigators also evaluate LV ejection fraction and global longitudinal strain in transthoracic echocardiography performed at the ED (baseline) and within seven days (follow-up). The investigators also assessed the association between neurocognitive outcomes using the global deterioration scale (at 1, 6, and 12 months after CO exposure) and the presence of LGE positive.
Read the detailed description
In the US, carbon monoxide (CO) poisoning accounts for 1,300 deaths and 50,000 emergency department visits annually. Previous report showed that 37% of patients with moderate to severe CO poisoning experience a myocardial injury defined as elevated cardiac enzyme [creatine kinase, CK-MB, and cardiac troponin I (TnI)] or ischemic electrocardiogram (ECG) change. In other study, there was a mortality of 24% of patients during a median follow-up of 7.6 years. A mortality among the patients who experienced the myocardial injury was higher than patients without the myocardial injury. The death caused by cardiovascular problems occurred more among patients with a history of the myocardial injury (44% vs. 18%). The myocardial injury was the major predictor of mortality. In addition, in the Taiwanese nationwide population-based cohort study, a history of CO poisoning showed a higher risk of a major adverse cardiovascular event.
The investigators reported that myocardial injury (defined as elevated TnI or change of ischemic ECG) developed in 20% of CO poisoned patients and elevated TnI was normalized within 65.0 hours. According to previous study of the investigators, among CO poisoned patients with myocardial injury, 74.4% of patients experienced CO-induced cardiomyopathy. All CO-induced cardiomyopathy recovered to normal status. In this situation, there is no definite approved reason why more cardiovascular events are occurred in CO poisoned patients with myocardial injury during long term follow-up period despite normalization of CO-induced elevated TnI and cardiac dysfunction.
One case reported an image related to a CO poisoned patient with acute myocardial injury found by cardiac magnetic resonance imaging (CMR) with a normal coronary artery confirmed by coronary angiography. In that case, a patient showed that patient had mildly depressed left ventricular (LV) systolic function with hypokinesis of the anterior wall and regional akinesis of the inferior wall on the transthoracic echocardiography performed during hospitalization and late gadolinium-enhancement (LGE) images of CMR demonstrated multiple focal areas of high signal consistent with myocardial necrosis or fibrosis. Through this case, the investigators thought that CO poisoning might result in acute myocardial necrosis, demonstrating another type of myocardial injury that can be detected by CMR. In addition, Other case reported an image case that in cardiac MRI, inferolateral mid-wall myocardial fibrosis, which was defined as LGE, was present despite the setting of a completely normal echocardiogram at 4-month follow-up in a patient who experienced severe CO poisoning.
Mid-wall myocardial fibrosis has been reported in dilated cardiomyopathy (DCMP) of unclear origin. In a follow-up study of 101 consecutive patients with DCMP, mid-wall fibrosis (presented in 35% of patients) predicted a combined endpoint of all-cause mortality, cardiovascular hospitalization, and sudden cardiac death. Myocardial fibrosis has also been demonstrated in hypertrophic cardiomyopathy. The myocardial fibrosis has been linked to known markers for sudden cardiac death, although the independent prognostic value of CMR has yet to be determined.
Through above results, the investigators thought that the normal LV cardiac function may not reflect that there is no problem with the heart, and it could lead to myocardial fibrosis in the chronic phase. Myocardial damage seen through CMR may be related to the patient's prognosis. Therefore, the investigators evaluate prevalence (frequency of LGE positive) and patterns (involved LV wall and range of LGE positive) of myocardial fibrosis (LGE positive) in acute CO-poisoned patients during acute (within 7 days after CO exposure) and chronic phase (at 4-5 months after CO exposure) and whether LGE positive developed in the acute phase has been changed in cardiac MRI performed at chronic phase. The investigators also evaluate LV ejection fraction and global longitudinal strain in transthoracic echocardiography performed at the ED (baseline) and within seven days (follow-up). The investigators also assessed the association between neurocognitive outcomes using the global deterioration scale (at 1, 6, and 12 months after CO exposure) and the presence of LGE positive.
- Conditions
- Carbon Monoxide Poisoning, Myocardial Injury, Image, Body
- Being tested
- Cardiac MRI
- Medical subject headings
- Carbon Monoxide Poisoning
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
Cardiac MRIDiagnostic test
Also called Transthoracic echocardiography (TTE)
- Cardiac MRI be taken to acute CO poisoned patients with elevated TnI [during acute (within 7 days after CO exposure) and chronic phase (at 4-5 months after CO exposure)]
- TTE be taken to acute CO poisoned patients with elevated TnI [At the ED and during admission (within 7 days after CO exposure)]
| Study group | Role | What they receive |
|---|---|---|
| Acute CO poisoning with myocardial injury | A diagnosis of CO poisoning was made according to medical history and carboxyhaemoglobin >5% (>10% in smokers).
Myocardial injury was defined as elevated high-sensitivity TnI level above the upper limit (> 0.046 ng/mL) when measured in the emergency department (ED) or repeatedly within 24 hours after ED arrival. Receives: Diagnostic Test: Cardiac MRI |
What is being measured
The primary outcome is the main question the study is designed to answer.
Late gadolinium enhancement (LGE) in CMR
Prevalence (percent) of presence of LGE in CMR
Measured: Within 7 days after acute CO poisoning
LGE involved wall in CMR
Injured left ventricular wall according to LGE in CMR
Measured: Within 7 days after acute CO poisoning
Secondary outcomes (9)
LGE size in CMR
Injury size according to LGE in CMR
Measured: Within 7 days after acute CO poisoning
Change of LGE between first CMR and follow-up CMR
Change of LGE between first CMR (within 7 days after CO exposure) and follow-up CMR (at 4-5 months after CO exposure)
Measured: Within 7 days after CO exposure and at 4-5 months after CO exposure
LV ejection fraction (EF) of TTE performed at the ED
Baseline LV EF of TTE performed at the ED
Measured: Within 3 hours at the ED
LV global longitudinal strain (GLS) of TTE performed at the ED
Baseline LV GLS of TTE performed at the ED
Measured: Within 3 hours at the ED
LV EF of TTE performed during admission
Follow-up LV EF of TTE performed during admission
Measured: Within 7 days after CO exposure
LV GLS of TTE performed during admission
Follow-up LV GLS of TTE performed during admission
Measured: Within 7 days after CO exposure
Change of LV EF between ED TTE and follow-up TTE
Change of LV EF between baseline TTE and follow-up TTE
Measured: Within 3 hours at the ED and within 7 days after CO exposure
Change of LV GLS between ED TTE and follow-up TTE
Change of LV GLS between baseline TTE and follow-up TTE
Measured: Within 3 hours at the ED and within 7 days after CO exposure
Correlation between presence of LGE and poor neurocognitive outcome at 1, 6, and 12 months
Correlation between presence of LGE and poor neurocognitive outcome [global deterioration scale (GDS) 4-7] evaluated by GDS at 1, 6, and 12 months after CO exposure
Measured: GDS (minimum 1 - maximum 7) evaluated at 1, 6, and 12 months after CO exposure
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted5 Jun 2020
- Study start1 Aug 2017
- Primary completion23 May 2019
- Study completion25 May 2020
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 Carbon Monoxide PoisoningStudies 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
- Observational
- Observational model
- Cohort
- Time perspective
- Prospective
- Enrolment
- 104 participants (actual)
Sponsor and investigators
- Lead sponsor
- Wonju Severance Christian Hospital
- Sponsor type
- University, hospital or other
- Collaborators
- National Research Foundation of Korea
- Responsible party
- Principal investigator, Yong Sung Cha, Wonju Severance Christian Hospital
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT04419298
- Sponsor's protocol ID
- CMR-CO
- Status last verified
- Jun 2020
- First submitted
- 28 May 2020
- Last updated
- 5 Jun 2020
- Results posted
- No
- Data monitoring committee
- No
- FDA-regulated drug
- No
- FDA-regulated device
- No
- Individual data sharing
- No
Publications
Cho DH, Ko SM, Son JW, Park EJ, Cha YS. Myocardial Injury and Fibrosis From Acute Carbon Monoxide Poisoning: A Prospective Observational Study. JACC Cardiovasc Imaging. 2021 Sep;14(9):1758-1770. doi: 10.1016/j.jcmg.2021.02.020. Epub 2021 Apr 14.
PubMed 33865788
Study at a glance
From the registry record, last updated by the sponsor on 5 Jun 2020. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Evaluation for Acute and Chronic Features of Cardiac Injury by CMR in Acute CO Poisoned Patients With Elevated Troponin I (TnI)
- ClinicalTrials.gov ID
- NCT04419298
- Acronym / sponsor ID
- CMR-CO
- Conditions
- Carbon Monoxide Poisoning, Myocardial Injury, Image, Body
- Study type
- Observational
- Recruitment status
- Completed
- Enrolment
- 104 participants (actual)
- Lead sponsor
- Wonju Severance Christian HospitalUniversity, hospital or other
- Collaborators
- National Research Foundation of Korea
- Study start
- 1 Aug 2017 (actual)
- Primary completion
- 23 May 2019 (actual)
- Study completion
- 25 May 2020 (actual)
- First posted
- 5 Jun 2020 (actual)
- 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.
Previous report showed that 37% of patients with moderate to severe carbon monoxide (CO) poisoning experienced a myocardial injury, defined as elevated cardiac enzyme [creatine kinase, CK-MB, and cardiac troponin I (TnI)] or ischemic electrocardiogram (ECG) change. In other study, 24% of the patients with the myocardial injury after CO poisoning died during a median follow-up of 7.6 years. The myocardial injury was the major predictor of mortality. In addition, in the Taiwanese nationwide population-based cohort study, CO poisoning itself reported as a higher risk of a major adverse cardiovascular event.
According to the previous study of investigators, among CO poisoned patients with myocardial injury, 74.4% of patients experienced CO-induced cardiomyopathy. All CO-induced cardiomyopathy recovered to normal status. In this situation, there is no definite approved reason why more cardiovascular events are occurred in CO poisoned patients with myocardial injury during long term follow-up period despite normalization of CO-induced elevated TnI and cardiac dysfunction.
Two image cases related to cardiac magnetic resonance imaging (CMR) in acute CO poisoning previously reported. One image case reported that patient had mildly depressed left ventricular (LV) systolic function with hypokinesis of the anterior wall and regional akinesis of the inferior wall on the transthoracic echocardiography performed during hospitalization and late gadolinium-enhancement (LGE) images of CMR demonstrated multiple focal areas of high signal consistent with myocardial necrosis or fibrosis. Another image case reported an image case that in CMR, inferolateral mid-wall myocardial fibrosis, which was defined as LGE, was present despite the setting of a completely normal echocardiogram at 4-month follow-up in CO poisoned patients.
Therefore, the investigators evaluate prevalence (frequency of LGE positive) and patterns (involved LV wall and range of LGE positive) of myocardial fibrosis (LGE positive) in acute CO-poisoned patients during acute (within seven days after CO exposure) and chronic phase (at 4-5 months after CO exposure) and whether LGE positive developed in acute phase have been changed through cardiac MRI performed at chronic phase. The investigators also evaluate LV ejection fraction and global longitudinal strain in transthoracic echocardiography performed at the ED (baseline) and within seven days (follow-up). The investigators also assessed the association between neurocognitive outcomes using the global deterioration scale (at 1, 6, and 12 months after CO exposure) and the presence of LGE positive.
Detailed description
In the US, carbon monoxide (CO) poisoning accounts for 1,300 deaths and 50,000 emergency department visits annually. Previous report showed that 37% of patients with moderate to severe CO poisoning experience a myocardial injury defined as elevated cardiac enzyme [creatine kinase, CK-MB, and cardiac troponin I (TnI)] or ischemic electrocardiogram (ECG) change. In other study, there was a mortality of 24% of patients during a median follow-up of 7.6 years. A mortality among the patients who experienced the myocardial injury was higher than patients without the myocardial injury. The death caused by cardiovascular problems occurred more among patients with a history of the myocardial injury (44% vs. 18%). The myocardial injury was the major predictor of mortality. In addition, in the Taiwanese nationwide population-based cohort study, a history of CO poisoning showed a higher risk of a major adverse cardiovascular event.
The investigators reported that myocardial injury (defined as elevated TnI or change of ischemic ECG) developed in 20% of CO poisoned patients and elevated TnI was normalized within 65.0 hours. According to previous study of the investigators, among CO poisoned patients with myocardial injury, 74.4% of patients experienced CO-induced cardiomyopathy. All CO-induced cardiomyopathy recovered to normal status. In this situation, there is no definite approved reason why more cardiovascular events are occurred in CO poisoned patients with myocardial injury during long term follow-up period despite normalization of CO-induced elevated TnI and cardiac dysfunction.
One case reported an image related to a CO poisoned patient with acute myocardial injury found by cardiac magnetic resonance imaging (CMR) with a normal coronary artery confirmed by coronary angiography. In that case, a patient showed that patient had mildly depressed left ventricular (LV) systolic function with hypokinesis of the anterior wall and regional akinesis of the inferior wall on the transthoracic echocardiography performed during hospitalization and late gadolinium-enhancement (LGE) images of CMR demonstrated multiple focal areas of high signal consistent with myocardial necrosis or fibrosis. Through this case, the investigators thought that CO poisoning might result in acute myocardial necrosis, demonstrating another type of myocardial injury that can be detected by CMR. In addition, Other case reported an image case that in cardiac MRI, inferolateral mid-wall myocardial fibrosis, which was defined as LGE, was present despite the setting of a completely normal echocardiogram at 4-month follow-up in a patient who experienced severe CO poisoning.
Mid-wall myocardial fibrosis has been reported in dilated cardiomyopathy (DCMP) of unclear origin. In a follow-up study of 101 consecutive patients with DCMP, mid-wall fibrosis (presented in 35% of patients) predicted a combined endpoint of all-cause mortality, cardiovascular hospitalization, and sudden cardiac death. Myocardial fibrosis has also been demonstrated in hypertrophic cardiomyopathy. The myocardial fibrosis has been linked to known markers for sudden cardiac death, although the independent prognostic value of CMR has yet to be determined.
Through above results, the investigators thought that the normal LV cardiac function may not reflect that there is no problem with the heart, and it could lead to myocardial fibrosis in the chronic phase. Myocardial damage seen through CMR may be related to the patient's prognosis. Therefore, the investigators evaluate prevalence (frequency of LGE positive) and patterns (involved LV wall and range of LGE positive) of myocardial fibrosis (LGE positive) in acute CO-poisoned patients during acute (within 7 days after CO exposure) and chronic phase (at 4-5 months after CO exposure) and whether LGE positive developed in the acute phase has been changed in cardiac MRI performed at chronic phase. The investigators also evaluate LV ejection fraction and global longitudinal strain in transthoracic echocardiography performed at the ED (baseline) and within seven days (follow-up). The investigators also assessed the association between neurocognitive outcomes using the global deterioration scale (at 1, 6, and 12 months after CO exposure) and the presence of LGE positive.
Study design
- Observational model
- Cohort
- Time perspective
- Prospective
- Number of arms
- 1
| Arm | Type | Receives |
|---|---|---|
| Acute CO poisoning with myocardial injury | – | Diagnostic Test: Cardiac MRIA diagnosis of CO poisoning was made according to medical history and carboxyhaemoglobin >5% (>10% in smokers). Myocardial injury was defined as elevated high-sensitivity TnI level above the upper limit (> 0.046 ng/mL) when measured in the emergency department (ED) or repeatedly within 24 hours after ED arrival. |
Who may qualify
- Ages
- 19 years and older
- Sex
- All
- Healthy volunteers
- Not accepted
- Age groups
- Adult, Older adult
- Study population
- Acute CO poisoning with myocardial injury, which was defined as elevated TnI (reference range < 0.045 ng/mL), within 24 hours after ED arrival.
Key inclusion criteria (1 listed)
- Acute CO poisoning with myocardial injury, which was defined as elevated TnI (reference range < 0.045 ng/mL), within 24 hours after ED arrival.
Key exclusion criteria (12 listed)
- Age <19 years
- No elevated TnI within 24 hours after ED arrival
- Cardiac arrest upon ED arrival or before taking a CMR
- Co-ingestion of cardiac toxic drugs
- Transferred patients without admission
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 |
|---|---|---|
| Cardiac MRIAlso: Transthoracic echocardiography (TTE)1. Cardiac MRI be taken to acute CO poisoned patients with elevated TnI [during acute (within 7 days after CO exposure) and chronic phase (at 4-5 months after CO exposure)] 2. TTE be taken to acute CO poisoned patients with elevated TnI [At the ED and during admission (within 7 days after CO exposure)] | Diagnostic test | Acute CO poisoning with myocardial injury |
Primary outcome
Late gadolinium enhancement (LGE) in CMR
Time frame: Within 7 days after acute CO poisoning
Prevalence (percent) of presence of LGE in CMR
LGE involved wall in CMR
Time frame: Within 7 days after acute CO poisoning
Injured left ventricular wall according to LGE in CMR
9 secondary outcomes
LGE size in CMR
Time frame: Within 7 days after acute CO poisoning
Change of LGE between first CMR and follow-up CMR
Time frame: Within 7 days after CO exposure and at 4-5 months after CO exposure
LV ejection fraction (EF) of TTE performed at the ED
Time frame: Within 3 hours at the ED
LV global longitudinal strain (GLS) of TTE performed at the ED
Time frame: Within 3 hours at the ED
LV EF of TTE performed during admission
Time frame: Within 7 days after CO exposure
LV GLS of TTE performed during admission
Time frame: Within 7 days after CO exposure
Change of LV EF between ED TTE and follow-up TTE
Time frame: Within 3 hours at the ED and within 7 days after CO exposure
Change of LV GLS between ED TTE and follow-up TTE
Time frame: Within 3 hours at the ED and within 7 days after CO exposure
Correlation between presence of LGE and poor neurocognitive outcome at 1, 6, and 12 months
Time frame: GDS (minimum 1 - maximum 7) evaluated at 1, 6, and 12 months after CO exposure
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 5 Jun 2020.
- Derived from this study: PubMed 33865788Cho DH, Ko SM, Son JW, Park EJ, Cha YS. Myocardial Injury and Fibrosis From Acute Carbon Monoxide Poisoning: A Prospective Observational Study. JACC Cardiovasc Imaging. 2021 Sep;14(9):1758-1770. doi: 10.1016/j.jcmg.2021.02.020. Epub 2021 Apr 14.
- Individual participant dataSharing planned: No
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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.
The record lists no contact. Use the official record to reach the sponsor.
1 site in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
An observational study of Carbon Monoxide Poisoning and Myocardial Injury, run by Wonju Severance Christian Hospital at 1 site in South Korea.
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 1 inclusion and 12 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 5 Jun 2020. Status can change between updates, so confirm with the study contact before making plans.
Where is the study taking place?
The record lists 1 site in South Korea. 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.
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?
Late gadolinium enhancement (LGE) in CMR (time frame: Within 7 days after acute CO poisoning). The study lists 2 primary outcomes in all. 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 NCT04419298, 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 5 Jun 2020.