<clinical_study>
  <!-- This xml conforms to an XML Schema at:
    https://clinicaltrials.gov/ct2/html/images/info/public.xsd -->
  <required_header>
    <download_date>ClinicalTrials.gov processed this data on September 20, 2023</download_date>
    <link_text>Link to the current ClinicalTrials.gov record.</link_text>
    <url>https://clinicaltrials.gov/ct2/show/NCT04419298</url>
  </required_header>
  <id_info>
    <org_study_id>CMR-CO</org_study_id>
    <nct_id>NCT04419298</nct_id>
  </id_info>
  <brief_title>Cardiac Magnetic Resonance Image (CMR) in Acute Carbon Monoxide (CO) Poisoning</brief_title>
  <official_title>Evaluation for Acute and Chronic Features of Cardiac Injury by CMR in Acute CO Poisoned Patients With Elevated Troponin I (TnI)</official_title>
  <sponsors>
    <lead_sponsor>
      <agency>Wonju Severance Christian Hospital</agency>
      <agency_class>Other</agency_class>
    </lead_sponsor>
    <collaborator>
      <agency>National Research Foundation of Korea</agency>
      <agency_class>Other</agency_class>
    </collaborator>
  </sponsors>
  <source>Wonju Severance Christian Hospital</source>
  <oversight_info>
    <has_dmc>No</has_dmc>
    <is_fda_regulated_drug>No</is_fda_regulated_drug>
    <is_fda_regulated_device>No</is_fda_regulated_device>
  </oversight_info>
  <brief_summary>
    <textblock>
      Previous report showed that 37% of patients with moderate to severe carbon monoxide (CO)&#xD;
      poisoning experienced a myocardial injury, defined as elevated cardiac enzyme [creatine&#xD;
      kinase, CK-MB, and cardiac troponin I (TnI)] or ischemic electrocardiogram (ECG) change. In&#xD;
      other study, 24% of the patients with the myocardial injury after CO poisoning died during a&#xD;
      median follow-up of 7.6 years. The myocardial injury was the major predictor of mortality. In&#xD;
      addition, in the Taiwanese nationwide population-based cohort study, CO poisoning itself&#xD;
      reported as a higher risk of a major adverse cardiovascular event.&#xD;
&#xD;
      According to the previous study of investigators, among CO poisoned patients with myocardial&#xD;
      injury, 74.4% of patients experienced CO-induced cardiomyopathy. All CO-induced&#xD;
      cardiomyopathy recovered to normal status. In this situation, there is no definite approved&#xD;
      reason why more cardiovascular events are occurred in CO poisoned patients with myocardial&#xD;
      injury during long term follow-up period despite normalization of CO-induced elevated TnI and&#xD;
      cardiac dysfunction.&#xD;
&#xD;
      Two image cases related to cardiac magnetic resonance imaging (CMR) in acute CO poisoning&#xD;
      previously reported. One image case reported that patient had mildly depressed left&#xD;
      ventricular (LV) systolic function with hypokinesis of the anterior wall and regional&#xD;
      akinesis of the inferior wall on the transthoracic echocardiography performed during&#xD;
      hospitalization and late gadolinium-enhancement (LGE) images of CMR demonstrated multiple&#xD;
      focal areas of high signal consistent with myocardial necrosis or fibrosis. Another image&#xD;
      case reported an image case that in CMR, inferolateral mid-wall myocardial fibrosis, which&#xD;
      was defined as LGE, was present despite the setting of a completely normal echocardiogram at&#xD;
      4-month follow-up in CO poisoned patients.&#xD;
&#xD;
      Therefore, the investigators evaluate prevalence (frequency of LGE positive) and patterns&#xD;
      (involved LV wall and range of LGE positive) of myocardial fibrosis (LGE positive) in acute&#xD;
      CO-poisoned patients during acute (within seven days after CO exposure) and chronic phase (at&#xD;
      4-5 months after CO exposure) and whether LGE positive developed in acute phase have been&#xD;
      changed through cardiac MRI performed at chronic phase. The investigators also evaluate LV&#xD;
      ejection fraction and global longitudinal strain in transthoracic echocardiography performed&#xD;
      at the ED (baseline) and within seven days (follow-up). The investigators also assessed the&#xD;
      association between neurocognitive outcomes using the global deterioration scale (at 1, 6,&#xD;
      and 12 months after CO exposure) and the presence of LGE positive.&#xD;
    </textblock>
  </brief_summary>
  <detailed_description>
    <textblock>
      In the US, carbon monoxide (CO) poisoning accounts for 1,300 deaths and 50,000 emergency&#xD;
      department visits annually. Previous report showed that 37% of patients with moderate to&#xD;
      severe CO poisoning experience a myocardial injury defined as elevated cardiac enzyme&#xD;
      [creatine kinase, CK-MB, and cardiac troponin I (TnI)] or ischemic electrocardiogram (ECG)&#xD;
      change. In other study, there was a mortality of 24% of patients during a median follow-up of&#xD;
      7.6 years. A mortality among the patients who experienced the myocardial injury was higher&#xD;
      than patients without the myocardial injury. The death caused by cardiovascular problems&#xD;
      occurred more among patients with a history of the myocardial injury (44% vs. 18%). The&#xD;
      myocardial injury was the major predictor of mortality. In addition, in the Taiwanese&#xD;
      nationwide population-based cohort study, a history of CO poisoning showed a higher risk of a&#xD;
      major adverse cardiovascular event.&#xD;
&#xD;
      The investigators reported that myocardial injury (defined as elevated TnI or change of&#xD;
      ischemic ECG) developed in 20% of CO poisoned patients and elevated TnI was normalized within&#xD;
      65.0 hours. According to previous study of the investigators, among CO poisoned patients with&#xD;
      myocardial injury, 74.4% of patients experienced CO-induced cardiomyopathy. All CO-induced&#xD;
      cardiomyopathy recovered to normal status. In this situation, there is no definite approved&#xD;
      reason why more cardiovascular events are occurred in CO poisoned patients with myocardial&#xD;
      injury during long term follow-up period despite normalization of CO-induced elevated TnI and&#xD;
      cardiac dysfunction.&#xD;
&#xD;
      One case reported an image related to a CO poisoned patient with acute myocardial injury&#xD;
      found by cardiac magnetic resonance imaging (CMR) with a normal coronary artery confirmed by&#xD;
      coronary angiography. In that case, a patient showed that patient had mildly depressed left&#xD;
      ventricular (LV) systolic function with hypokinesis of the anterior wall and regional&#xD;
      akinesis of the inferior wall on the transthoracic echocardiography performed during&#xD;
      hospitalization and late gadolinium-enhancement (LGE) images of CMR demonstrated multiple&#xD;
      focal areas of high signal consistent with myocardial necrosis or fibrosis. Through this&#xD;
      case, the investigators thought that CO poisoning might result in acute myocardial necrosis,&#xD;
      demonstrating another type of myocardial injury that can be detected by CMR. In addition,&#xD;
      Other case reported an image case that in cardiac MRI, inferolateral mid-wall myocardial&#xD;
      fibrosis, which was defined as LGE, was present despite the setting of a completely normal&#xD;
      echocardiogram at 4-month follow-up in a patient who experienced severe CO poisoning.&#xD;
&#xD;
      Mid-wall myocardial fibrosis has been reported in dilated cardiomyopathy (DCMP) of unclear&#xD;
      origin. In a follow-up study of 101 consecutive patients with DCMP, mid-wall fibrosis&#xD;
      (presented in 35% of patients) predicted a combined endpoint of all-cause mortality,&#xD;
      cardiovascular hospitalization, and sudden cardiac death. Myocardial fibrosis has also been&#xD;
      demonstrated in hypertrophic cardiomyopathy. The myocardial fibrosis has been linked to known&#xD;
      markers for sudden cardiac death, although the independent prognostic value of CMR has yet to&#xD;
      be determined.&#xD;
&#xD;
      Through above results, the investigators thought that the normal LV cardiac function may not&#xD;
      reflect that there is no problem with the heart, and it could lead to myocardial fibrosis in&#xD;
      the chronic phase. Myocardial damage seen through CMR may be related to the patient's&#xD;
      prognosis. Therefore, the investigators evaluate prevalence (frequency of LGE positive) and&#xD;
      patterns (involved LV wall and range of LGE positive) of myocardial fibrosis (LGE positive)&#xD;
      in acute CO-poisoned patients during acute (within 7 days after CO exposure) and chronic&#xD;
      phase (at 4-5 months after CO exposure) and whether LGE positive developed in the acute phase&#xD;
      has been changed in cardiac MRI performed at chronic phase. The investigators also evaluate&#xD;
      LV ejection fraction and global longitudinal strain in transthoracic echocardiography&#xD;
      performed at the ED (baseline) and within seven days (follow-up). The investigators also&#xD;
      assessed the association between neurocognitive outcomes using the global deterioration scale&#xD;
      (at 1, 6, and 12 months after CO exposure) and the presence of LGE positive.&#xD;
    </textblock>
  </detailed_description>
  <overall_status>Completed</overall_status>
  <start_date type="Actual">August 1, 2017</start_date>
  <completion_date type="Actual">May 25, 2020</completion_date>
  <primary_completion_date type="Actual">May 23, 2019</primary_completion_date>
  <study_type>Observational</study_type>
  <has_expanded_access>No</has_expanded_access>
  <study_design_info>
    <observational_model>Cohort</observational_model>
    <time_perspective>Prospective</time_perspective>
  </study_design_info>
  <primary_outcome>
    <measure>Late gadolinium enhancement (LGE) in CMR</measure>
    <time_frame>Within 7 days after acute CO poisoning</time_frame>
    <description>Prevalence (percent) of presence of LGE in CMR</description>
  </primary_outcome>
  <primary_outcome>
    <measure>LGE involved wall in CMR</measure>
    <time_frame>Within 7 days after acute CO poisoning</time_frame>
    <description>Injured left ventricular wall according to LGE in CMR</description>
  </primary_outcome>
  <secondary_outcome>
    <measure>LGE size in CMR</measure>
    <time_frame>Within 7 days after acute CO poisoning</time_frame>
    <description>Injury size according to LGE in CMR</description>
  </secondary_outcome>
  <secondary_outcome>
    <measure>Change of LGE between first CMR and follow-up CMR</measure>
    <time_frame>Within 7 days after CO exposure and at 4-5 months after CO exposure</time_frame>
    <description>Change of LGE between first CMR (within 7 days after CO exposure) and follow-up CMR (at 4-5 months after CO exposure)</description>
  </secondary_outcome>
  <secondary_outcome>
    <measure>LV ejection fraction (EF) of TTE performed at the ED</measure>
    <time_frame>Within 3 hours at the ED</time_frame>
    <description>Baseline LV EF of TTE performed at the ED</description>
  </secondary_outcome>
  <secondary_outcome>
    <measure>LV global longitudinal strain (GLS) of TTE performed at the ED</measure>
    <time_frame>Within 3 hours at the ED</time_frame>
    <description>Baseline LV GLS of TTE performed at the ED</description>
  </secondary_outcome>
  <secondary_outcome>
    <measure>LV EF of TTE performed during admission</measure>
    <time_frame>Within 7 days after CO exposure</time_frame>
    <description>Follow-up LV EF of TTE performed during admission</description>
  </secondary_outcome>
  <secondary_outcome>
    <measure>LV GLS of TTE performed during admission</measure>
    <time_frame>Within 7 days after CO exposure</time_frame>
    <description>Follow-up LV GLS of TTE performed during admission</description>
  </secondary_outcome>
  <secondary_outcome>
    <measure>Change of LV EF between ED TTE and follow-up TTE</measure>
    <time_frame>Within 3 hours at the ED and within 7 days after CO exposure</time_frame>
    <description>Change of LV EF between baseline TTE and follow-up TTE</description>
  </secondary_outcome>
  <secondary_outcome>
    <measure>Change of LV GLS between ED TTE and follow-up TTE</measure>
    <time_frame>Within 3 hours at the ED and within 7 days after CO exposure</time_frame>
    <description>Change of LV GLS between baseline TTE and follow-up TTE</description>
  </secondary_outcome>
  <secondary_outcome>
    <measure>Correlation between presence of LGE and poor neurocognitive outcome at 1, 6, and 12 months</measure>
    <time_frame>GDS (minimum 1 - maximum 7) evaluated at 1, 6, and 12 months after CO exposure</time_frame>
    <description>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</description>
  </secondary_outcome>
  <number_of_groups>1</number_of_groups>
  <enrollment type="Actual">104</enrollment>
  <condition>Carbon Monoxide Poisoning</condition>
  <condition>Myocardial Injury</condition>
  <condition>Image, Body</condition>
  <arm_group>
    <arm_group_label>Acute CO poisoning with myocardial injury</arm_group_label>
    <description>A diagnosis of CO poisoning was made according to medical history and carboxyhaemoglobin &gt;5% (&gt;10% in smokers).&#xD;
Myocardial injury was defined as elevated high-sensitivity TnI level above the upper limit (&gt; 0.046 ng/mL) when measured in the emergency department (ED) or repeatedly within 24 hours after ED arrival.</description>
  </arm_group>
  <intervention>
    <intervention_type>Diagnostic Test</intervention_type>
    <intervention_name>Cardiac MRI</intervention_name>
    <description>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)]&#xD;
TTE be taken to acute CO poisoned patients with elevated TnI [At the ED and during admission (within 7 days after CO exposure)]</description>
    <arm_group_label>Acute CO poisoning with myocardial injury</arm_group_label>
    <other_name>Transthoracic echocardiography (TTE)</other_name>
  </intervention>
  <eligibility>
    <study_pop>
      <textblock>
        Acute CO poisoning with myocardial injury, which was defined as elevated TnI (reference&#xD;
        range &lt; 0.045 ng/mL), within 24 hours after ED arrival.&#xD;
      </textblock>
    </study_pop>
    <sampling_method>Probability Sample</sampling_method>
    <criteria>
      <textblock>
        Inclusion Criteria:&#xD;
&#xD;
          -  Acute CO poisoning with myocardial injury, which was defined as elevated TnI&#xD;
             (reference range &lt; 0.045 ng/mL), within 24 hours after ED arrival.&#xD;
&#xD;
        Exclusion Criteria:&#xD;
&#xD;
          -  Age &lt;19 years&#xD;
&#xD;
          -  No elevated TnI within 24 hours after ED arrival&#xD;
&#xD;
          -  Cardiac arrest upon ED arrival or before taking a CMR&#xD;
&#xD;
          -  Co-ingestion of cardiac toxic drugs&#xD;
&#xD;
          -  Transferred patients without admission&#xD;
&#xD;
          -  Declined to enrollment in the study&#xD;
&#xD;
          -  Impossible CMR due to artificial device&#xD;
&#xD;
          -  Calculated creatinine clearance (Ccr) &lt; 30 mL/min&#xD;
&#xD;
          -  Previous known history of hypersensitivity of gadolinium&#xD;
&#xD;
          -  History of acute coronary syndrome, heart failure, or cardiomyopathy&#xD;
&#xD;
          -  Patients who refuse CMR or fail to take a CMR although written informed consent was&#xD;
             obtained&#xD;
&#xD;
          -  Impossible of interpretation of CMR although CMR was taken&#xD;
      </textblock>
    </criteria>
    <gender>All</gender>
    <minimum_age>19 Years</minimum_age>
    <maximum_age>N/A</maximum_age>
    <healthy_volunteers>No</healthy_volunteers>
  </eligibility>
  <location>
    <facility>
      <name>Wonju Severance Christian Hospital</name>
      <address>
        <city>Wonju</city>
        <state>Gangwon</state>
        <zip>26426</zip>
        <country>Korea, Republic of</country>
      </address>
    </facility>
  </location>
  <location_countries>
    <country>Korea, Republic of</country>
  </location_countries>
  <verification_date>June 2020</verification_date>
  <study_first_submitted>May 28, 2020</study_first_submitted>
  <study_first_submitted_qc>June 2, 2020</study_first_submitted_qc>
  <study_first_posted type="Actual">June 5, 2020</study_first_posted>
  <last_update_submitted>June 2, 2020</last_update_submitted>
  <last_update_submitted_qc>June 2, 2020</last_update_submitted_qc>
  <last_update_posted type="Actual">June 5, 2020</last_update_posted>
  <responsible_party>
    <responsible_party_type>Principal Investigator</responsible_party_type>
    <investigator_affiliation>Wonju Severance Christian Hospital</investigator_affiliation>
    <investigator_full_name>Yong Sung Cha</investigator_full_name>
    <investigator_title>Assistant Professor</investigator_title>
  </responsible_party>
  <condition_browse>
    <!-- CAUTION:  The following MeSH terms are assigned with an imperfect algorithm            -->
    <mesh_term>Poisoning</mesh_term>
    <mesh_term>Carbon Monoxide Poisoning</mesh_term>
  </condition_browse>
  <patient_data>
    <sharing_ipd>No</sharing_ipd>
  </patient_data>
  <!-- Results have not yet been posted for this study                                          -->
</clinical_study>


download date: ClinicalTrials.gov processed this data on September 20, 2023
link text: Link to the current ClinicalTrials.gov record.
url: https://clinicaltrials.gov/ct2/show/NCT04419298
org study id: CMR-CO
nct id: NCT04419298
lead sponsor: 
collaborator: 
has dmc: No
is fda regulated drug: No
is fda regulated device: No
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.
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.
observational model: Cohort
time perspective: Prospective
measure: Late gadolinium enhancement (LGE) in CMR
time frame: Within 7 days after acute CO poisoning
description: Prevalence (percent) of presence of LGE in CMR
measure: LGE involved wall in CMR
time frame: Within 7 days after acute CO poisoning
description: Injured left ventricular wall according to LGE in CMR
measure: LGE size in CMR
time frame: Within 7 days after acute CO poisoning
description: Injury size according to LGE in CMR
measure: 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
description: Change of LGE between first CMR (within 7 days after CO exposure) and follow-up CMR (at 4-5 months after CO exposure)
measure: LV ejection fraction (EF) of TTE performed at the ED
time frame: Within 3 hours at the ED
description: Baseline LV EF of TTE performed at the ED
measure: LV global longitudinal strain (GLS) of TTE performed at the ED
time frame: Within 3 hours at the ED
description: Baseline LV GLS of TTE performed at the ED
measure: LV EF of TTE performed during admission
time frame: Within 7 days after CO exposure
description: Follow-up LV EF of TTE performed during admission
measure: LV GLS of TTE performed during admission
time frame: Within 7 days after CO exposure
description: Follow-up LV GLS of TTE performed during admission
measure: 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
description: Change of LV EF between baseline TTE and follow-up TTE
measure: 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
description: Change of LV GLS between baseline TTE and follow-up TTE
measure: 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
description: 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
arm group label: Acute CO poisoning with myocardial injury
description: 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.
intervention type: Diagnostic Test
intervention name: Cardiac MRI
description: 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)]
arm group label: Acute CO poisoning with myocardial injury
other name: Transthoracic echocardiography (TTE)
study pop: 
sampling method: Probability Sample
criteria: 
gender: All
minimum age: 19 Years
maximum age: N/A
healthy volunteers: No
facility: 
country: Korea, Republic of
responsible party type: Principal Investigator
investigator affiliation: Wonju Severance Christian Hospital
investigator full name: Yong Sung Cha
investigator title: Assistant Professor
mesh term: Poisoning
mesh term: Carbon Monoxide Poisoning
sharing ipd: No