Cardiac Magnetic Resonance Image (CMR) in Acute Carbon Monoxide (CO) Poisoning

June 2, 2020 updated by: Yong Sung Cha, Wonju Severance Christian Hospital

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.

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.

Study Overview

Status

Completed

Intervention / Treatment

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 Type

Observational

Enrollment (Actual)

104

Contacts and Locations

This section provides the contact details for those conducting the study, and information on where this study is being conducted.

Study Locations

    • Gangwon
      • Wonju, Gangwon, Korea, Republic of, 26426
        • Wonju Severance Christian Hospital

Participation Criteria

Researchers look for people who fit a certain description, called eligibility criteria. Some examples of these criteria are a person's general health condition or prior treatments.

Eligibility Criteria

Ages Eligible for Study

19 years and older (Adult, Older Adult)

Accepts Healthy Volunteers

No

Genders Eligible for Study

All

Sampling Method

Probability Sample

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.

Description

Inclusion Criteria:

  • Acute CO poisoning with myocardial injury, which was defined as elevated TnI (reference range < 0.045 ng/mL), within 24 hours after ED arrival.

Exclusion Criteria:

  • 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
  • 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

Study Plan

This section provides details of the study plan, including how the study is designed and what the study is measuring.

How is the study designed?

Design Details

  • Observational Models: Cohort
  • Time Perspectives: Prospective

Cohorts and Interventions

Group / Cohort
Intervention / Treatment
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.

  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)]
Other Names:
  • Transthoracic echocardiography (TTE)

What is the study measuring?

Primary Outcome Measures

Outcome Measure
Measure Description
Time Frame
Late gadolinium enhancement (LGE) in CMR
Time Frame: Within 7 days after acute CO poisoning
Prevalence (percent) of presence of LGE in CMR
Within 7 days after acute CO poisoning
LGE involved wall in CMR
Time Frame: Within 7 days after acute CO poisoning
Injured left ventricular wall according to LGE in CMR
Within 7 days after acute CO poisoning

Secondary Outcome Measures

Outcome Measure
Measure Description
Time Frame
LGE size in CMR
Time Frame: Within 7 days after acute CO poisoning
Injury size according to LGE in CMR
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
Change of LGE between first CMR (within 7 days after CO exposure) and follow-up CMR (at 4-5 months after CO exposure)
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
Baseline LV EF of TTE performed at the ED
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
Baseline LV GLS of TTE performed at the ED
Within 3 hours at the ED
LV EF of TTE performed during admission
Time Frame: Within 7 days after CO exposure
Follow-up LV EF of TTE performed during admission
Within 7 days after CO exposure
LV GLS of TTE performed during admission
Time Frame: Within 7 days after CO exposure
Follow-up LV GLS of TTE performed during admission
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 EF between baseline TTE and follow-up TTE
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
Change of LV GLS between baseline TTE and follow-up TTE
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
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
GDS (minimum 1 - maximum 7) evaluated at 1, 6, and 12 months after CO exposure

Collaborators and Investigators

This is where you will find people and organizations involved with this study.

Publications and helpful links

The person responsible for entering information about the study voluntarily provides these publications. These may be about anything related to the study.

Study record dates

These dates track the progress of study record and summary results submissions to ClinicalTrials.gov. Study records and reported results are reviewed by the National Library of Medicine (NLM) to make sure they meet specific quality control standards before being posted on the public website.

Study Major Dates

Study Start (Actual)

August 1, 2017

Primary Completion (Actual)

May 23, 2019

Study Completion (Actual)

May 25, 2020

Study Registration Dates

First Submitted

May 28, 2020

First Submitted That Met QC Criteria

June 2, 2020

First Posted (Actual)

June 5, 2020

Study Record Updates

Last Update Posted (Actual)

June 5, 2020

Last Update Submitted That Met QC Criteria

June 2, 2020

Last Verified

June 1, 2020

More Information

Terms related to this study

Other Study ID Numbers

  • CMR-CO

Plan for Individual participant data (IPD)

Plan to Share Individual Participant Data (IPD)?

No

Drug and device information, study documents

Studies a U.S. FDA-regulated drug product

No

Studies a U.S. FDA-regulated device product

No

This information was retrieved directly from the website clinicaltrials.gov without any changes. If you have any requests to change, remove or update your study details, please contact register@clinicaltrials.gov. As soon as a change is implemented on clinicaltrials.gov, this will be updated automatically on our website as well.

Clinical Trials on Myocardial Injury

Clinical Trials on Cardiac MRI

Subscribe