Introduction In acute carbon monoxide (CO) poisoning, cardiac injury can predict mortality. However, it remains unclear why increased mortality and cardiovascular events occur despite normalization of CO-induced elevated troponin I (TnI) and cardiac dysfunction. We evaluated the prevalence and patterns of late gadolinium enhancement (LGE) after CO poisoning using cardiac magnetic resonance imaging (CMRI) and transthoracic echocardiography (TTE). Material & Method This prospective, observational study evaluated consecutive patients with acute CO poisoning and myocardial injury admitted to an emergency department between August 2017 and May 2019. CMRI was performed within 7 days of CO exposure and after 4?5 months. Patients were divided into LGE (n=72, 69.2%) and no-LGE (n=32, 30.8%) groups. Result In the LGE group, 39.4%, 4.8%, and 25.0% of patients exhibited mid-wall, subendocardial, and right ventricular insertion point injury, respectively. Diffuse injury was observed in 22.1% of patients, and 67.6% of the 37 patients who underwent follow-up CMRI showed no interval change. On TTE, baseline left ventricular ejection fraction and global longitudinal strain (GLS) were significantly deteriorated in the LGE group; serial TTE within 7 days indicated that only left ventricular GLS remained significantly deteriorated. Three cases of mortality occurred in the LGE group during the 1-year follow-up. Conclusion LGE prevalence in acute CO-poisoned patients with elevated TnI levels, without underlying cardiovascular diseases, and eligible for CMRI was 69.2%, and this comprised patients with mid-wall injury. Of the 37 patients who underwent follow-up CMRI, most chronic phase images showed no interval change. Myocardial fibrosis detected on CMR images was related to acute myocardial dysfunction and subacute deterioration of myocardial strain on TTE.