Myocardial Injury and Fibrosis From Acute Carbon Monoxide Poisoning: A Prospective Observational Study

Abstract

ObjectivesThis study sought to evaluate the prevalence and patterns of late gadolinium enhancement (LGE) after carbon monoxide (CO) poisoning using cardiac magnetic resonance (CMR) imaging (CMRI) and transthoracic echocardiography (TTE). BackgroundIn acute 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. MethodsPatients with acute CO poisoning with elevated TnI were evaluated. CMRI was performed within 7 days of CO exposure and after 4 to 5 months. Patients were divided into LGE (n = 72; 69.2%) and no-LGE (n = 32; 30.8%) groups. ResultsIn the LGE group, 39.4%, 4.8%, and 25.0% of patients exhibited midwall, 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 were significantly deteriorated in the LGE group; serial TTE within 7 days indicated that only left ventricular global longitudinal strain remained significantly deteriorated. Three cases of mortality occurred in the LGE group during the 1-year follow-up. ConclusionsThe LGE prevalence in patients with acute CO poisoning with elevated TnI levels, with no underlying cardiovascular diseases and eligible for CMRI, was 69.2%; this proportion primarily comprised patients with a midwall 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. (Cardiac Magnetic Resonance Image in Acute Carbon Monoxide Poisoning; NCT04419298)