Carbon monoxide-induced myocardial injury: Mechanisms, structural Remodeling, and clinical implications

Carbon monoxide (CO) poisoning remains a leading cause of toxic exposure worldwide. Beyond hypoxic injury, CO exerts direct cardiotoxic effects that contribute to both short- and long-term morbidity and mortality. Myocardial injury occurs frequently after CO exposure, including in patients without known coronary artery disease, and is associated with an increased risk of death, heart failure, and arrhythmias months to years after exposure. Nonetheless, cardiac injury often goes clinically unrecognized and is inconsistently evaluated in acute care settings.

A comprehensive scoping review was performed to summarize evidence published from between January 1990 and to December 2025 on the epidemiology, pathophysiology, clinical manifestations, and diagnostic evaluation of CO-related myocardial injury, with an emphasis on early detection and risk stratification in the ED. Findings were summarized qualitatively with emphasis on clinical relevance to acute care.

Across studies, 20-40% of patients with moderate to severe CO poisoning demonstrated evidence of myocardial injury, as identified by elevated cardiac biomarkers or abnormal electrocardiography. Such injury is linked to a twofold increase in long-term mortality and adverse cardiovascular events. Mechanisms extend beyond hypoxia and include mitochondrial dysfunction, oxidative stress, endothelial injury, and catecholamine-mediated toxicity. Advanced imaging studies reveal persistent myocardial fibrosis and subclinical dysfunction even after apparent clinical recovery.

As cardiac involvement is often clinically occult, reliance on symptoms alone may miss clinically significant myocardial injury, particularly in younger patients and those without known cardiac disease. Routine use of electrocardiography, cardiac biomarkers, and bedside echocardiography may improve early detection and risk stratification.