• Yong Sung Cha, Hyun Kim, Yoonsuk Lee, Woocheol Kwon, Jung-Woo Son, Hyun Youk, Hyung Il Kim, Oh Hyun Kim, Kyung Hye Park, Kyoung-Chul Cha, Kang Hyun Lee, and Sung Oh Hwang.
• a Department of Emergency Medicine , Yonsei University Wonju College of Medicine , Wonju , Republic of Korea.
• Clin Toxicol (Phila). 2018 Jan 1; 56 (1): 30-36.

ObjectivesWhether coronary artery changes are a main mechanism in the development of carbon monoxide (CO)-induced cardiomyopathy remains unknown. We investigated the effects of coronary artery stenosis on the presence or patterns of cardiomyopathy in CO-poisoned patients with myocardial injury defined as elevation of troponin I.Materials And MethodsThis prospective observational study collected data from consecutive patients who were diagnosed with CO poisoning and myocardial injury during the 24-month study period. Transthoracic echocardiography (TTE) and coronary computed tomography angiography (CCTA) were performed to evaluate cardiac function and coronary artery status.ResultsTTE and CCTA were performed in 32 consecutive patients. The observed echocardiographic patterns included non-cardiomyopathy (59.4%), left ventricular global dysfunction (25%), Takotsubo cardiomyopathy (6.3%), and cardiomyopathy matching the distribution of the left anterior descending (LAD) artery (9.4%). Four patients had more than moderate stenosis, while stenoses of the LAD, left circumflex, and right coronary arteries were observed in two (6.3%), three (9.4%), and zero patients, respectively. Patients with coronary artery stenosis did not develop cardiomyopathy except for one patient; this patient also did not have regional wall motion abnormalities (RWMA) matched with the stenosis territory.ConclusionsBecause there was no difference in coronary artery stenosis according to the presence or patterns of CO-induced cardiomyopathy, coronary artery stenosis is not the main mechanism for the development of CO-induced cardiomyopathy. Thus, the evaluation of coronary arteries is not necessary in all patients with CO-induced cardiomyopathy unless there is RWMA consistent with ischemic changes in electrocardiograms and elevated troponin I levels.

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