Evaluation of relationship between coronary artery status evaluated by coronary computed tomography angiography and development of cardiomyopathy in carbon monoxide poisoned patients with myocardial injury: a prospective observational study. (2nd January 2018)

• Record Type: Journal Article
• Authors: Cha, Yong Sung; Kim, Hyun; Lee, Yoonsuk; Kwon, Woocheol; Son, Jung-Woo; Youk, Hyun; Kim, Hyung Il; Kim, Oh Hyun; Park, Kyung Hye; Cha, Kyoung-Chul; Lee, Kang Hyun; Hwang, Sung Oh
• Is Part Of: Clinical toxicology. Volume 56:Number 1(2018)
• Page Start: 30
• Page End: 36
• Publication Date: 2018-01-02
• Subjects: Carbon monoxide poisoning -- pathophysiology -- coronary artery stenosis -- cardiomyopathy; Toxicology -- Periodicals; Toxicological emergencies -- Periodicals; 615.9
• DOI: 10.1080/15563650.2017.1337910
• Languages: English
• ISSNs: 1556-3650

Abstract

Abstract: Objectives: Whether 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 methods: This 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. Results: TTE 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. Conclusions: Because 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.