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Transient ST Segment Elevation Caused by Intracoronary Thrombus after Acute Carbon Monoxide Poisoning

Published online by Cambridge University Press:  09 October 2019

Ercan Akşit*
Affiliation:
Canakkale Onsekiz Mart University Faculty of Medicine, Department of Cardiology, Canakkale, Turkey
Özge Turgay Yildirim
Affiliation:
Eskisehir State Hospital, Department of Cardiology, Eskişehir, Turkey
Fatih Aydin
Affiliation:
Eskisehir State Hospital, Department of Cardiology, Eskişehir, Turkey
Okan Bardakci
Affiliation:
Canakkale Onsekiz Mart University Faculty of Medicine, Department of Emergency Service, Canakkale, Turkey
Ayşe Hüseyınoğlu Aydin
Affiliation:
Eskisehir State Hospital, Department of Cardiology, Eskişehir, Turkey
*
Correspondence: Ercan Akşit Barbaros Street Terzioglu Campus B Block No: 4 Onsekiz Mart University Faculty of Medicine Department of Cardiology Canakkale/Turkey E-mail: [email protected]

Abstract

Carbon monoxide (CO) poisoning is the most common cause of death and injury among all poisonings. Myocardial injury is detected in one-third of CO poisonings. In this Case Report, a previously healthy 41-year-old man was referred for CO poisoning. The initial electrocardiogram (ECG) showed 1mm ST segment elevation in leads DII, DIII, and aVF. As the patient did not describe chest pain and had no cardiac symptoms, ECG was repeated 10 minutes later and it was seen that ST segment elevation disappeared. As the patient had a transient ST segment elevation and elevated high-sensitive Tn-T (HsTn-T), the patient was transferred to the coronary angiography laboratory. The patient’s left coronary system was normal, but a thrombus image narrowing the lumen by approximately 60% was observed in the right coronary artery. Intravenous tirofiban was administered for 48 hours. Control coronary angiography showed continuing thrombus formation and a bare metal stent was successfully implanted. This is the first reported case with transient ST segment elevation associated with acute coronary thrombus caused by CO poisoning. It may be recommended that patients with CO poisoning should be followed-up with a 12-lead ECG monitor or 24-hour ECG Holter monitoring, even if they show no cardiac symptoms and echocardiography shows no wall motion abnormality. Early coronary angiography upon detection of such dynamic ECG changes in these recordings as ST segment elevation can reduce the risk of myocardial infarction (MI) and mortality in these patients.

Type
Case Report
Copyright
© World Association for Disaster and Emergency Medicine 2019 

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References

Hampson, NB, Weaver, LK. Carbon monoxide poisoning: a new incidence for an old disease. Undersea Hyperb Med. 2007;34(3):163168.Google ScholarPubMed
Lippi, G, Rastelli, G, Meschi, T, Borghi, L, Cervellin, G., Pathophysiology, clinics, diagnosis and treatment of heart involvement in carbon monoxide poisoning. Clin Biochem. 2012;45(16-17):12781285.CrossRefGoogle ScholarPubMed
Huang, CC, Ho, CH, Chen, YC, et al. Risk of myocardial infarction after carbon monoxide poisoning: a nationwide population-based cohort study. Cardiovasc Toxicol. 2019;19(2):147155.CrossRefGoogle ScholarPubMed
Reumuth, G, Alharbi, Z, Houschyar, KS, et al. Carbon monoxide intoxication: what we know. Burns. 2019;45(3):526530.CrossRefGoogle ScholarPubMed
Kalay, N, Ozdogru, I, Cetinkaya, Y, et al. Cardiovascular effects of carbon monoxide poisoning. Am J Cardiol. 2007;99(3):322324.CrossRefGoogle ScholarPubMed
Genç, S, Baydın, A, Aygün, D, İncealtın, O. Two carbon monoxide poisoning cases with similar carboxihemoglobin levels and different clinical presentations. J Acad Emerg Med. 2008;7:4748.Google Scholar
Gülbay, BE, Önen, ZP. Carbon monoxide poisoning. J Surg Med. 2006;2:109112.Google Scholar
Rose, JJ, Wang, L, Xu, Q, et al. Carbon monoxide poisoning: pathogenesis, management, and future directions of therapy. Am J Respir Crit Care Med. 2017;195(5):596606.CrossRefGoogle ScholarPubMed
Unlu, M, Ozturk, C, Demirkol, S, et al. Thrombolytic therapy in a patient with inferolateral myocardial infarction after carbon monoxide poisoning. Hum Exp Toxicol. 2016;35(1):101105.CrossRefGoogle Scholar
Hsu, PC, Lin, TH, Su, HM, et al. Acute carbon monoxide poisoning resulting in ST elevation myocardial infarction: a rare case report. Kaohsiung J Med Sci. 2010;26(5):271275.CrossRefGoogle Scholar
Dziewierz, A, Ciszowski, K, Gawlikowski, T, et al. Primary angioplasty in patient with STsegment elevation myocardial infarction in the setting of intentional carbon monoxide poisoning. J Emerg Med. 2013;45(6):831834.CrossRefGoogle Scholar
Nelson, LH. Carbon Monoxide. Goldfrank’s Toxicologic Emergencies. 7th edition. New York, USA: McGraw-Hill; 2002:16891704.Google Scholar
Tritapepe, L, Macchiarelli, G, Rocco, M, et al. Functional and ultrastructural evidence of myocardial stunning after acute carbon monoxide poisoning. Crit Care Med. 1998;26(4):797801.CrossRefGoogle ScholarPubMed
Satran, D, Henry, CR, Adkinson, C, Nicholson, CI, Bracha, Y, Henry, TD. Cardiovascular manifestations of moderate to severe carbon monoxide poisoning. J Am Coll Cardiol. 2005;45(9):15131516.CrossRefGoogle ScholarPubMed
Kaya, H, Coşkun, A, Beton, O, et al. COHgb levels predict the long-term development of acute myocardial infarction in CO poisoning. Am J Emerg Med. 2016;34(5):840844.CrossRefGoogle ScholarPubMed