Acute Carbon Monoxide Poisoning Resulting in ST Elevation Myocardial Infarction: A Rare Case Report

Abstract

Acute carbon monoxide (CO) poisoning with cardiac complications is well documented in the literature. However, ST segment elevation is a rare presentation, and most of these cases with ST elevation have revealed non-occlusive or normal coronary arteries. We report a case of CO poisoning complicated with ST elevation myocardial infarction. Emergency coronary angiography revealed total occlusion of the left anterior descending artery and primary percutaneous coronary intervention was performed. This report of a rare case should remind physicians that cardiovascular investigations, including electrocardiography, must be performed in cases with CO poisoning because mortality might increase if reperfusion therapy or appropriate medical treatments are not performed in patients with acute coronary artery occlusion.

Carbon monoxide: Anticoagulant or procoagulant?

“…In the case of myocardial infarction, it has been demonstrated that CO poisoning causes myocardial injury in the presence of normal coronary arteries [34][35][36][37][38][39][40] and thrombosis of a Nielsen et al 7 7 coronary arterial stent [41], with COHb values observed as small as 2.6% [40] to as high as 52.2% noted [34], with typical values averaging in the 10-20% range [34][35][36][37][38][39][40][41]. While a likely contributor to myocardial necrosis was hypoxia secondary to decreased oxyhemoglobin and increased COHb, the acute occurrence of coronary artery occlusion/thrombus [38][39][40] and coronary artery shunt thrombus [41] formation serve as evidence of an acute CO associated thrombophilic event. Even more impressive are the reports of acute intracardiac thrombus in the right atrium [42][43][44] or left ventricle [45] and pulmonary embolism [46] in patients with the diagnosis of acute CO poisoning;…”

“…In addition to these case reports and series [34][35][36][37][38][39][40][41][42][43][44][45] portraying a procoagulant feature of marked CO exposure, one recent article linked in vitro measures of coagulation with clinical CO poisoning in victims with COHb concentrations over 10% [47]. Compared to normal subjects, 48 CO poisoning victims (COHb=21.97.9%, meanSD) had significantly greater plasma concentrations of prothrombin fragment 1+2, plasminogen activator inhibitor-1 and tissue type plasminogen activator with normal fibrinogen concentrations [47].…”

“…Spectrophotometric measures of resistance to fibrinolysis also demonstrated that these CO poisoning victims had increased plasmatic resistance to fibrinolysis [47]. Taken as a whole, these aforementioned investigations potentially link CO exposure to thrombophilia [28][29][30][31][32][33][34][35][36][37][38][39][40][41][42][43][44][45][46], with increased systemic thrombin generation and hypofibrinolysis being possible mechanisms by which CO were posited to mediate thrombotic events [47].…”

“…There is evidence that excessive CO exposure may result in decreased in vivo and in vitro hemostasis in humans and rodents [4][5][6][7][8][18][19][20][21][22][23], potentially by inhibition of platelet aggregation [9][10][11][12][13]15,16,[20][21][22][23]. However, there is also evidence that increased CO exposure can enhance platelet activation [14,17] and cause enhanced coagulation/decreased fibrinolysis in humans and other mammalian species [28][29][30][31][32][33][34][35][36][37][38][39][40][41][42][43][44][45][46][47][67][68][69][70]…”

ST Elevation Myocardial Infarction Due to Carbon Monoxide Poisoning

“…Though myocardial infarction (MI) is rarely reported after CO intoxication, no distinct ratio is given [6][7][8]. In this study, a patient with no known prior history of coronary artery disease, who developed MI following CO intoxication, is described, along with a review of the relevant literature.…”