Carbon monoxide poisoning and intracardiac ...

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Aug 28, 2015 - We read the article entitled ''Intracardiac Throm- bus Formation Induced by Carbon Monoxide. Poisoning'' published recently in Human ...
Letter to the Editor

Carbon monoxide poisoning and intracardiac thrombus formation: Additional mechanisms

Human and Experimental Toxicology 2015, Vol. 34(3) 333–334 ª The Author(s) 2015 Reprints and permission: sagepub.co.uk/journalsPermissions.nav DOI: 10.1177/0960327114537324 het.sagepub.com

S Senthilkumaran1, RG Menezes2, R Meenakshisundaram3 and P Thirumalaikolundusubramanian3

We read the article entitled ‘‘Intracardiac Thrombus Formation Induced by Carbon Monoxide Poisoning’’ published recently in Human & Experimental Toxicology with keen interest.1 Herein, we would like to mention additional mechanisms for the formation of intracardiac thrombus following exposure to carbon monoxide. Apart from inhibition of platelet aggregation and alteration of blood flow, carbon monoxide also augments coagulation by increasing the velocity of clot formation, and it also attenuates the susceptibility of clot lysis.2 Furthermore, carbon monoxide makes the thrombus resistant to tissue plasminogen activator by enhancing a2-antiplasmin interaction as documented by thrombelastography.3 The preclinical investigation demonstrated an abnormal increase in density of fibrin fiber and matting after exposure to carbon monoxide.4 Gawlikowski et al.5 have put forward that the formation of less permeable and denser fibrin clot structure with impaired lysis of fibrin clots might have contributed to ischemic manifestations in carbon monoxide-poisoned individuals. However, prolonged exposure to carbon monoxide modulates fibrin clot to fibrinolytic proteins. Apart from activation of nitric oxide and release of other free radicals in carbon monoxide poisoning, the other contributory factors for thrombus formation are mitochondrial dysfunction, microvascular impairment, and oxidative stress and leads to endothelial damage that subsequently increases thrombin formation as evidenced by enhanced tissue factor expression.6 It is likely that oxidative stress might have contributed to the activation of the coagulation cascade. Unfortunately, the influence of subclinical exposure to carbon monoxide on endothelial damage and effects of carbon monoxide on the pharmacokinetics

of therapeutic agents have not been realized by clinicians and research scholars. Elevated levels of carbon monoxide cause a havoc on the health of individuals and precipitates the occurrence of illnesses as well as interferes with therapeutic agents, which are not considered in general during clinical rounds or discussion. Interestingly, one has to find out whether the usefulness of carbon monoxidereleasing molecules could be utilized as hemostatic agents. References 1. Ryoo SM, Sohn CH, Kim HJ, et al. Intracardiac thrombus formation induced by carbon monoxide poisoning. Hum Exp Toxicol 2013; 32: 1193–1196. 2. Nielsen VG, Kirklin JK, and George JF. Carbon monoxide releasing molecule-2 increases the velocity of thrombus growth and strength in human plasma. Blood Coagul Fibrinolysis 2009; 20: 377–380. 3. Malayaman SN, Cohen JB, Machovec KA, et al. Carbon monoxide releasing molecule-2 enhances a2-antiplasmin activity. Blood Coagul Fibrinolysis 2011; 22: 345–348. 1 Department of Emergency and Critical Care Medicine, Sri Gokulam Hospital and Research Institute, Salem, Tamil Nadu, India 2 College of Medicine, King Fahd Hospital of the University, University of Dammam, Dammam, Kingdom of Saudi Arabia 3 Department of Internal Medicine, Chennai Medical College Hospital and Research Center, Irungalur, Trichy, Tamil Nadu, India

Corresponding author: RG Menezes, College of Medicine, King Fahd Hospital of the University, University of Dammam, Dammam, Kingdom of Saudi Arabia. Email: [email protected]

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4. Nielsen VG, Kirklin JK, and George JF. Carbon monoxide-releasing molecule-2 decreases fibrinolysis in human plasma. Blood Coagul Fibrinolysis 2009; 20: 448–455. 5. Gawlikowski T, Gomolka E, Piekoszewski W, et al. Acute CO poisoning is associated with impaired

fibrinolysis and increased thrombin generation. Basic Clin Pharmacol Toxicol 2013; 112: 352–356. 6. Kavakli HS, Erel O, Delice O, et al. Oxidative stress increases in carbon monoxide poisoning patients. Hum Exp Toxicol 2011; 30: 160–164.

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