Abstract
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 α2-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 monoxide-releasing molecules could be utilized as hemostatic agents.