2022
DOI: 10.7759/cureus.24309
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A Rare yet Morbid Complication of Cocaine Use: Brugada Type 1 on Electrocardiogram

Abstract: Cocaine is considered a leading non-opioid cause of drug overdose in the US. It acts as a sympathomimetic and increases the amount of catecholamines, thereby increasing the risk of ventricular irritability and resultant arrhythmias. Its sodium (Na) channel blockage is the principal mechanism behind the Brugada pattern on an electrocardiogram (ECG), which is often transient but is indistinguishable from that of Brugada syndrome, the autosomal dominant channelopathy.We are presenting a case of a 32-year-old male… Show more

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Cited by 2 publications
(5 citation statements)
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“…In Brugada syndrome, findings associated with a loss-of-function mutation in the SCN5A gene reveal alterations in the encoding of alpha subunits of myocardial sodium channels. These genetic defects result in defective sodium channels that decrease sodium influx while enhancing outward current, thereby leading to a plateaued action potential and increasing susceptibility to reentry ventricular arrhythmias [ 4 , 5 ]. Cocaine is a known cardiac sodium channel blocker and inhibits these channels by preferentially binding to open or inactivated states, inducing concentration-dependent inhibition and slowing channel repriming, suggesting a pore-blocking mechanism and stabilization of the channels in an inactivated state [ 6 ].…”
Section: Discussionmentioning
confidence: 99%
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“…In Brugada syndrome, findings associated with a loss-of-function mutation in the SCN5A gene reveal alterations in the encoding of alpha subunits of myocardial sodium channels. These genetic defects result in defective sodium channels that decrease sodium influx while enhancing outward current, thereby leading to a plateaued action potential and increasing susceptibility to reentry ventricular arrhythmias [ 4 , 5 ]. Cocaine is a known cardiac sodium channel blocker and inhibits these channels by preferentially binding to open or inactivated states, inducing concentration-dependent inhibition and slowing channel repriming, suggesting a pore-blocking mechanism and stabilization of the channels in an inactivated state [ 6 ].…”
Section: Discussionmentioning
confidence: 99%
“…Cocaine is a known cardiac sodium channel blocker and inhibits these channels by preferentially binding to open or inactivated states, inducing concentration-dependent inhibition and slowing channel repriming, suggesting a pore-blocking mechanism and stabilization of the channels in an inactivated state [ 6 ]. Therefore, we predict that in a mechanism similar to that of the loss of function mutation within the SCN5A gene, cocaine may either directly produce Brugada-like ECG findings or may actually serve to unmask underlying Brugada syndrome in otherwise asymptomatic patients through the decreased cardiac sodium influx [ 4 ].…”
Section: Discussionmentioning
confidence: 99%
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