Drug-induced Brugada Syndrome

Yee Guan Yap; Elijah R. Behr; A. John Camm

Disclosures

Europace. 2009;11(8):989-994. 

In This Article

Cocaine

Sudden unexpected death due to cocaine in young otherwise healthy individuals occurs in an idiosyncratic manner and is commonly felt to be arrhythmogenic in nature, although the exact cause of death is rarely documented. In addition to indirect sympathomimetic actions, cocaine has a potent sodium channel blocking effect resembling that of flecainide.[52] The sodium channel blocking property of cocaine is now thought to be a major mechanism behind cocaine-induced sudden cardiac death.

A case of transient Brugada type 1 ECG pattern provoked by recreational cocaine use has been reported in an individual with a normal baseline ECG.[53] An electrophysiological study performed in the presence of these changes was unremarkable and challenge with procainamide, propranolol, and noradrenaline failed to re-induce the pattern. Its clinical importance is unclear.

More commonly, cocaine-induced Brugada syndrome has been reported following overdose with the drug. In one case, a patient with massive cocaine ingestion complicated by generalized seizures, an asystolic cardiac arrest and severe metabolic acidosis, developed right bundle branch block, left anterior fascicular block, QRS and QT prolongation, and coved ST-segment elevation in leads V1 and V2. Sodium bicarbonate administration rapidly normalized cardiac conduction and the Brugada pattern settled slowly. Subsequent flecainide challenge was unremarkable.[54] Several similar cases of drug-induced Brugada syndrome following cocaine overdose have also been reported.[55–57] Cocaine significantly prolonged the PR, QRS, QTc, AH, and HV intervals in a canine model.[58] During cocaine toxicity, myocardial depression, malignant arrhythmias, and sudden death could relate in part to its potent sodium channel blockade[59,60] resembling flecainide.[52]

Interestingly, the class IB antiarrhythmic lidocaine, much like cocaine, inhibits the voltage-gated cardiac sodium channels but has an antiarrhythmic effect, whereas cocaine may be pro-arrhythmic. This may be explained by lidocaine's other actions on INa that are not shared with cocaine: a strong voltage-dependence of INa inhibition; and a large leftward shift of the steady-state inactivation to hyperpolarized potentials which appeared to be very important in the prevention of fatal arrhythmias by lidocaine.[61]

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