Drug-induced Brugada Syndrome

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


Europace. 2009;11(8):989-994. 

In This Article

Calcium Channel Blockers

Although there has only been one report of verapamil-induced Brugada syndrome among all the calcium channel blockers,[65] co-administration of diltiazem and isosorbide-5-mononitrate had also been reported to induce the Brugada ECG pattern and ventricular tachycardia in the patient aforementioned.

Fish and Antzelevitch proposed a cellular mechanism for the Brugada syndrome in which accentuation of the epicardial action potential notch and eventual loss of the epicardial action potential dome results in ST-segment elevation, phase 2 re-entry, and polymorphic VT/VF.[11] The proposed mechanism involves a rebalancing of the currents available at the end of phase 1 of the epicardial action potential. Diminution of inward currents (I Na and I Ca) or enhancement of outward currents (I to and I K-ATP) results in a slowing of the second upstroke of the epicardial action potential, eventually leading to loss of the action potential dome as a consequence of all-or-none repolarization at the end of phase 1. Thus, mechanistically, the pro-arrhythmic action of calcium channel blockers could be explained by the additional I Ca block by calcium channel blockers a situation with pre-existing defective I Na channel resulting in a synergistic loss of the epicardial action potential dome and precipitates the syndrome.


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