Drug-induced Brugada Syndrome

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

Disclosures

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.

Comments

3090D553-9492-4563-8681-AD288FA52ACE
Comments on Medscape are moderated and should be professional in tone and on topic. You must declare any conflicts of interest related to your comments and responses. Please see our Commenting Guide for further information. We reserve the right to remove posts at our sole discretion.

processing....