Brugada syndrome

Antzelevitch C, Brugada P, Brugada J, Brugada R, Shimizu W, Gussak I, Perez Riera AR. Brugada syndrome a decade of progress. Circ Res 2002 91 1114— 1118. 

Tada H, Sticherling C, Oral H, Morady F. Brugada syndrome mimicked by tricyclic antidepressant overdose. J Cardiovasc Electrophysiol 2001 12 275. 

The authors of this report thought that the Brugada syndrome was probably not due to chlorpromazine or lithium in this patient, and it has not been previously described with heroin. It may have been due to hyperkalemia (as the Brugada pattern normalized when the serum potassium concentration normalized), perhaps facilitated by cocaine. Another case of Brugada syndrome is described under Drug overdose . 

Brugada J, Brugada P, Brugada R. The ajmaUne challenge in Brugada syndrome. A useful tool or misleading information European Heart J. 2003 24 1085-1086. 

Marquez ME, SaUca G, Hermosillo AG, PasteUn G, Gomez-Hores J, Nava S, Cardenas M. onic basis of pharmacological therapy in Brugada syndrome. J. Cardiovasc. Electrophysiol. 2007 18 234— 240. 

It is unwise to give antidysrhythmic drugs to patients with Brugada syndrome. 

Pinar Bermudez E, Garcia-Alberola A, Martinez Sanchez J, Sanchez Munoz JJ, Valdes Chavarri M. Spontaneous sustained monomorphic ventricular tachycardia after administration of ajmaline in a patient with Brugada syndrome. Pacing Clin Electrophysiol 2000 23(3) 407-9. 

Class Ic antidysrhjdhmic drugs have been reported to cause the characteristic electrocardiographic changes of Brugada syndrome, which consists of right bundle branch block, persistent ST segment elevation, and sudden... 

Fujiki A, Usui M, Nagasawa H, Mizumaki K, Hayashi H, Inoue H. ST segment elevation in the right precordial leads induced with class IC antiarrhythmic drugs insight into the mechanism of Brugada syndrome. J Cardiovasc Electrophysiol 1999 10(2) 214-18. 

Chandrasekaran B, Kurbaan AS. Brugada syndrome a review. Br J Cardiol 2002 9 406-10. 

Priori SG, Napolitano C, Schwartz PJ, Bloise R, Crotti L, Ronchetti E. The elusive link betw een LQT3 and Brugada syndrome the role of flecainide challenge. Circulation 2000 102(9) 945-7. 

Bezzina C, Veldkamp MW, Van Den Berg MP, Postma AV, Rook MB, et al. 1999. A single Na(+) channel mutation causing both long-QT and Brugada syndromes. Circ. Res. 85 1206-13... 

Shu J, Zhu T, Yang L, Cui C, Yan GX. ST-segment elevation in the early repolarization syndrome, idiopathic ventricular fibrillation, and the Brugada syndrome cellular and clinical linkage. J Electrocardiol 2005 38 26. 

Wilde AA, Antzelevitch C, Borggrefe M et al. Proposed diagnostic criteria for the Brugada syndrome consensus report. Circulation 2002 106 2514. 

Bean What about patients with Brugada syndrome, which is caused by the other mutation in SCNSA ... 

Makita N, Shirai N, Wang D et al 2000 Cardiac Na channel dysfunction in Brugada syndrome is aggravated by jSl-subunit. Circulation 101 54-60... 

Note LQTS can be provoked by potassium channel blockers (e.g., quinidine, sotalol), and Brugada syndrome can be provoked by potent sodium channel blockers (e.g., cocaine, flecainide). LQTS3 and Brugada may coexist. 

Ventricular fibrillation is electrical anarchy of the ventricle resulting in no cardiac output and cardiovascular collapse. Death wiU ensue rapidly if effective treatment measures are not taken. Patients who die abruptly (within 1 hour of initial symptoms) and unexpectedly (i.e., sudden death) usually have ventricular fibrillation recorded at the time of death. Sudden cardiac death accounts for about 400,000 deaths per year or 1000 deaths per day in the United States. Sudden cardiac death occurs most commonly in patients with ischemic heart disease and primary myocardial disease associated with LV dysfunction, less commonly in those with WPW syndrome and mitral valve prolapse, and occasionally, in those without associated heart disease (e.g., Brugada syndrome). Patients who have sudden cardiac death (not associated with acute MI) but survive because of appropriate CPR often have inducible sustained ventricular tachycardia and/or ventricular fibrillation during electrophysiologic studies. These individuals are at high risk for the recurrence of ventricular tachycardia and/or ventricular fibrillation. 

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