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Europace Advance Access originally published online on October 15, 2007
Europace 2007 9(12):1216; doi:10.1093/europace/eum229
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2007. For permissions please email: journals.permissions@oxfordjournals.org

ELECTROCARDIOLOGY

Unmasking the Brugada syndrome with high parasternal leads

Manlio F. Márquez*, Ricardo Allende and José L. Morales

Department of Electrophysiology, Instituto Nacional de Cardiología "Ignacio Chávez", Juan Badiano 1, Sección XVI, Tlalpan 14080, Mexico City, Mexico

Manuscript submitted 9 August 2007. Accepted after revision 23 September 2007.

* Corresponding author. Tel: +5255 55133740; fax: +5255 55730994. E-mail address: manliomarquez{at}yahoo.com

Key Words: Brugada syndrome, Electrocardiography, Sudden death

A 37-year-old man underwent implantation of a defibrillator in 1996 for ‘idiopathic ventricular fibrillation’ (nocturnal sudden death in the absence of heart disease).

Retrospective examination of all standard electrocardiograms recorded since then showed intermittent repolarization abnormalities. These were of the ‘saddle-back’ (type II) morphology of Brugada syndrome. The typical coved-type (type I) pattern of Brugada syndrome became evident only when placing standard V1–V3 leads on the 1st, 2nd and 3rd right parasternal spaces and V4–V6 on the left parasternal spaces (Figure 1), as first suggested by Shimizu et al.1Go


Figure 1
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  		Figure 1 Right (RP) and left (LP) high parasternal leads compared with standard V1 and V2 leads.

 

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[1] Shimizu W, Matsuo K, Takagi M, Tanabe Y, Aiba T, Taguchi A, et al. Body surface distribution and response to drugs of ST segment elevation in Brugada syndrome: clinical implication of eighty-seven-lead body surface potential mapping and its application to twelve-lead electrocardiograms. J Cardiovasc Electrophysiol (2000) 11:396–404.[Web of Science][Medline]


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This Article
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