Elsevier

Journal of Electrocardiology

Volume 45, Issue 5, September–October 2012, Pages 433-442
Journal of Electrocardiology

Current electrocardiographic criteria for diagnosis of Brugada pattern: a consensus report

https://doi.org/10.1016/j.jelectrocard.2012.06.004Get rights and content

Abstract

Brugada syndrome is an inherited heart disease without structural abnormalities that is thought to arise as a result of accelerated inactivation of Na channels and predominance of transient outward K current (Ito) to generate a voltage gradient in the right ventricular layers. This gradient triggers ventricular tachycardia/ventricular fibrillation possibly through a phase 2 reentrant mechanism.

The Brugada electrocardiographic (ECG) pattern, which can be dynamic and is sometimes concealed, being only recorded in upper precordial leads, is the hallmark of Brugada syndrome. Because of limitations of previous consensus documents describing the Brugada ECG pattern, especially in relation to the differences between types 2 and 3, a new consensus report to establish a set of new ECG criteria with higher accuracy has been considered necessary. In the new ECG criteria, only 2 ECG patterns are considered: pattern 1 identical to classic type 1 of other consensus (coved pattern) and pattern 2 that joins patterns 2 and 3 of previous consensus (saddle-back pattern). This consensus document describes the most important characteristics of 2 patterns and also the key points of differential diagnosis with different conditions that lead to Brugada-like pattern in the right precordial leads, especially right bundle-branch block, athletes, pectus excavatum, and arrhythmogenic right ventricular dysplasia/cardiomyopathy.

Also discussed is the concept of Brugada phenocopies that are ECG patterns characteristic of Brugada pattern that may appear and disappear in relation with multiple causes but are not related with Brugada syndrome.

Section snippets

Concept

Brugada syndrome (BrS)1 is a familial, genetically determined syndrome characterized by autosomal dominant inheritance in about 50% of cases with variable penetrance. More than 70 mutations, most commonly in the cardiac Na+ channel, have been described. In around 20% of cases, there are SCN5A mutations that explain the accelerated inactivation of Na channels.2

The diagnosis of BrS is suggested by the clinical history in a patient with specific electrocardiographic (ECG) pattern (Brugada pattern

ECG abnormalities of the BrP

Firstly, we have to say that the abnormal ECG constitutes the hallmark of BrS; but it is necessary to emphasize that the ECG changes can be dynamic and sometimes are concealed. Indeed, the ECG BrP is sometimes intermittent; and it may be observed only in certain situations, such as fever, intoxication, vagal stimulation, and electrolyte imbalance (Table 1).17, 18 Furthermore, there are some drugs (sodium channels blockers) that may unmask a BrP.19 The ECG pattern characteristic of BrS that may

Differential diagnosis

We have to distinguish (a) the cases of spontaneous typical BrP type 1 in case of BrS; (b) the typical BrP type 1 induced by some drugs (sodium channel blockers) or other circumstances (fever, etc) that unmask a BrS; (c) the cases of ECG BrP especially type 1 induced by many circumstances that disappear upon resolution of the injury and that do not present BrS (named phenocopies) (These include acute ischemia, pericarditis, myocarditis, pulmonary embolism, metabolic disorders, ionic disorders,

Conclusions

We have exposed the current ECG criteria of BrP, including the ones described after the last consensus statement,24, 25 which have very high accuracy and could used by nonexperienced physicians for a reliable diagnosis of both types of BrP, especially type 1. The most important points are the following:

  • 1.

    Only 2 ECG patterns should be considered: type 1 (coved type) and type 2 (saddle-back type) that encompass the patterns 2 and 3 of previous consensus (Table 2).

  • 2.

    In both types 1 and 2, the end of

References (52)

  • S. Chevallier et al.

    New electrocardiographic criteria for discriminating between Brugada types 2 and 3 patterns and incomplete right bundle branch block

    J Am Coll Cardiol

    (2011)
  • M. Nishizaki et al.

    Classification and assessment of computerized diagnostic criteria for Brugada-type electrocardiograms

    Heart Rhythm

    (2010)
  • T. Kurita et al.

    The electrophysiologic mechanism of ST segment elevation in Brugada syndrome

    J Am Coll Cardiol

    (2002)
  • J.B. Jayroe et al.

    Differentiating ST elevation myocardial infarction and nonischemic causes of ST elevation by analyzing the presenting electrocardiogram

    Am J Cardiol

    (2009)
  • R. Rosso et al.

    J-point elevation in survivors of primary ventricular fibrillation and matched control subjects: incidence and clinical significance

    J Am Coll Cardiol

    (2008)
  • W. McIntyre et al.

    Coexisting early repolarization pattern and Brugada syndromes recognition of potentially overlapping entities

    J Electrocardiol

    (2012)
  • M.V. Pitzalis et al.

    QT interval prolongation in right precordial leads in Brugada syndrome

    J Am Coll Cardiol

    (2003)
  • M. Babai Bigi et al.

    aVR sign as a risk factor for life-threatening arrhythmic events in patients with Brugada syndrome

    Heart Rhythm

    (2007)
  • H. Makimoto et al.

    Augmented ST-segment elevation during recovery from exercise predicts cardiac events in patients with Brugada syndrome

    J Am Coll Cardiol

    (2010)
  • Z. Huang et al.

    Role of signal-averaged electrocardiograms in arrhythmic risk stratification of patients with Brugada syndrome: a prospective study

    Heart Rhythm

    (2009)
  • V. Probst et al.

    SCN5A mutations and the role of genetic background in the pathophysiology of Brugada syndrome

    Circ Cardiovasc Genet

    (2009)
  • A. Frustaci et al.

    Cardiac histological substrate in patients with clinical phenotype of Brugada syndrome

    Circulation

    (2005)
  • G.X. Yan et al.

    Cellular basis for the Brugada syndrome and other mechanisms of arrhythmogenesis associated with ST-segment elevation

    Circulation

    (1999)
  • P.D. Lambiase et al.

    High-density substrate mapping in Brugada syndrome: combined role of conduction and repolarization heterogeneities in arrhythmogenesis

    Circulation

    (2009)
  • K. Nademanee et al.

    Prevention of ventricular fibrillation episodes in Brugada syndrome by catheter ablation over the anterior right ventricular outflow tract epicardium

    Circulation

    (2011)
  • R. Tukkie et al.

    Delay in right ventricular activation contributes to Brugada syndrome

    Circulation

    (2004)
  • Cited by (287)

    View all citing articles on Scopus

    Sponsored by the International Society for Holter and Noninvasive Electrocardiology (ISHNE).

    View full text