Abstract/Text: Patients with a suspected acute coronary syndrome and left bundle branch block (LBBB) present a unique diagnostic and therapeutic challenge to the clinician. Although current guidelines recommend that patients with new or presumed new LBBB undergo early reperfusion therapy, data suggest that only a minority of patients with LBBB are ultimately diagnosed with acute myocardial infarction, regardless of LBBB chronicity, and that a significant proportion of patients will not have an occluded culprit artery at cardiac catheterization. The current treatment approach exposes a significant proportion of patients to the risks of fibrinolytic therapy without the likelihood of significant benefit and leads to increased rates of false-positive cardiac catheterization laboratory activation, unnecessary risks, and costs. Therefore, alternative strategies to those for patients with ST-segment elevation myocardial infarction are needed to guide selection of appropriate patients with a suspected acute coronary syndrome and LBBB for urgent reperfusion therapy. In this article, we describe the evolving epidemiology of LBBB in acute coronary syndromes and discuss controversies related to current clinical practice. We propose a more judicious diagnostic approach among clinically stable patients with LBBB who do not have electrocardiographic findings highly specific for ST-segment elevation myocardial infarction.

Copyright © 2012 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.

Abstract/Text: In an effort to standardize terminology and criteria for clinical electrocardiography, and as a follow-up of its work on definitions of terms related to cardiac rhythm, an Ad Hoc Working Group established by the World Health Organization and the International Society and Federation of Cardiology reviewed criteria for the diagnosis of conduction disturbances and pre-excitation. Recommendations resulting from these discussions are summarized for the diagnosis of complete and incomplete right and left bundle branch block, left anterior and left posterior fascicular block, nonspecific intraventricular block, Wolff-Parkinson-White syndrome and related pre-excitation patterns. Criteria for intraatrial conduction disturbances are also briefly reviewed. The criteria are described in clinical terms. A concise description of the criteria using formal Boolean logic is given in the Appendix. For the incorporation into computer electrocardiographic analysis programs, the limits of some interval measurements may need to be adjusted.

Abstract/Text: 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 (I(to)) 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.

Copyright © 2012 Elsevier Inc. All rights reserved.

Abstract/Text: Two decades ago, a series of 8 idiopathic ventricular fibrillation patients who each had an abnormal ECG (right bundle branch block with coved-type ECG), but otherwise had normal hearts were described by Brugada and Brugada. Since then, the clinical entity has become known as Brugada syndrome (BS). Shortly thereafter, mutations of the SCN5A gene that encodes for the α-subunit of the sodium channel were found, galvanizing the field of ion channelopathies following in the footsteps of the breakthrough in long QT syndrome. Over the past 20 years, extensive research in this field has produced major progress toward better understanding of BS and the gaining of knowledge of the genetic background, pathophysiology and new management. Two consensus reports were published to help define the diagnostic criteria, risk stratification and management of BS patients. However, there are controversies. In this review, we will share our experiences of BS patients in Thailand and discuss advances in many aspects of the syndrome (ie, genetics and pathophysiology) and some of these pertinent controversies, as well as new treatment of the syndrome with catheter ablation.