Javier García-Niebla
Hospital Universitario de Canarias
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Featured researches published by Javier García-Niebla.
Journal of Electrocardiology | 2012
Antonio Bayés de Luna; Josep Brugada; Adrian Baranchuk; Martin Borggrefe; Guenter Breithardt; Diego Goldwasser; Pier D. Lambiase; Andres Ricardo Perez Riera; Javier García-Niebla; Carlos Alberto Pastore; Giuseppe Oreto; William J. McKenna; Wojciech Zareba; Ramon Brugada; Pedro Brugada
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.
Journal of Electrocardiology | 2012
Antonio Bayés de Luna; Pyotr G. Platonov; Francisco G. Cosio; Iwona Cygankiewicz; Carlos Alberto Pastore; Rafa Baranowski; Antoni Bayes-Genis; Josep Guindo; Xavier Viñolas; Javier García-Niebla; Raimundo Barbosa; Shlomo Stern; David H. Spodick
Impaired interatrial conduction or interatrial block is well documented but is not described as an individual electrocardiographic (ECG) pattern in most of ECG books, although the term atrial abnormalities to encompass both concepts, left atrial enlargement (LAE) and interatrial block, has been coined. In fact, LAE and interatrial block are often associated, similarly to what happens with ventricular enlargement and ventricular block. The interatrial blocks, that is, the presence of delay of conduction between the right and left atria, are the most frequent atrial blocks. These may be of first degree (P-wave duration >120 milliseconds), third degree (longer P wave with biphasic [±] morphology in inferior leads), and second degree when these patterns appear transiently in the same ECG recording (atrial aberrancy). There are evidences that these electrocardiographic P-wave patterns are due to a block because they may (a) appear transiently, (b) be without associated atrial enlargement, and (c) may be reproduced experimentally. The presence of interatrial blocks may be seen in the absence of atrial enlargement but often are present in case of LAE. The most important clinical implications of interatrial block are the following: (a) the first degree interatrial blocks are very common, and their relation with atrial fibrillation and an increased risk for global and cardiovascular mortality has been demonstrated; (b) the third degree interatrial blocks are less frequent but are strong markers of LAE and paroxysmal supraventricular tachyarrhythmias. Their presence has been considered a true arrhythmological syndrome.
Annals of Noninvasive Electrocardiology | 2013
Sara F.M. Awad; Raimundo Barbosa-Barros; Lucia de Sousa Belem; Camila Pinto Cavalcante; Andrés Ricardo Pérez Riera; Javier García-Niebla; Daniel D. Anselm; Adrian Baranchuk
Brugada phenocopies (BrP) have emerged as new clinical entities that are etiologically distinct from true Brugada syndrome (BrS). BrP are characterized by an ECG pattern that is phenotypically identical to true BrS (type 1 or type 2); however, BrP are caused by various other factors such as mechanical mediastinal compression, myocardial ischemia, pericarditis, myocarditis, pulmonary embolism, and metabolic disturbances. We report a case of an electrocardiographic BrP in a patient with pectus excavatum deformity in the absence of true BrS using currently defined BrP diagnostic criteria. A systematic review of ECG manifestations associated with pectus excavatum is also discussed.
Journal of Electrocardiology | 2009
Javier García-Niebla; Guillem Serra-Autonell
Some technical aspects in the ECG recording, although basic, are not well enough known. In this short communication we present two examples in which the low-pass filter attenuates or eliminates electrocardiographic signals which are important from the clinical point of view.
Annals of Noninvasive Electrocardiology | 2015
Adrian Baranchuk; Andres Enriquez; Javier García-Niebla; Antoni Bayes-Genis; Roger Villuendas; Antoni Bayés de Luna
One of the more frequent dilemmas in ECG interpretation is the differential diagnosis of an rSr’ pattern in leads V1‐V2. We often face this finding in asymptomatic and otherwise healthy individuals and the causes may vary from benign nonpathological variants to severe or life‐threatening heart diseases, such as Brugada syndrome or arrhythmogenic right ventricular dysplasia. In other cases, a normal variant of rSr’ pattern can be misinterpreted as pathological after the occurrence of certain clinical events such as cardiac arrest or syncope of unknown cause. In this review we analyze in detail all the possible conditions, both benign and pathological that may explain the presence of this electrocardiographic pattern. We also propose a simple electrocardiographic algorithm for differential diagnosis.
Journal of the American College of Cardiology | 2010
Andrés Carrillo; Miquel Fiol; Javier García-Niebla; Antonio Bayés de Luna
Kosuge et al. ([1][1]) present an interesting analysis on differentiating Takotsubo cardiomyopathy from anterior acute myocardial infarction using electrocardiographic criteria. However, we would like to draw attention to certain aspects of this paper. The authors do not report how the Takotsubo
Current Cardiology Reviews | 2014
Antonio Bayés de Luna; Javier García-Niebla; Adrian Baranchuk
Brugada syndrome is a genetically determined familial disease with autosomal dominant transmission and variable penetrance, conferring a predisposition to sudden cardiac death due to ventricular arrhythmias. The syndrome is characterized by a typical electrocardiographic pattern in the right precordial leads. This article will focus on the new electrocardiographic features recently agreed on by expert consensus helping to identify this infequent electrocardiographic pattern.
Journal of Electrocardiology | 2009
Javier García-Niebla; Diego Goldwasser; Antonio Bayés de Luna
We present a case of a 55-year-old-man with acute coronary syndrome due to occlusion of the right coronary artery. Electrocardiogram showed ST-segment elevation in nine leads. We explain the causes of this exceptional electrocardiographic pattern.
Journal of Electrocardiology | 2008
Javier García-Niebla; Pablo Llontop García
Accidental interchange between precordial and limb leads, although unusual, can be possible given that some of them share the same color. We present the case where interchange of V(2) and left arm cables produced significant electrocardiographic abnormalities, which created many doubts and discussion within the clinical team.
Journal of Electrocardiology | 2016
Byron H. Gottschalk; Javier García-Niebla; Daniel D. Anselm; Atul Jaidka; Antoni Bayés de Luna; Adrian Baranchuk
BACKGROUND Brugada phenocopies (BrP) are clinical entities characterized by ECG patterns that are identical to true Brugada syndrome (BrS), but are elicited by various clinical circumstances. A recent study demonstrated that the patterns of BrP and BrS are indistinguishable under the naked eye, thereby validating the concept that the patterns are identical. OBJECTIVE The aim of our study was to determine whether recently developed ECG criteria would allow for discrimination between type-2 BrS ECG pattern and type-2 BrP ECG pattern. METHODS Ten ECGs from confirmed BrS (aborted sudden death, transformation into type 1 upon sodium channel blocking test and/or ventricular arrhythmias, positive genetics) cases and 9 ECGs from confirmed BrP were included in the study. Surface 12-lead ECGs were scanned, saved in JPEG format for blind measurement of two values: (i) β-angle; and (ii) the base of the triangle. Cut-off values of ≥58° for the β-angle and ≥4mm for the base of the triangle were used to determine the BrS ECG pattern. RESULTS Mean values for the β-angle in leads V1 and V2 were 66.7±25.5 and 55.4±28.1 for BrS and 54.1±26.5 and 43.1±16.1 for BrP respectively (p=NS). Mean values for the base of the triangle in V1 and V2 were 7.5±3.9 and 5.7±3.9 for BrS and 5.6±3.2 and 4.7±2.7 for BrP respectively (p=NS). The β-angle had a sensitivity of 60%, specificity of 78% (LR+ 2.7, LR- 0.5). The base of the triangle had a sensitivity of 80%, specificity of 40% (LR+ 1.4, LR- 0.5). CONCLUSIONS New ECG criteria presented relatively low sensitivity and specificity, positive and negative predictive values to discriminate between BrS and BrP ECG patterns, providing further evidence that the two patterns are identical.