Vectocardiographic analysis of right ventricular electrical conduction delay

Introdução: A interpretação eletrocardiográfica do atraso final da condução no ramo do ventrículo direito do coração já gerou algumas hipóteses de que esse ramo direito não é único como demonstrado anatomicamente e que pode ser divido em ramos terminais distintos quando analisamos o traçado através do vetocardiograma.Método: Separados 227 eletrocardiogramas com características típicas definidas como atraso final de condução dos pacientes do serviço de eletrocardiografia do Centro Universitário FMABC, de ambos os sexos na faixa de idade de 18 a 87 anos, etnias, peso e estatura variadas com fatores de risco cardiovascular ou sem fator de risco, realizamos vetocardiograma nesses pacientes para observar o comportamento da porção final da condução elétrica. Resultado: Analisando os traçados vetocardiográficos dos pacientes que apresentavam o atraso final de condução no eletrocardiograma, confirmamos no registro pelo plano frontal, a presença do atraso final de condução, porém registravam em três regiões distintas; 103 pacientes no quadrante superior direito entre -120º e -150º, 45 pacientes no quadrante inferior direito entre +170º e -170º e medial e 79 pacientes no quadrante inferior direito entre +110º e + 140º.Conclusão: A despolarização elétrica do coração no ventrículo direito no traçado eletrocardiográfico aparentemente registra alterações típicas que podemos diagnosticar como uma despolarização de um feixe único, porém ao realizarmos vetocardiograma, registramos três zonas distintas de despolarização ventricular direita com atraso, ou seja, três setores distintos da parede livre do ventrículo direito como atraso Tipo I (superior), Tipo II (inferior), e Tipo III (medial).

Introduction: The electrocardiographic interpretation of end conduction delay (ECD) in the right ventricular branch of the heart has already generated some hypotheses that this right branch is not single, as anatomically demonstrated, and can be divided into distinct terminal branches when we analyze tracings through the vectorcardiogram.Methods: There were 227 electrocardiograms selected, with typical characteristics defined as ECD of patients from the electrocardiography service of the Centro Universitário Saúde ABC, of both sexes, in the age range of 18 to 87 years, with varied ethnicities, weight and height, with cardiovascular risk factors or without them. We performed vectorcardiograms in these patients to observe the behavior of the final portion of electrical conduction.Results: Analyzing the vectorcardiographic tracings of patients who presented ECD in electrocardiogram, we confirmed in the recording by the frontal plane, the presence of ECD but recorded in three distinct regions; 103 patients in the right upper quadrant between -120° and -150°, 45 patients in the right lower quadrant between +170° and -170°, and medial, and 79 patients in the right lower quadrant between +110° and + 140°.Conclusion: Electrical depolarization of the heart in the right ventricle in electrocardiographic tracings apparently records typical alterations that we can diagnose as depolarization of a single bundle; but when we performed vectorcardiograms, we recorded three distinct zones of right ventricular depolarization with delay; i.e., three distinct sectors of right ventricle free wall delay, such as type I (upper), type II (lower) and type III (medial).

Brugada syndrome unmasked by fever and paradoxical lower degree of dromotropic disturbance in the right ventricular outflow tract

Brugada syndrome (BrS) is an inherited clinical-electrocardiographic arrhythmic entity with an autosomal dominant genetic pattern of inheritance or de novo variant. The syndrome has low worldwide prevalence, but is endemic in Southeast Asian countries (Thailand, Philippines and Japan). The BrS is a subtle structural heart disease (SHD), and the diagnosis is only possible when the so-called type 1 Brugada ECG pattern is spontaneously present or induced for example with fever. Repolarization-depolarization disturbances in BrS patients can be caused by genetic mutations, abnormal neural crest cell migration, low expression of connexin-43 gap junction protein, or connexome disturbances. A recent autopsy study revealed increase in biventricular collagen with myocardial fibrosis when compared with control subjects although the main affected cardiac territory is the right ventricular outflow tract (RVOT). In this location, there is abnormally low expression of significant connexin-43 gap junction responsible for the electro-vectorcardiographic manifestations of terminal QRS conduction delay in the right standard precordial leads (V1-V2), high right precordial leads (V1H-V2H), as well as in the unipolar aVR lead ("the forgotten lead"). Based on their location, these leads reflect the electrical activity of the RVOT.

A síndrome de Brugada (SBr) é uma entidade arrítmica clínico-eletrocardiográfica hereditária com padrão genético autossômico dominante de herança ou variante de novo. A síndrome tem baixa prevalência mundial, porém sendo endêmica no Sudeste Asiático (Tailândia, Filipinas e Japão). A SBr é uma doença cardíaca minimamente estrutural, sendo o diagnóstico só possível na presença do chamado padrão ECG de Brugada tipo 1 espontâneo ou induzido, por exemplo, a febre. Os distúrbios de repolarização-despolarização em pacientes com SBr podem ser causados por mutações genéticas responsáveis pela migração anormal de células da crista neural, baixa expressão "gap junctions" conexina-43 ou distúrbios do conexoma. Um estudo recente de autópsia revelou aumento do colágeno biventricular com fibrose miocárdica quando comparado aos controles, embora o principal território cardíaco afetado seja a via de saída do ventrículo direito (VSVD). Nessa área, há menor expressão da conexina-43, o que se traduz no ECG-VCG por atraso final de condução do QRS nas derivações precordiais direitas (V1-V2), precordiais direitas altas (V1H-V2H), bem como na derivação unipolar aVR ("a derivação esquecida"). Com base em sua localização, esses eletrodos refletem a atividade elétrica da VSVD

COVID-19 and influenza: implications in the public health context / COVID-19 e influenza: implicações no contexto da saúde pública

The COVID-19 pandemic caused by the novel coronavirus SARS-CoV-2 continues to have a major impact on health and social systems around the world. The COVID-19 and influenza manifest themselves in a similar way, causing respiratory diseases that can present asymptomatically, as well as from the cold to severe respiratory problems until death. The form of transmission is similar, through contact with droplets or particles of saliva and secretions, which implies preventive actions that involve the same hygiene measures, use of masks and the need to cough using the elbow or disposable tissues. This characterizes a syndemic. It becomes necessary to monitor these diseases so that there are parameters for better decision-making on the appropriate clinical management of these respective diseases.

A pandemia de COVID-19 causada pelo novo coronavírus SARS-CoV-2 continua a ter um grande im-pacto nos sistemas de saúde e sociais em todo o mundo. torna-se necessário que haja monitoramento dessas doenças para que assim, tenha-se parâmetros para melhor tomada de decisão sobre a gestão clínica adequada sobre essas respectivas doenças. Os dois vírus se manifestam de forma semelhante, ao causarem doenças respiratórias que podem se apresentar de forma assintomáticas, assim como do resfriado a problemas respiratórios graves até a morte. A forma de transmissão são parecidas, por contato com gotículas ou partículas de saliva e secreções, o que implica nas ações de prevenção que perpassam pelas mesmas medidas higienização, uso de máscaras e a necessidade de tossir usando o cotovelo ou lenções descartáveis. Isto caracteriza uma sindemia.

Transient ascending ST-segment depression and widening of the S wave in 3-channel Holter monitoring-A sign of dromotropic disturbance in the right ventricular outflow tract in the Brugada syndrome: A report of five cases.

BACKGROUND: Brugada syndrome (BrS) is somewhat a challenging diagnosis, due to its dynamic pattern. One of the aspects of this disease is a significant conduction disorder located in the right ventricular outflow tract (RVOT), which can be explained as a consequence of low expression of Connexin-43. This decreased conduction speed is responsible for the typical electrocardiographic pattern. Opposite leads located preferably in inferior leads of the electrocardiogram may show a deep and widened S wave associated with ascending ST segment depression. Holter monitoring electrocardiographic (ECG) aspects is still a new frontier of knowledge in BrS, especially in intermittent clinical presentations. METHODS: We describe, as an exploratory analysis, five case series of intermittent type 1 BrS to demonstrate the appearance of ascending ST segment depression and widening of the S wave, during 3-channel 24h-Holter monitoring (C1, C2 and C3) with bipolar leads. RESULTS: In the five cases described, the ST segment depression was observed mainly in C2, but in some cases also in C1 and C3. Only case 1 presented concomitant intermittent elevation of the ST segment in C1. All cases were intermittent. CONCLUSION: The recognition of an ECG pattern with ascending ST-segment depression and widening of the S wave in 3-channel Holter described in this case series should raise a suspicion of the BrS and suggests the counterpart of a dromotropic disturbance registered in the RVOT and/or reciprocal changes.

Brugada syndrome: current concepts and genetic background / Síndrome de Brugada: conceitos atuais e antecedentes genéticos

BACKGROUNG: Brugada syndrome (BrS) is a hereditary clinical-electrocardiographic arrhythmic entity with low worldwide prevalence. The syndrome is caused by changes in the structure and function of certain cardiac ion channels and reduced expression of Connexin 43 (Cx43) in the Right Ventricle (RV), predominantly in the Right Ventricular Outflow Tract (VSVD), causing electromechanical abnormalities. The diagnosis is based on the presence of spontaneous or medicated ST elevation, characterized by boost of the J point and the ST segment ≥2 mm, of superior convexity "hollow type" (subtype 1A) or descending rectilinear model (subtype 1B). BrS is associated with an increased risk of syncope, palpitations, chest pain, convulsions, difficulty in breathing (nocturnal agonal breathing) and/or Sudden Cardiac Death (SCD) secondary to PVT/VF, unexplained cardiac arrest or documented PVT/VF or Paroxysmal atrial fibrillation (AF) in the absence of apparent macroscopic or structural heart disease, electrolyte disturbance, use of certain medications or coronary heart disease and fever. In less than three decades since the discovery of Brugada syndrome, the concept of Mendelian heredity has come undone. The enormous variants and mutations found mean that we are still far from being able to concretely clarify a genotype-phenotype relationship. There is no doubt that the entity is oligogenetic, associated with environmental factors, and that there are variants of uncertain significance, especially the rare variants of the SCN5A mutation, with European or Japanese ancestors, as well as a spontaneous type 1 or induced pattern, thanks to gnomAD (coalition) researchers who seek to aggregate and harmonize exome and genome sequencing data from a variety of large-scale sequencing projects and make summary data available to the scientific community at large). Thus, we believe that this in-depth analytical study of the countless mutations attributed to BrS may constitute a real cornerstone that will help to better understand this intriguing syndrome.

INTRODUÇÃO: A Síndrome de Brugada (SBr) é uma entidade arrítmica clínico-eletrocardiográfica hereditária com baixa prevalência mundial. A síndrome é causada por alterações na estrutura e função de certos canais iônicos cardíacos e redução da expressão da Connexina 43 (Cx43) no Ventrículo Direito (VD), predominantemente no Trato de Saída do Ventricular Direito (VSVD), causando anormalidades eletromecânicas. O diagnóstico é baseado na presença de supradesnivelamento de ST espontâneo ou medicamentoso caracterizado por supradesnivelamento do ponto J e do segmento ST ≥2 mm, de convexidade superior "tipo covado" (subtipo 1A) ou modelo retilíneo descendente (subtipo 1B). A SBr está associado a um risco aumentado de síncope, palpitações, dor precordial, convulsões, dificuldade em respirar (respiração agonal noturna) e/ou Morte Cardíaca Súbita (MSC) secundária a PVT/VF, parada cardíaca inexplicada ou PVT/VF documentado ou Fibrilação atrial paroxística (FA) na ausência de doença cardíaca macroscópica ou estrutural aparente, distúrbio eletrolítico, uso de certos medicamentos ou coração coronário e febre. Em menos de três décadas desde a descoberta da síndrome de Brugada, o conceito de hereditariedade mendeliana se desfez. As enormes variantes e mutações encontradas significam que ainda estamos longe de sermos capazes de esclarecer concretamente uma relação genótipo-fenótipo. Não há dúvida de que a entidade é oligogenética associada a fatores ambientais, e que há variantes de significado incerto, principalmente as raras variantes da mutação SCN5A, com ancestrais europeus ou japoneses, bem como padrão espontâneo tipo 1 ou induzido, graças ao gnomAD (coalizão de pesquisadores que buscam agregar e harmonizar dados de sequenciamento de exoma e genoma de uma variedade de projetos de sequenciamento em grande escala e disponibilizar dados resumidos para a comunidade científica em geral). As enormes variantes e mutações encontradas significam que ainda estamos longe de sermos capazes de esclarecer concretamente uma relação genótipo-fenótipo. Assim, acreditamos que este estudo analítico em profundidade das inúmeras mutações atribuídas à BrS pode constituir uma verdadeira pedra angular que ajudará a compreender melhor esta síndrome intrigante.

A rare combination of atrial and intraventricular conduction disturbances: Atypical type I advanced interatrial block, left posterior fascicular block and transient right bundle branch block.

According to the first 2012 consensus report about interatrial block, the diagnosis of advanced interatrial block (A-IAB) consists of a P-wave duration ≥120 ms with biphasic "plus-minus" (±) polarity in the three leads of the inferior wall in the electrocardiogram. At the end of 2018, a new concept was introduced: the atypical A-IAB due to changes in the polarity or duration of the P-wave. The prevalence of these atypical patterns in different scenarios is currently unknown, but the patterns should be considered as risk factors of embolic stroke of undetermined source. When the A-IAB pattern is associated with clinical arrhythmic manifestations, it is known as the Bayés' Syndrome. We present a characteristic case of atypical A-IAB, and the rare left posterior fascicular block and transient right bundle branch block.

Electrocardiographic and Echocardiographic Abnormalities in Patients with Risk Factors for Atrial Fibrillation.

The electrocardiogram and various echocardiography modalities are important risk markers for atrial fibrillation (AF). Electrocardiographic criteria of left atrial enlargement, advanced interatrial block, and PR-interval prolongation are atrial risk markers for AF. Transthoracic echocardiography is elementary for risk stratification of AF. Transesophageal echocardiography is a valuable tool to detect cardiac sources of embolism if early cardioversion is necessary. Intracardiac echocardiography is a real-time tool for guidance of percutaneous interventions, including radiofrequency ablation and left atrial appendage closure in patients with AF.

The Vectorcardiogram and the Main Dromotropic Disturbances.

Until the mid-1980s, it was believed that the vectorcardiogram (VCG) presented a greater specificity, sensitivity and accuracy in comparison to the 12-lead electrocardiogram (ECG), in the cardiology diagnosis. Currently, the VCG still is superior to the ECG in specific situations, such as in the evaluation of myocardial infarctions when associated with intraventricular conduction disturbances, in the identification and location of accessory pathways in ventricular preexcitation, in the differential diagnosis of patterns varying from normal of electrical axis deviation, in the evaluation of particular aspects of Brugada syndrome, Brugada phenocopies, concealed form of arrhythmogenic right ventricular cardiomyopathy and zonal or fascicular blocks of the right bundle branch on right ventricular free wall.VCG allows us to analyze the presence of left septal fascicular block more accurately than ECG and in the diagnosis of the interatrial blocks and severity of some chambers enlargements. The three-dimensional spatial orientation of both the atrial and the ventricular activity provides a far more complete observation tool than the linear ECG. We believe that the ECG/VCG binomial simultaneously obtained by the technique called electro-vectorcardiography (ECG/VCG) brought a significant gain for the differential diagnosis of several pathologies. Finally, in the field of education and research, VCG provided a better and more rational tridimensional insight into the electrical phenomena that occurs spatially, and represented an important impact on the progress of electrocardiography.

Andersen-Tawil Syndrome: A Comprehensive Review.

Andersen-Tawil syndrome (ATS) is a very rare orphan genetic multisystem channelopathy without structural heart disease (with rare exceptions). ATS type 1 is inherited in an autosomal dominant fashion and is caused by mutations in the KCNJ2 gene, which encodes the α subunit of the K+ channel protein Kir2.1 (in ≈ 50-60% of cases). ATS type 2 is in turn linked to a rare mutation in the KCNJ5-GIRK4 gene that encodes the G protein-sensitive-activated inwardly rectifying K+ channel Kir3.4 (15%), which carries the acetylcholine-induced potassium current. About 30% of cases are de novo/sporadic, suggesting that additional as-yet unidentified genes also cause the disorder. A triad of periodic muscle paralysis, repolarization changes in the electrocardiogram, and structural body changes characterize ATS. The typical muscular change is episodic flaccid muscle weakness. Prolongation of the QU/QUc intervals and normal or minimally prolonged QT/QTc intervals with a tendency to ventricular arrhythmias are typical repolarization changes. Bidirectional ventricular tachycardia is the hallmark ventricular arrhythmia, but also premature ventricular contractions, and rarely, polymorphic ventricular tachycardia of torsade de pointes type may be present. Patients with ATS have characteristic physical developmental dysmorphisms that affect the face, skull, limbs, thorax, and stature. Mild learning difficulties and a distinct neurocognitive phenotype (deficits in executive function and abstract reasoning) have been described. About 60% of affected individuals have all features of the major triad. The purpose of this review is to present historical aspects, nomenclature (observations/criticisms), epidemiology, genetics, electrocardiography, arrhythmias, electrophysiological mechanisms, diagnostic criteria/clues of periodic paralysis, prognosis, and management of ATS.

The numerous denominations of the Brugada syndrome and proposal about how to put an end to an old controversy - a historical-critical perspective

BACKGROUNG: The eponymous Brugada Syndrome (BrS) in honor of its discovery as an independent entity by the Spanish/Catalan Brugada brothers, Pedro and Josep, has deserved numerous denominations derived mainly from the clinical genotype/phenotype correlation. The purpose of this manuscript is to present and analyze the nomenclatures that this intriguing and challenging syndrome has received over the past 28 years. We also compared the main features between cases from the first report of the Brugada brothers and an article by Martini et al. The nomenclatures used by these authors are closely linked to the BrS, but the cases (except one) presented in the article by Martini et al do not present the type 1 Brugada ECG pattern, which is mandatory for the diagnosis of BrS

INTRODUÇÃO: A Síndrome de Brugada (SB), em homenagem à sua descoberta como entidade independente pelos irmãos espanhóis / catalães Pedro e Josep Brugada, tem merecido inúmeras denominações derivadas principalmente da correlação genótipo /fenótipo clínico. O objetivo deste manuscrito é apresentar e analisar as nomenclaturas que esta intrigante e desafiadora síndrome recebeu nos últimos 28 anos. Também comparamos as principais características entre os casos do primeiro relato dos irmãos Brugada e um artigo de Martini e col. As nomenclaturas utilizadas por esses autores estão intimamente ligadas à SB, mas os casos (exceto um) apresentados no artigo de Martini e cols. não apresentam o padrão eletrocardiográfico de Brugada tipo 1, obrigatório para o diagnóstico da SB

Unusual ventricular activation produced by temporary transvenous cardiac pacing: electrovectorcardiographic findings / Activación ventricular inusual producida por estimulación cardíaca transvenosa temporal: hallazgos electrovectorcardiográficos

Abstract Complete heart block (CHB) results from dysfunction of the cardiac conduction system, which results in complete electrical dissociation. The ventricular escape rhythm can have its origin anywhere from the atrioventricular node to the bundle branch-Purkinje system. CHB typically results in bradycardia, hypotension, fatigue, hemodynamic instability, syncope, or even Stokes-Adams syndrome. Escape rhythm originating above the bifurcation of the His bundle (HB) produces narrow QRSs with relatively rapid heart rate (HR) (except in cases of His system disease). We present a middle-aged man with an HR of 34 bpm, progressive fatigue, in whom a temporary pacemaker was implanted in the subtricuspid region. The post-intervention electrocardiogram had unusual features.

Resumen El bloqueo cardíaco completo (BCC) resulta de la disfunción del sistema de conducción cardíaco, lo que ocasiona una disociación eléctrica completa entre aurículas y ventrículos. El ritmo de escape resultante puede tener su origen en cualquier lugar desde el nodo auriculoventricular hasta el sistema His Purkinje. El BCC generalmente produce bradicardia, hipotensión, fatiga, inestabilidad hemodinámica, síncope o incluso el síndrome de Stokes-Adams. El ritmo de escape que se origina por encima de la bifurcación del haz de His produce intervalos QRS estrechos con frecuencia cardíaca no muy lenta (excepto en casos de enfermedad del sistema Hisiano). Presentamos a un hombre de mediana edad con una frecuencia cardíaca de 34 lpm, fatiga progresiva, en el que se implantó un marcapasos temporario en la región subtricuspídea. El electrocardiograma resultante a la intervención presentó características inusuales.

Unusual ventricular activation produced by temporary transvenous cardiac pacing: electrovectorcardiographic findings.

Complete heart block (CHB) results from dysfunction of the cardiac conduction system, which results in complete electrical dissociation. The ventricular escape rhythm can have its origin anywhere from the atrioventricular node to the bundle branch-Purkinje system. CHB typically results in bradycardia, hypotension, fatigue, hemodynamic instability, syncope, or even Stokes-Adams syndrome. Escape rhythm originating above the bifurcation of the His bundle (HB) produces narrow QRSs with relatively rapid heart rate (HR) (except in cases of His system disease). We present a middle-aged man with an HR of 34 bpm, progressive fatigue, in whom a temporary pacemaker was implanted in the subtricuspid region. The post-intervention electrocardiogram had unusual features.

El bloqueo cardíaco completo (BCC) resulta de la disfunción del sistema de conducción cardíaco, lo que ocasiona una disociación eléctrica completa entre aurículas y ventrículos. El ritmo de escape resultante puede tener su origen en cualquier lugar desde el nodo auriculoventricular hasta el sistema His Purkinje. El BCC generalmente produce bradicardia, hipotensión, fatiga, inestabilidad hemodinámica, síncope o incluso el síndrome de Stokes-Adams. El ritmo de escape que se origina por encima de la bifurcación del haz de His produce intervalos QRS estrechos con frecuencia cardíaca no muy lenta (excepto en casos de enfermedad del sistema Hisiano). Presentamos a un hombre de mediana edad con una frecuencia cardíaca de 34 lpm, fatiga progresiva, en el que se implantó un marcapasos temporario en la región subtricuspídea. El electrocardiograma resultante a la intervención presentó características inusuales.

Transient high-degree right bundle branch block masking the type 1 Brugada ECG pattern associated with possible transient early repolarization syndrome.

The Brugada syndrome (BrS) was the last electrocardiographic syndrome described in the 20th century. The initial description included right bundle branch block (RBBB), persistent ST-segment elevation in the right precordial leads, absence of structural heart disease, and propensity to unexplained syncope and/or sudden death mainly during nocturnal rest. Currently, we know that the first three components are not constant or true since RBBB is present in only 28% of cases, the ST-segment elevation is dynamic, at times absent, and there are discrete structural changes in the right ventricular outflow tract. Additionally, the presence of RBBB can hide the typical type 1 Brugada ECG pattern. We present a very unusual case of spontaneous transient RBBB that revealed a hidden type 1 Brugada ECG pattern that could be seen in the beat with normal ventricular conduction.

Electrocardiographic "Northwest QRS Axis" in the Brugada Syndrome: A Potential Marker to Predict Poor Outcome.

Conduction delay in the right ventricular outflow tract as manifested in the electrocardiogram constitutes a high-risk predictor of ventricular arrhythmias in patients with Brugada syndrome. We present a case with a right QRS axis between -90° and ±180°. This feature has never been reported in the context of Brugada syndrome. (Level of Difficulty: Advanced.).

Authorship: From credit to accountability - Reflections from the Editors' network.

The Editors' Network of the European Society of Cardiology (ESC) provides a dynamic forum for editorial discussions and endorses the recommendations of the International Committee of Medical Journal Editors (ICMJE) to improve the scientific quality of biomedical journals. Authorship confers credit and important academic rewards. Recently, however, the ICMJE emphasized that authorship also requires responsibility and accountability. These issues are now covered by the new -(fourth) criterion for authorship. Authors should agree to be accountable and ensure that questions regarding the accuracy and integrity of the entire work will be appropriately addressed. This review discusses the implications of this paradigm shift on authorship requirements with the aim of increasing awareness on good scientific and editorial practices.

La Red de Editores de la Sociedad Europea de Cardiología (SEC) proporciona un foro dinámico para debates editoriales y respalda las recomendaciones del Comité Internacional de Editores de Revistas Médicas (ICMJE) para mejorar la calidad científica de las revistas biomédicas. La autoría confiere crédito e importantes recompensas académicas. Recientemente, sin embargo, el ICMJE enfatizó que la autoría también requiere responsabilidad y compromiso. Estos problemas ahora están cubiertos por el nuevo (cuarto) criterio de autoría. Los autores deben aceptar ser responsables y garantizar que las preguntas sobre la precisión y la integridad de todo el trabajo será abordado adecuadamente. Esta revisión discute las implicaciones de este cambio de paradigma en requisitos de autoría con el objetivo de aumentar la conciencia sobre las buenas prácticas científicas y editoriales.

Autoría: desde el crédito a la responsabilidad. Reflexiones de la Red de Editores / Authorship: from credit to accountability. Reflections from the Editors´ Network / Autoria: do crédito à responsabilidade. Reflexões da Rede de Editores

Resumen: La Red de Editores de la Sociedad Europea de Cardiología (ESC, por su sigla en inglés) constituye un foro dinámico dedicado a discusiones editoriales y respalda las recomendaciones del Comité Internacional de Editores de Revistas Médicas (ICMJE, por su sigla en inglés) destinadas a mejorar la calidad científica de las revistas biomédicas. La paternidad literaria confiere crédito, además de importantes recompensas académicas. Recientemente, sin embargo, el ICMJE ha destacado que la autoría también exige que los autores sean responsables y se hagan cargo de lo que publican. Estas cuestiones ahora están cubiertas por el nuevo (cuarto) criterio para la autoría. Los autores deben aceptar hacerse responsables de lo que escriben y garantizar un adecuado enfoque de las cuestiones concernientes a la precisión e integridad de todo el trabajo. Esta revisión analiza las implicancias de este cambio de paradigma en los requisitos de autoría con el objetivo de aumentar la conciencia sobre las buenas prácticas científicas y editoriales.

Summary: The Editors´ Network of the European Society of Cardiology provides a dynamic forum for editorial discussions and endorses the recommendations of the International Committee of Medical Journal Editors to improve the scientific quality of biomedical journals. Authorship confers credit and important academic rewards. Recently, however, the International Committee of Medical Journal Editors emphasized that authorship also requires responsibility and accountability. These issues are now covered by the new (fourth) criterion for authorship. Authors should agree to be accountable and ensure that questions regarding the accuracy and integrity of the entire work will be appropriately addressed. This review discusses the implications of this paradigm shift on authorship requirements with the aim of increasing awareness on good scientific and editorial practices.

Resumo: A Rede de Editores da Sociedade Europeia de Cardiologia é um fórum dinâmico para discussões editoriais e apoia as recomendações do Comitê Internacional de Editores de Revistas Médicas, visando melhorar a qualidade científica das revistas biomédicas. A autoria confere crédito, além de importantes recompensas acadêmicas. Recentemente, no entanto, o Comitê Internacional de Editores de Revistas Médicas enfatizou que a autoria também requer que os autores sejam responsáveis do que escrevem e se encarreguem do que publicam. Essas questões agora estão cobertas pelo novo (quarto) critério de autoria. Os autores devem concordar em ser responsáveis e garantir que as questões relativas à precisão e integridade de todo o trabalho sejam abordadas de maneira apropriada. Esta revisão discute as implicações dessa mudança de paradigma nos requisitos de autoria, com o objetivo de aumentar a conscientização sobre as boas práticas científicas e editoriais.