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

A counterpoint paper: Comments on the electrocardiographic part of the 2018 Fourth Universal Definition of Myocardial Infarction.

The Fourth Universal Definition of Myocardial Infarction (FUDMI) [published simultaneously in 2018 in numerous journals including Circulation, Journal of the American College of Cardiology and European Heart Journal] focuses mainly on the distinction between non-ischemic myocardial injury and myocardial infarction (MI), along with the role of cardiovascular magnetic resonance, in order to define the etiology of myocardial injury. As a consequence, there is less emphasis on updating the parts of the definition concerning the electrocardiographic (ECG) changes related to MI. Evidence of myocardial ischemia is a prerequisite for the diagnosis of MI and the ECG is the main available tool for i) detecting acute ischemia, ii) triage and iii) risk stratification upon presentation. This review focuses on multiple aspects of ECG interpretation that we firmly believe should be considered for incorporation in any future update to the Universal Definition of MI. Our counterpoint view is that: a) the use of the ECG following coronary artery bypass surgery should be better explored and defined; b) the emphasis in the FUDMI on convex versus concave ST-elevation, which is questionable, should be balanced by the fact that many patients with true ST-elevation MI (STEMI) present with a concave form of ST elevation; c) reciprocal ST-depression in STEMI caused by right coronary artery or left circumflex artery occlusion, should be set against the fact that not all anterior STEMIs present with reciprocal ST-depression which can also be seen in cardiomyopathy and left ventricular hypertrophy; d) the "posterior" leads V7-V9 should be placed on a horizontal line from V4, rather than follow the 5th intercostal space; e) ST-depression in V1-V3 is not a manifestation of ischemia of the basal inferior segment, placed horizontally; f) Interpreting ST-T changes in patients with conduction abnormalities and pacemakers should be further defined.

Transient ST-segment elevation in precordial leads by acute marginal branch occlusion during stent implantation.

The isolated right ventricular infarction is a rare entity. Our case presented a selective occlusion of an acute marginal branch that supplies the right ventricular free wall with isolated ST elevation in precordial leads simulating an occlusion of the left anterior descending artery and without pseudonormalization in inferior due to the non-involvement of the main branch in the ischemic process. Our case clearly illustrates a rare differential diagnosis when a new ST segment elevation appears in earlier precordial leads in patients with symptoms of myocardial ischemia.