Contribution of the vectorcardiogram in the differential diagnosis of Brugada electrocardiographic pattern.

BACKGROUND: The electrocardiogram (ECG) is a powerful tool for differential diagnosis among a group of pathologies with different therapeutic approaches/prognoses, the so-called J-wave syndrome. The vectorcardiogram (VCG) can be used as a complementary method to the ECG in several dubious electrocardiographic alterations. OBJECTIVE: We carried out a VCG analysis after conceiving and measuring a novel parameter (JT-distance) that allows diagnosis of the Brugada ECG pattern. METHODS: A retrospective cohort study selected ninety-six ECGs with J-point elevation in V1/V2, ECG superior leads and VCGs, all performed on the same day. A new VCG measurement by Frank method (JT-distance) was conceived and designed in transverse and right sagittal planes by 3 lines drawn 1) at the final third of the QRS loop, comprehending the J-point; 2) at the initial portion of the T loop; 3) a parallel of the J-point line at the beginning of the T loop. JT measure was determined by the distance between parallels. A validation cohort was established in a new sample of thirty-five patients. RESULTS: JT-distance ≥1.5 mm (tranverse plane) and JT-distance >1.25 mm, in the sagittal plane, differentiated Brugada type-1 from Brugada type-2, early repolarization and others, with 95% sensitivity and 68% specificity. JT-distance <1.5 mm (transverse plane) and JT >1.25 mm (sagittal plane) had 100% sensitivity and 85% specificity for Brugada type-1 diagnosis. A validation cohort showed very similar Cohen's kappa levels (0.65 and 0.77, test and validation cohorts, respectively), with overlapping 95% confidence intervals. CONCLUSIONS: The novel vectorcardiogram measurement (JT-distance) presented a new diagnostic criterion to identify Brugada pattern. Nevertheless, prospective studies should be performed by other centers to confirm these findings.

T-wave alternans: clinical performance, limitations and analysis methodologies.

Accurate recognition of individuals at higher immediate risk of sudden cardiac death (SCD) is still an open question. The fortuitous nature of acute cardiovascular events just does not seem to fit the well-known model of ventricular tachycardia/fibrillation induction in a static arrhythmogenic substrate by a synchronous trigger. On the mechanism of SCD, a dynamical electrical instability would better explain the rarity of the simultaneous association of a correct trigger and an appropriate cardiac substrate. Several studies have been conducted trying to measure this cardiac electrical instability (or any valid surrogate) in an ECG beat stream. Among the current possible candidates we can number QT prolongation, QT dispersion, late potentials, T-wave alternans (TWA), and heart rate turbulence. This article reviews the particular role of TWA in the current cardiac risk stratification scenario. TWA findings are still heterogeneous, ranging from very good to nearly null prognostic performance depending on the clinical population observed and clinical protocol in use. To fill the current gaps in the TWA base of knowledge, practitioners, and researchers should better explore the technical features of the several technologies available for TWA evaluation and pay greater attention to the fact that TWA values are responsive to several factors other than medications. Information about the cellular and subcellular mechanisms of TWA is outside the scope of this article, but the reader is referred to some of the good papers available on this topic whenever this extra information could help the understanding of the concepts and facts covered herein.

T-wave alternans: desempenho clínico, limitações, metodologias de análise / T-wave alternans: clinical performance, limitations and analysis methodologies / T-wave alternans: desempeño clínico, limitaciones, metodologías de análisis

Reconhecer com precisão indivíduos com maior risco imediato de morte súbita cardíaca (MSC) ainda é uma questão em aberto. A natureza fortuita dos eventos cardiovasculares agudos não parece se adequar ao conhecido modelo de indução de taquicardia/fibrilação ventricular por um gatilho em sincronia a um substrato arritmogênico estático. Quanto ao mecanismo da MSC, uma instabilidade elétrica dinâmica explicaria melhor a raridade da associação simultânea de um gatilho certo a um substrato cardíaco apropriado. Diversos estudos tentaram medir essa instabilidade elétrica cardíaca (ou um equivalente válido) em uma sequência de batimentos cardíacos no ECG. Dentre os mecanismos possíveis podemos citar o prolongamento do QT, dispersão do QT, potenciais tardios, alternância de onda T ou T-wave alternans (TWA), e turbulência da frequência cardíaca. Este artigo se atém em particular ao papel da TWA no panorama atual da estratificação de risco cardíaco. Os achados sobre TWA ainda são heterogêneos, variando de um desempenho prognóstico muito bom até um quase nulo, dependendo da população clínica observada e protocolo clínico usado. Para preencher as atuais lacunas no conhecimento sobre TWA, profissionais médicos e pesquisadores devem explorar melhor as características técnicas das diversas tecnologias disponíveis para a avaliação de TWA e atentar ao fato de que os valores de TWA respondem a diversos outros fatores, além de medicamentos. Informações sobre mecanismos celulares e subcelulares da TWA estão fora do escopo deste artigo, mas são referenciados alguns dos principais trabalhos sobre este tópico, com o intuito de auxiliar no entendimento dos conceitos e fatos cobertos neste artigo.

Accurate recognition of individuals at higher immediate risk of sudden cardiac death (SCD) is still an open question. The fortuitous nature of acute cardiovascular events just does not seem to fit the well-known model of ventricular tachycardia/fibrillation induction in a static arrhythmogenic substrate by a synchronous trigger. On the mechanism of SCD, a dynamical electrical instability would better explain the rarity of the simultaneous association of a correct trigger and an appropriate cardiac substrate. Several studies have been conducted trying to measure this cardiac electrical instability (or any valid surrogate) in an ECG beat stream. Among the current possible candidates we can number QT prolongation, QT dispersion, late potentials, T-wave alternans (TWA), and heart rate turbulence. This article reviews the particular role of TWA in the current cardiac risk stratification scenario. TWA findings are still heterogeneous, ranging from very good to nearly null prognostic performance depending on the clinical population observed and clinical protocol in use. To fill the current gaps in the TWA base of knowledge, practitioners, and researchers should better explore the technical features of the several technologies available for TWA evaluation and pay greater attention to the fact that TWA values are responsive to several factors other than medications. Information about the cellular and subcellular mechanisms of TWA is outside the scope of this article, but the reader is referred to some of the good papers available on this topic whenever this extra information could help the understanding of the concepts and facts covered herein.

Reconocer con precisión individuos con mayor riesgo inmediato de muerte súbita cardíaca (MSC) aun es una cuestión en abierto. La naturaleza fortuita de los eventos cardiovasculares agudos no parece adecuarse al conocido modelo de inducción de taquicardia/fibrilación ventricular por un gatillo en sincronía con un substrato arritmogénico estático. En cuanto al mecanismo de la MSC, una inestabilidad eléctrica dinámica explicaría mejor la rareza de la asociación simultánea de un gatillo correcto a un substrato cardíaco apropiado. Diversos estudios trataron de medir esa inestabilidad eléctrica cardíaca (o un equivalente válido) en una secuencia de latidos cardíacos en el ECG. Entre los mecanismos posibles podemos citar la prolongación del QT, dispersión del QT, potenciales tardíos, alternancia de onda T o T-wave alternans (TWA), y turbulencia de la frecuencia cardíaca. Este artículo se atiene en particular al papel de la TWA en el panorama actual de la estratificación de riesgo cardíaco. Los hallazgos sobre TWA aun son heterogéneos, variando de un desempeño pronóstico muy bueno hasta uno casi nulo, dependiendo de la población clínica observada y protocolo clínico usado. Para llenar las actuales lagunas en el conocimiento sobre TWA, profesionales médicos e investigadores deben explotar mejor las características técnicas de las diversas tecnologías disponibles para la evaluación de TWA y estar atento al hecho de que los valores de TWA responden a otros diversos factores, además de medicamentos. Informaciones sobre mecanismos celulares y subcelulares de la TWA están fuera del objetivo de este artículo, pero son referenciados algunos de los principales trabajos sobre este tópico, con el propósito de auxiliar en la comprensión de los conceptos y hechos cubiertos en este artículo.