The electrocardiogram (ECG) has been reinvigorated by the identification of
electrical alterations that were not definitely clarified before. In this
context, and mainly regarding the definition of arrhythmogenic substrates, the
association of the ECG with the vectorcardiogram (VCG) has gathered much more
information about the cardiac electrical phenomena, thus allowing us to
differentiate potentially fatal cases from benign ones. Obtaining a VCG
concomitantly with the performance of an ECG has led to a significant gain in
the definition of extremely sophisticated pathologies, which function suffer
some type of structural or dynamic alterations, involving either the reduction
or enhancement of ionic channels and currents.
The classic aspects of the ECG/VCG association in the differential diagnosis of
myocardial infarctions, conduction disorders, atrial and ventricular
hypertrophies, and the correlations between these electrical disorders are still
valid and assertive. The association of these pathologies is further clarified
when they are seen through the ECG/VCG dyad.
The three-dimensional spatial orientation of both the atrial and the ventricular
activity provides a far more complete observation tool than the ECG linear form.
The modern analysis of the ECG and its respective VCG, simultaneously obtained
by the recent technique called electro-vectorcardiogram (ECG/VCG), brought a
significant gain for the differential diagnosis of some pathologies. Therefore,
we illustrate how this type of analysis can elucidate some of the most important
diagnoses found in our daily clinical practice as cardiologists.
Heart rate variability (HRV) analysis is a useful method to assess abnormal functioning in the autonomic nervous system and to predict cardiac events in patients with heart failure (HF). HRV measurements with heart rate monitors have been validated with an electrocardiograph in healthy subjects but not in patients with HF. We explored the reproducibility of HRV in two consecutive six-minute walk tests (6MW), 60-minute apart, using a heart rate monitor (PolarS810i) and a portable electrocardiograph (called Holter) in 50 HF patients (mean age 59 years, NYHA II, left ventricular ejection fraction ~35%). The reproducibility for each device was analysed using a paired t-test or the Wilcoxon signed-rank test. Additionally, we assessed the agreement between the two devices based on the HRV indices at rest, during the 6MW and during recovery using concordance correlation coefficients (CCC), 95% confidence intervals and Bland-Altman plots. The test-retest for the HRV analyses was reproducible using Holter and PolarS810i at rest but not during recovery. In the second 6MW, patients showed significant increases in rMSSD and walking distance. The PolarS810i measurements had remarkably high concordance correlation [0.86
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.
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