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Cardiac electrical alternans (CEA), manifested as T-wave alternans in ECG, is a clinical biomarker for predicting cardiac arrhythmias and sudden death. However, the mechanism underlying the spontaneous transition from CEA to arrhythmias remains incompletely elucidated. In this study, multiscale rabbit ventricular models were used to study the transition and a potential role of INa in perpetuating such a transition. It was shown CEA evolved into either concordant or discordant action potential (AP) conduction alternans in a homogeneous one-dimensional tissue model, depending on tissue AP duration and conduction velocity (CV) restitution properties. Discordant alternans was able to cause conduction failure in the model, which was promoted by impaired sodium channel with either a reduced or increased channel current. In a two-dimensional homogeneous tissue model, a combined effect of rate- and curvature-dependent CV broke-up alternating wavefronts at localised points, facilitating a spontaneous transition from CEA to re-entry. Tissue inhomogeneity or anisotropy further promoted break-up of re-entry, leading to multiple wavelets. Similar observations have also been seen in human atrial cellular and tissue models. In conclusion, our results identify a mechanism by which CEA spontaneously evolves into re-entry without a requirement for premature ventricular complexes or pre-existing tissue heterogeneities, and demonstrated the important pro-arrhythmic role of impaired sodium channel activity. These findings are model-independent and have potential human relevance. [ABSTRACT FROM AUTHOR]

Aims: Atrial fibrillation (AF) is one of the commonest sustained arrhythmias in chronic heart failure (CHF), although the prognostic implications of the presence of AF in CHF remain controversial. We have therefore performed this meta-analysis to study the effects of the presence of AF on mortality in CHF patients. [ABSTRACT FROM PUBLISHER]

The article discusses the upstream management of atrial fibrillation (AF) which involves treating the abnormalities that are thought to predispose certain patient groups to this arrhythmia. It examines the predisposing clinical factors for AF. It also explains the underlying electrophysiological mechanisms of AF, AF development in animal models, and effects of therapies in animal models of AF in the setting of structural heart disease or inflammation.

FITCHET, A., et al. : Holter Monitoring vs Tilt Testing in the Investigation of Suspected Vasovagal Syncope. --> The aim of this study was to compare the diagnostic yield of 48‐hour Holter monitoring with head‐up tilt (HUT) test in patients presenting with blackouts suggestive of vasovagal syncope. One hundred and eighteen consecutive patients, 68 women, aged (mean [SD])50 ± 20  years(range 16–88 years), underwent 48‐hour Holter monitoring and 60° HUT test within 3 months. Endpoints were symptom‐ECG correlation during Holter monitoring and positive HUT test. Syncope occurred in 3 (3%) patients during Holter monitoring, the rhythm being sinus tachycardia in all. Presyncope was reported in 22 (19%), the rhythm being sinus tachycardia in 6, persistent atrial fibrillation in 2, and normal sinus rhythm in the remainder. Asymptomatic arrhythmias were recorded in 103 (87%) patients. Positive HUT tests occurred in 39 (33%), the pattern being mixed (VASIS type 1) in 14 (36%), cardioinhibitory (VASIS type 2) in 3 (8%), and vasodepressor (VASIS type 3) in 22 (56%). Change in patient management occurred in 3 (3%) patients following Holter monitoring and 39 (33%) patients following HUT test. Holter monitoring produces a low yield of clinically useful information in the investigation of suspected vasovagal syncope. An HUT test should be considered the primary investigation of choice in such patients. (PACE 2003; 26[Pt. I]:1523–1527) [ABSTRACT FROM AUTHOR]

Introduction: The mechanisms by which Class IC drugs slow the rate of functional reentrant arrhythmias are not completely understood. We hypothesized that flecainide widens the excitable gap beyond the pivot point of premature turning wavefronts. Methods and Results: In eight perfused subepicardial layers of rahbit left ventricle, a linear lesion was made by radiofrequency (RF) ablation parallel to the fiber orientation. One end of the RF lesion was extended by a short incision. Pacing next to the lesion induced a wavefront propagating with a sharp U-turn around the end of the lesion in either the clockwise or counterclockwise direction. A high-density mapping electrode (240 electrodes, 350-μm resolution) was used to record unipolar electrograms at the pivot point During control, the shortest V1-V2 interval proximal to the pivot point was 162 ± 12 msec compared with 173 ± 13 msec distal to the pivot point difference 11 ± 8 msec; P < 0.01). After infusion of flecainide 2 mg/L, the shortest V1-V2 interval proximal and distal to the pivot point were 217 ± 29 msec and 244 ± 36 msec (difference 27 ± 16 msec; P < 0.01). Due to the increase in V1-V2 interval at the pivot point, flecainide widened the temporal excitable gap in the returning limb of the turning wavefront from 30 ± 11 msec to 55 ± 22 msec (P < 0.01). High-density mapping at the pivot point revealed that this widening of the excitable gap was due to both macroscopic discoutinuous conduction and functional conduction block at the pivot point. Conclusion: Flecainide widens the excitable gap in the returning limb of premature U-turning wavefronts by causing macroscopic discontinuous conduction and functional conduction block at the pivot point. [ABSTRACT FROM AUTHOR]

Introduction: QTc dispersion has traditionally been calculated from all 12 leads of a standard electrocardiogram (ECG). It is possible that alternative, quicker methods using fewer than 12 leads could be used to provide the same information. Methods and Results: We have previously shown a difference in QTc dispersion from ECGs recorded at least 1 month after myocardial infarction between patients who subsequently died and long-term survivors. In the current study, we recalculated QTc dispersion in these ECGs using different methods to determine if the observed difference in QTc dispersion measurements between the two groups, as calculated from 12-lead ECGs, persisted when using smaller sets of leads. QTc dispersion was recalculated by four methods: (1) with the two extreme QTc intervals excluded; (2) from the six precordial leads; (3) from the three leads most likely to contribute to QTc dispersion (aVF, V1, V4); and (4) from the three quasi-orthogonal leads (aVF, I, V2). For each of the 270 12-lead ECGs examined, a mean of 9.9 leads (SD 1.5 leads) had a QT interval analyzed; the QT interval could not be accurately measured in the remaining leads. Using the standard 12-lead measurement of QTc dispersion, there was a difference in the fall in QTc dispersion from early to late ECG between the groups: 9.1 (SD 60.8) msec for deaths versus 34.4 (55.2) msec for survivors (P = 0.016). This difference in QTc dispersion between early and late ECGs was maintained using either three-lead method (quasi-orthogonal leads: -2.6 [56.2] msec for deaths vs 26.9 [54.3] msec for survivors [P = 0.003]; "likeliest" leads: 8.6 [64.9] msec vs 29.5 [54.2] msec [P = 0.05]), but not when using the other two methods (precordial leads: 19.1 [55.5] msec vs 22 [50.8] msec [P = 0.76]; extreme leads removed: 9.2 [50.1] msec vs 21.8 [42] msec [P = 0.13]). Conclusion: QTc dispersion calculated from three leads may be as useful a measurement as QTc dispersion calculated from all leads of a standard ECG. Its advantages over the standard measurement are its simplicity and the lack of problems with lead adjustment. [ABSTRACT FROM AUTHOR]

Focuses on the substrate for atrioventricular nodal reentrant tachycardia. Evolution of the clinical concept of multiple AV nodal pathways; Evidence for the reentrant mechanism of AVNRT.

Most signal averaging processes used for cardiac signals align successive waveforms using a template matching process. In addition to achieving accurate temporal alignment of the signals, this operation must also ensure that the signal average comprises signals of the same morphology. For P wave signal averaging, systems designed for QRS complex averaging are often used, with the template acquisition window shifted to include the P wave. Theoretically, with this technique, variations in P wave morphology could reduce the high frequency content of the signal. We tested this hypothesis by comparing the performance of a selective P wave averaging system with a conventional system, based on template matching by cross-correlation over a fixed acquisition window, on identical P wave recordings from 15 subjects. The selective system identifies variations in P wave morphology and generates up to five candidate templates for averaging. Subsequently, the most frequently matched template over a 100-beat sample is used for averaging. Only P waves with the same morphology as this template are averaged. Selective averaging mainly increased the measured high frequency P wave energy, without affecting P wave duration after high pass filtering at 40 Hz, (Duration: 157(4)ms selective vs 155(4) nonselective. Energy 80–150 Hz: 1.77(0.28)µV².s selective vs 1.61(0.3)µV².s non selective, P < 0.01). These observations confirm that nonselective P wave averaging can reduce apparent P wave energy, especially at high frequency. Before meaningful studies of the value of frequency domain analysis of the P wave can be performed, it is important that signal averaging systems of sufficient fidelity are utilized. [ABSTRACT FROM AUTHOR]