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The volumetric method in cardiac magnetic resonance (CMR), the reference standard for right ventricular ejection fraction (RVEF), requires expertise because of the complex right ventricular geometry and anatomical landmarks.The aim of our retrospective study was to describe a new method to evaluate RVEF based on wall motion score index (WMSI) in CMR.Visual assessment of wall motion was performed using an eight-segment model (normokinesia=1, hypokinesia=2, akinesia=3). Correlation between WMSI (WMS/8) and the reference volumetric RVEF was analysed. A regression equation was derived to convert the WMSI into RVEF. The accuracy of CMR WMSI-derived RVEF compared with CMR volumetric RVEF was evaluated using Bland-Altman analysis.In the 112 patients using the volumetric method, the mean RVEF was 48±14%. Fifty-nine patients had normal RV kinetics (WMSI=1), which corresponded to a volumetric RVEF of 56% (standard deviation 7%; range 43-76%). CMR WMSI showed a strong correlation with CMR volumetric RVEF (Spearman's Rho=-0.69). A regression equation was created: RVEF=80-22×WMSI. Overall, the WMSI-derived RVEF resulted in good agreement with the CMR volumetric RVEF (mean bias-3%, standard deviation±7.5%). In addition, using a WMSI cut-off of≥1.5 was highly accurate (92%) to predict a reference RVEF of˂45%, an important prognostic indicator in CMR.Our results suggest that using the WMS in CMR (eight-segment) to estimate RVEF is accurate, and correlates well with the volumetric method. A WMSI≥1.5 is optimal to categorize patients in the higher-risk subset of CMR RVEF˂45%.

The present work aims at investigating the coupling between thermal ageing/degradation and creep behavior of PEKK and C/PEKK composites at 200 °C, above the glass transition temperature (which is close to 160 °C). Ageing tests were carried out at 200 °C, under 5 bar of oxygen conditioned atmosphere. DSC scans and DMA tests were carried out. Tests results discussion were supported by indentation tests and image analysis of the aged specimen cross-section. Coupled oxidation-thermomechanical-creep tests were carried out on C/PEKK samples at 200 °C under a 5 bar O2 environment. The resulting strain response was compared to creep tests carried out on C/PEKK samples at 200 °C under air at similar creep stress. Such comparison allowed to investigate the presence of degradation phenomena in C/PEKK samples. The analysis of X-rays µ-tomography scans allowed investigating the possible occurrence of degradation, and to discriminate between pure thermal and thermomechanical coupling with degradation phenomena.

International audience; Differential scanning calorimetry and polarized optical microscopy were used in this study to identify the contributions and interactions of both primary and secondary crystallization processes during the isothermal crystallization of a PEKK 70/30. Primary crystallization, which is related to the growth of spherulites, was monitored by polarized optical microscopy. The data collected allowed identifying the corresponding nucleation density and crystal growth rate that were subsequently used to feed a kinetic model derived from Hillier’s equation and already been reported in literature. The DSC data were then used to determine the contribution of the secondary crystallization mechanism, considering that primary crystallization is related to the instantaneous nucleation and growth of spherulites. From these data, an inverse approach was used to identify the few remaining parameters of the model. The proposed approach has the advantage of providing kinetic parameters representative of the secondary crystallization mechanism that are not dependent on the inverse identification procedure. Doing so, a non-integer Avrami exponent equal to 2.7 is obtained and discussed.

Background Many diagnostic criteria for the differential diagnosis of wide complex tachycardia (WCT) are complex and not completely accurate. Incorrect diagnosis is also related to error in applying criteria. Objectives To propose a novel reliable criterion for wide QRS complexes' differential diagnosis. Material and methods One hundred Electrocardiograms (ECGs) with wide QRS complexes were analyzed using the ECG software. Five variables were measured during the first 20 ms of QRS in leads V1 and V2 and compared between premature ventricular contraction (PVC) and conducted supraventricular impulse with bundle branch block (BBB) groups. The best discriminant variable was identified. The validity of this variable was tested on a group of 20 patients who had WCT during an electrophysiology study. Results Almost all variables were statistically different between PVC and BBB groups. The sum of voltages in absolute value of vectors during the initial 20 ms of the QRS in leads V1 and V2 (ΣV1 + V2) was the most discriminant between the two groups (131 ± 85 microvolt [μV] vs. 498 ± 392 μV, p Conclusions The ΣV1 + V2

Objective: In the electrocardiogram, adaptation of the QT interval to variations in heart rate is not instantaneous. Quantification of this hysteresis phenomenon relies on mathematical models describing the relation between the RR and QT time series. These models reproduce hysteresis through an effective RR interval computed as a linear combination of the history of past RR intervals. This filter depends on a time constant parameter that may be used as a biomarker. Approach: The most common hysteresis model is based on an autoregressive filter with an impulse response that decreases exponentially with the beat number (lag-based model). Recognizing that the QT time series is unevenly spaced, we propose two exponential moving average filters (time-based models) to define the effective RR interval: one with an impulse response that decreases exponentially with time in seconds, and one with a step response that relaxes exponentially with time in seconds. These two filters are neither linear nor time-invariant. Recurrence formulas are derived to enable efficient implementation. Main results: Application to clinical signals recorded during tilt table test, exercise and 24 h Holter demonstrates that the three models perform similarly in terms of goodness-of-fit. When comparing the hysteresis time constant in two conditions with different heart rates, however, the time-based models are shown to reduce the bias on the hysteresis time constant caused by heart rate acceleration and deceleration. Significance: Time-based models should be considered when intergroup differences in both heart rate and QT hysteresis are expected.

Correction of the QT interval in the ECG for changes in heart rate (RR interval) is needed to compare groups of patients and assess the risk of sudden cardiac death. The QTc represents the QT interval at 60 bpm, although most patients typically have a faster heart rate, thus requiring extrapolation of the QT-RR relationship. Objective This paper investigates the ability of QT-RR models with increasing number of parameters to fit beat-to-beat variations in the QT interval and provide a reliable estimate of the QTc. Approach One-, two- and three-parameter functions generalising the Bazett and Fridericia formulas were used in combination with hysteresis reduction (memory) obtained by time-averaging the history of RR intervals with exponentially-decaying weights. In normal men and women datasets of Holter recordings in normal subjects (24 h monitoring), two measures were computed for each model: the root mean square error (RMSE) of fitting and the difference between the estimated QTc and a reference QTc obtained by collecting data points around RR = 1000 ms. Main results The two- and three-parameter functions all gave similar low RMSE with uncorrelated residues. An optimal memory parameter was found that still minimized the RMSE and could be used for all functions and subjects. This reduction in RMSE resulted from changes in the parameters linked to the increased steepness of the QT-RR relation after hysteresis reduction. At optimal memory, the two and three-parameter models provided poorer prediction of the QTc as compared to the Fridericia's model in subjects with fast heart rates, since accurate representation of the steeper QT-RR relation worsened the extrapolation that was then needed to determine the QTc. Significance As a result, among all models investigated, the Fridericia formulation offered the best trade-off for QTc prediction robust to memory and fast heart rates.

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International audience; The properties of the thermoplastic matrix depend strongly on the crystalline morphology formed during the cooling.In order to predict the size of the crystalline entities, to evaluate the impact of the formation of a transcrystalline phasearound the fibers, and to make the link between kinetics of crystallization and morphology, a 3D simulation approachof crystallization is developed in this work. This approach validates identification methods based on the analysis ofmicrographs during crystallization and opens the way to material virtual testing based on realistic micro-structures; Les propriétés de la matrice thermoplastique dépendent fortement de la morphologie cristalline formée durant le refroi-dissement. Afin de prévoir la taille des entités cristallines, d’évaluer l’impact de la formation d’une phase transcristallineautour des fibres, et de faire le lien entre cinétique de cristallisation et la morphologie, une approche de simulation 3D de lacristallisation est développée dans cet article. Cette approche permet de valider des méthodes d’identifications basées surl’analyse de micrographies lors de la cristallisation et ouvre la voie au "virtual testing" de matériaux aux microstructures réalistes.

International audience; Activation mapping in animal models of atrial fibrillation (AF) has shown that activation patterns can repeat for several cycles and then be followed by different changing or repetitive patterns. Subsequent clinical studies have suggested a similar type of activity in human AF. Our purpose was to investigate whether a computer model of human AF can reproduce this behavior. We used a three-dimensional model of the human atria consisting of 0.2-mm volumetric elements with a detailed representation of bundle structures and fiber orientations. Propagating activation was simulated over 9 seconds with a monodomain reaction-diffusion model using human atrial membrane dynamics. AF was induced by rapid pacing. Pattern recurrence was quantified using a similarity measure based on transmembrane voltage at 1000 uniformly distributed points in the model. Recurrence plots demonstrated a continuous evolution of patterns, but the speed of evolution varied considerably. Groups of upto 15 similar cycles could be recognized, separated by rapid changes. In a few cases truly periodic patterns developed, which were related to macroscopic anatomical reentry. The drivers of non-periodic patterns could not be clearly identified. For example, a spiral wave could appear or disappear without an obvious impact on the similarity between cycles. We conclude that our model can indeed reproduce strong variations in similarity between subsequent cycles, but true periodicity only in case of anatomical reentry.

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Many diagnostic criteria for the differential diagnosis of wide complex tachycardia (WCT) are complex and not completely accurate. Incorrect diagnosis is also related to error in applying criteria.To propose a novel reliable criterion for wide QRS complexes' differential diagnosis.One hundred Electrocardiograms (ECGs) with wide QRS complexes were analyzed using the ECG software. Five variables were measured during the first 20 ms of QRS in leads V1 and V2 and compared between premature ventricular contraction (PVC) and conducted supraventricular impulse with bundle branch block (BBB) groups. The best discriminant variable was identified. The validity of this variable was tested on a group of 20 patients who had WCT during an electrophysiology study.Almost all variables were statistically different between PVC and BBB groups. The sum of voltages in absolute value of vectors during the initial 20 ms of the QRS in leads V1 and V2 (ΣV1 + V2) was the most discriminant between the two groups (131 ± 85 microvolt [μV] vs. 498 ± 392 μV, p 0.01). A ΣV1 + V2 258 μV (rounded to0.25 millivolt [mV]) diagnosed PVCs with good sensitivity and specificity (90% and 85% respectively). The ΣV1 + V2 in WCT group had lower values in VT versus supra-ventricular tachycardia (SVT) group (0.53 ± 0.35 mV vs. 1.79 ± 1.04 mV, p = 0.004).The ΣV1 + V2 258 μV is a reliable criterion for PVC diagnosis. It could be measured accurately using ECG Software, which could be programmed to calculate it automatically, limiting the risk of human error. The ΣV1 + V2 also seems capable of discriminating between VT and SVT.

Aim The autonomic nervous system modulates atrial activity, notably through acetylcholine (ACh) release. This time-dependent action may alter the dynamics of atrial arrhythmia. Our aim is to investigate in a computer model the changes induced by ACh release and degradation on the dynamical regime of a reentry. Methods and results A functional reentry was simulated in a 10 × 5 cm2 two-dimensional tissue with canine atrial membrane kinetics including an ACh-dependent K+ current. The local ACh concentration was altered over time in a circular region following a predefined spatiotemporal profile (ACh release and degradation) characterized by its maximum ACh level, time constant of release/degradation, and diameter of the region. Phase singularities were tracked to monitor the complexity of the dynamics. Four scenarios were identified: (i) the original reentry remained stable; (ii) repolarization gradients induced by ACh release caused wavebreaks, resulting in a transient complex dynamics that spontaneously converted to a single stable reentry; (iii) the reentry self-terminated through wavebreaks and wavefront interactions; (4) wavebreaks led to a complex dynamics that converted to two or three reentries that remained stable after ACh degradation. Higher ACh level, short ACh release time constant, larger heterogeneous region, and short distance between the heterogeneous region and the spiral tip were associated with higher occurrence of ACh-induced wavebreaks. Conclusion Variation of ACh concentration over time may modulate the complexity of atrial arrhythmias.

National audience; Pour les polymères thermoplastiques renforcés de fibres de carbone, le taux de cristallinité et la morphologie induite lors de la cristallisation ont un impact certain sur leurs propriétés physiques et mécaniques. Ces deux paramètres sont non seulement dépendants des conditions de mise oeuvre mais aussi des constituants du composite. Afin d'améliorer le contrôle et l'optimisation des cycles de fabrication de ces matériaux, il est nécessaire de construire une modélisation avancée de la cristallisation. Dans la littérature, de nombreux modèles ont été proposés afin de décrire la cinétique de cristallisation des polymères semi-cristallins [1-3]. Ces modèles s'avèrent peu adaptés pour décrire la cristallisation dans le cas d'un polymère de la famille des PAEK. En effet, comme pour le PEEK, le PEKK se distingue par une cristallisation particulière qui fait intervenir deux mécanismes. Une cristallisation primaire qui correspond aux étapes de germination-croissance décrites dans la théorie de Lauritzen et Hoffmann [4], suivi d'une cristallisation secondaire correspondant à une cristallisation interlamellaire ou à un perfectionnement des cristaux déjà présents. Des modèles ont été spécifiquement développés pour décrire les phénomènes de cristallisation particuliers du PEEK [5, 6]. Cette étude vise dans un premier temps à développer un modèle de cinétique adapté au PEKK, en se basant sur les étapes de germination-croissance pour le mécanisme 1 et sur une identification des paramètres à travers une loi d'Avrami (mécanisme 2). Nous pourrons ainsi mettre en évidence l'influence de différents paramètres, tels que la température du palier isotherme, la vitesse de refroidissement. Le développement de ce modèle s'appuie sur une étude expérimentale divisée en trois étapes. Tout d'abord des mesures calorimétriques à l'aide d'une DSC 8000 de Perkin Elmer permettant de quantifier les échanges thermiques lors de la cristallisation. Différents paliers isothermes entre 250 et 300°C ont été réalisés ainsi que six vitesses de refroidissement comprises entre 1 et 100°C/min. L'évolution du taux de cristallinité relative est tracée en fonction du temps de cristallisation sur la Fig. 1-a. Le temps de cristallisation dépend de la température du palier isotherme. En effet, plus la température du palier est haute, plus le temps de cristallisation sera long. Le PEKK cristallise au bout de 35 min à 315°C alors que le PEEK cristallise en moins de 6 min pour les paliers isothermes les plus hauts [6]. Le temps de cristallisation du PEKK chute à 2 min pour une cristallisation à 270°C. De plus, contrairement au PEEK qui cristallise toujours à au moins 20% [6] malgré des vitesses de refroidissement élevées (150°C/min), le PEKK est quasi amorphe lorsqu'il est refroidit au-delà de 50°C/min.

Atrial fibrillation is a disorganization of the electrical propagation in the atria often initiated by ectopic beats. This spontaneous activity might be associated with the appearance of sustained oscillations in some portion of the tissue. Adrenergic stress and specific gene polymorphisms known to promote atrial fibrillation are notably related to calcium and potassium channel conductances. We performed codimension-one and two bifurcation analysis along these conductances in an ionic canine atrial myocyte model. Two Hopf bifurcations were found, related to two distinct mechanisms: (1) a fast calcium gating-driven oscillator, and (2) a slow concentration-driven oscillator. These two mechanisms interact through a double Hopf bifurcation (HH) in a neighborhood of which a torus (Neimark–Sacker) bifurcation leads to bursting. A complex codimension-two theoretical scenario was identified around HH, through systematic comparison with the attractors found numerically. The concentration oscillator was further decomposed to reveal the minimal oscillating subnetwork, in which the Na + /Ca 2+ exchanger plays a prominent role.

Background and Purpose Measurement of QT intervals during atrial flutter (AFL) is relevant to monitor the safety of drug delivery. Our aim is to compare QT and QTc intervals in AFL patients before and after catheter ablation in order to validate QT measurement during AFL. Methods 25 patients suffering from AFL underwent catheter ablation; 9 were in sinus rhythm and 16 were in AFL at the time of the procedure. Holter ECGs were continuously recorded before, during and after the procedure. In AFL signals, flutter waves were subtracted using a previously-validated deconvolution-based method. Fridericia's QTc was computed before and after ablation after hysteresis reduction. Results Comparing QTc values obtained before and after ablation showed that (1) the intervention did not significantly affect QTc, and (2) the QTc during AFL was concordant with the QTc value in sinus rhythm. Conclusion QTc can be reliably measured in patients with AFL using flutter wave subtraction and hysteresis reduction.

Theaimsofthestudyweretodeterminehowaggregatesofintrinsiccardiac(IC)neurons transduce the cardiovascular milieu versus responding to changes in central neuronal drive and to determine IC network interactions subsequent to induced neural imbalances in the genesis of atrial fibrillation (AF). Activity from multiple IC neurons in the right atrial ganglionated plexus was recorded in eight anaesthetized canines using a 16-channel linear microelectrode array. Induced changes in IC neuronal activity were evaluated in response to: (1) focal cardiac mechanical distortion; (2) electrical activation of cervical vagi or stellate ganglia; (3) occlusion of the inferior vena cava or thoracic aorta; (4) transient ventricular ischaemia, and (5) neurally induced AF. Low level activity (ranging from 0 to 2.7 Hz) generated by 92 neurons was identified in basal states, activities that displayed functional interconnectivity. The majority (56%) of IC neurons so identified received indirect central inputs (vagus alone: 25%; stellate ganglion alone: 27%;both:48%).Fiftypercenttransducedthecardiacmilieurespondingtomultimodalstressors appliedtothegreatvesselsorheart.FiftypercentofICneuronsexhibitedcardiaccycleperiodicity, with activity occurring primarily in late diastole into isovolumetric contraction. Cardiac-related activityinICneuronswasprimarilyrelatedtodirectcardiacmechano-sensoryinputsandindirect autonomicefferentinputs.Inresponsetomediastinalnervestimulation,mostICneuronsbecame excessively activated; such network behaviour preceded and persisted throughout AF. It was

To quantify the sensitivity of QT heart-rate correction methods for detecting drug-induced QTc changes in thorough QT studies.Twenty-four-hour Holter ECGs were analyzed in 66 normal subjects during placebo and moxifloxacin delivery (single oral dose). QT and RR time series were extracted. Three QTc computation methods were used: (1) Fridericia's formula, (2) Fridericia's formula with hysteresis reduction, and (3) a subject-specific approach with transfer function-based hysteresis reduction and three-parameter non-linear fitting of the QT-RR relation. QTc distributions after placebo and moxifloxacin delivery were compared in sliding time windows using receiver operating characteristic (ROC) curves. The area under the ROC curve (AUC) served as a measure to quantify the ability of each method to detect moxifloxacin-induced QTc prolongation.Moxifloxacin prolonged the QTc by 10.6 ± 6.6 ms at peak effect. The AUC was significantly larger after hysteresis reduction (0.87 ± 0.13 vs. 0.82 ± 0.12, p0.01) at peak effect, indicating a better discriminating capability. Subject-specific correction further increased the AUC to 0.91 ± 0.11 (p0.01 vs. Fridericia with hysteresis reduction). The performance of the subject-specific approach was the consequence of a substantially lower intra-subject QTc standard deviation (5.7 ± 1.1 ms vs. 8.8 ± 1.2 ms for Fridericia).The ROC curve provides a tool for quantitative comparison of QT heart rate correction methods in the context of detecting drug-induced QTc prolongation. Results support a broader use of subject-specific QT correction.

Mediastinal nerve stimulation (MNS) reproducibly evokes atrial fibrillation (AF) by excessive and heterogeneous activation of intrinsic cardiac (IC) neurons. This study evaluated whether preemptive vagus nerve stimulation (VNS) impacts MNS-induced evoked changes in IC neural network activity to thereby alter susceptibility to AF. IC neuronal activity in the right atrial ganglionated plexus was directly recorded in anesthetized canines ( n = 8) using a linear microelectrode array concomitant with right atrial electrical activity in response to: 1) epicardial touch or great vessel occlusion vs. 2) stellate or vagal stimulation. From these stressors, post hoc analysis (based on the Skellam distribution) defined IC neurons so recorded as afferent, efferent, or convergent (afferent and efferent inputs) local circuit neurons (LCN). The capacity of right-sided MNS to modify IC activity in the induction of AF was determined before and after preemptive right (RCV)- vs. left (LCV)-sided VNS (15 Hz, 500 μs; 1.2× bradycardia threshold). Neuronal ( n = 89) activity at baseline (0.11 ± 0.29 Hz) increased during MNS-induced AF (0.51 ± 1.30 Hz; P < 0.001). Convergent LCNs were preferentially activated by MNS. Preemptive RCV reduced MNS-induced changes in LCN activity (by 70%) while mitigating MNS-induced AF (by 75%). Preemptive LCV reduced LCN activity by 60% while mitigating AF potential by 40%. IC neuronal synchrony increased during neurally induced AF, a local neural network response mitigated by preemptive VNS. These antiarrhythmic effects persisted post-VNS for, on average, 26 min. In conclusion, VNS preferentially targets convergent LCNs and their interactive coherence to mitigate the potential for neurally induced AF. The antiarrhythmic properties imposed by VNS exhibit memory.

The QT interval in the electrocardiogram (ECG) is a measure of total duration of depolarization and repolarization. Correction for heart rate is necessary to provide a single intrinsic physiological value that can be compared between subjects and within the same subject under different conditions. Standard formulas for the corrected QT (QTc) do not fully reproduce the complexity of the dependence in the preceding interbeat intervals (RR) and inter-subject variability. In this paper, a subject-specific, nonlinear, transfer function-based correction method is formulated to compute the QTc from Holter ECG recordings. The model includes five parameters: three describing the static QT-RR relationship and two representing memory/hysteresis effects that intervene in the calculation of effective RR values. The parameter identification procedure is designed to minimize QTc fluctuations and enforce zero correlation between QTc and effective RR. Weighted regression is used to better handle unbalanced or skewed RR distributions. The proposed optimization approach provides a general mathematical framework for further extensions of the model. Validation, robustness evaluation and comparison with existing QT correction formulas is performed on ECG signals recorded during sinus rhythm, atrial pacing, tilt-table tests, stress tests and atrial flutter (29 subjects in total). The resulting average modeling error on the QTc is 4.9 ± 1.1 ms with a sampling interval of 2 ms, which outperforms correction formulas currently used. The results demonstrate the benefits of subject-specific rate correction and hysteresis reduction.

BACKGROUND Recently, we demonstrated that ajmaline caused ST segment elevation in the heart of an SCN5A mutation carrier by excitation failure in structurally discontinuous myocardium. In patients with Brugada syndrome, ST segment elevation is modulated by cardiac sodium (I-Na), transient outward (I-to), and L-type calcium currents (I-CaL). OBJECTIVE To establish experimentally whether excitation failure by current-to-load mismatch causes ST segment elevation and is modulated by I-to and I-CaL. METHODS In porcine epicardial shavings, isthmuses of 0.9, 1.1, or 1.3 mm in width were created parallel to the fiber orientation. Local activation was recorded electrically or optically (di-4ANEPPS) simultaneously with a pseudo-electrocardiogram (ECG) before and after ajmaline application. Intra-and extracellular potentials and ECGs were simulated in a computer model of the heart and thorax before and after introduction of right ventricular structural discontinuities and during varying levels of I-Na, I-to, and I-CaL. RESULTS In epicardial shavings, conduction blocked after ajmaline in a frequency-dependent manner in all preparations with isthmuses = 1.1 mm (P

L’electrocardiogramme (ECG) resulte de la propagation dans le torse des courants electriques generes par le tissu cardiaque. Le potentiel d’action produit par les cardiomyocytes, qui prelude a leur contraction, est la source premiere de ces courants. L’echange de ces courants intra- et extracellulaires permet a l’activation de se propager d’une cellule a l’autre et de provoquer des differences de potentiels sur le torse. La modelisation de l’activite electrique peut donc se faire a plusieurs echelles : de la cellule isolee a l’organisme entier. Quelques exemples illustrent comment la nature du probleme a analyser determine l’echelle, le niveau de complexite minimale a considerer et le type de resultats qui peuvent etre atteints.

This paper describes an unsupervised signal processing method applied to three-channel unipolar electrograms recorded from human atria. These were obtained by epicardial wires sutured on the right and left atria after coronary artery bypass surgery. Atrial (A) and ventricular (V) activations had to be detected and identified on each channel, and gathered across the channels when belonging to the same global event. The algorithm was developed and optimized on a training set of 19 recordings of 5 min. It was assessed on twenty-seven 2 h recordings taken just before the onset of a prolonged atrial fibrillation for a total of 1593697 activations that were validated and classified as normal atrial or ventricular activations (A, V) and premature atrial or ventricular activations (PAA, PVA). 99.93% of the activations were detected, and amongst these, 99.89% of the A and 99.75% of the V activations were correctly labelled. In the subset of the 39705 PAA, 99.83% were detected and 99.3% were correctly classified as A. The false positive rate was 0.37%. In conclusion, a reliable fully automatic detection and classification algorithm was developed that can detect and discriminate A and V activations from atrial recordings. It can provide the time series needed to develop a monitoring system aiming to identify dynamic predictors of forthcoming cardiac events such as postoperative atrial fibrillation.

Potse M, Vinet A, Opthof T, Coronel R. Validation of a simple model for the morphology of the T wave in unipolar electrograms. Am J Physiol Heart Circ Physiol 297: H792-H801, 2009. First published May 22, 2009; doi: 10.1152/ajpheart.00064.2009.-Local unipolar electrograms (UEGs) permit assessment of local activation and repolarization times at multiple sites simultaneously. However, UEG-based indexes of local repolarization are still debated, in particular for positive T waves. Previous experimental and computer modeling studies have not been able to terminate the debate. In this study we validate a simple theoretical model of the UEG and use it to explain how repolarization statistics in the UEG relate to those in the action potential. The model reconstructs the UEG by taking the difference between an inverted local action potential and a position-independent remote signal. In normal tissue, this extremely simple model predicts T-wave morphology with surprising accuracy while explaining in a readily understandable way why the instant of repolarization is always related to the steepest upstroke of the UEG, both in positive and negative T waves, and why positive T waves are related to early repolarizing sites, whereas negative T waves are related to late repolarizing sites.

The boundary-element method (BEM) is widely used for electrocardiogram (ECG) simulation. Its major disadvantage is its perceived inability to deal with the anisotropic electric conductivity of the myocardial interstitium, which led researchers to represent only intracellular anisotropy or neglect anisotropy altogether. We computed ECGs with a BEM model based on dipole sources that accounted for a "compound" anisotropy ratio. The ECGs were compared with those computed by a finite-difference model, in which intracellular and interstitial anisotropy could be represented without compromise. For a given set of conductivities, we always found a compound anisotropy value that led to acceptable differences between BEM and finite-difference results. In contrast, a fully isotropic model produced unacceptably large differences. A model that accounted only for intracellular anisotropy showed intermediate performance. We conclude that using a compound anisotropy ratio allows BEM-based ECG models to more accurately represent both anisotropies.

Our objective was to determine whether neuronally induced atrial arrhythmias can be modified by α-adrenergic receptor blockade. In 30 anesthetized dogs, trains of five electrical stimuli (1 mA; 1 ms) were delivered immediately after the P wave of the ECG to mediastinal nerves associated with the superior vena cava. Regional atrial electrical events were monitored with 191 atrial unipolar electrodes. Mediastinal nerve sites were identified that reproducibly initiated atrial arrhythmias. These sites were then restimulated following 1 h (time control, n = 6), or the intravenous administration of naftopidil (α1-adrenergic blocker: 0.2 mg/kg, n = 6), yohimbine (α2-adrenergic blocker: 1 mg/kg, n = 6) or both ( n = 8). A ganglionic blocker (hexamethonium: 1 mg/kg) was tested in four dogs. Stimulation of mediastinal nerves sites consistently elicited atrial tachyarrhythmias. Repeat stimulation after 1 h in the time-control group exerted a 19% decrease of the sites still able to induce atrial tachyarrhythmias. Hexamethonium inactivated 78% of the previously active sites. Combined α-adrenoceptor blockade inactivated 72% of the previously active sites. Bradycardia responses induced by mediastinal nerve stimulation were blunted by hexamethonium, but not by α1,2-adrenergic blockade. Naftopidil or yohimbine alone eliminated atrial arrhythmia induction from 31% and 34% of the sites (similar to time control). We conclude that heterogeneous activation of the intrinsic cardiac nervous system results in atrial arrhythmias that involve intrinsic cardiac neuronal α-adrenoceptors. In contrast to the global suppression exerted by hexamethonium, we conclude that α-adrenoceptor blockade targets intrinsic cardiac local circuit neurons involved in arrhythmia formation and not the flow-through efferent projections of the cardiac nervous system.