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Permanent His-bundle pacing (PHBP) has become increasingly popular, as it provides the most physiological form of ventricular activation when compared to other pacing modalities.1 PHBP has been reported in patients with mitral and aortic prosthetic cardiac valves.2 To date, there have been no published reports regarding the feasibility of PHBP in the setting of prosthetic tricuspid valve (TV). We report 2 cases of patients with prosthetic TV who underwent PHBP.

We report the case of a man in his 60s who had dilated cardiomyopathy with severe functional mitral regurgitation. Four years after a cardiac resynchronization therapy (CRT) device with an implantable cardioverter defibrillator was implanted, this device was replaced with an adaptive CRT device because of battery consumption. Seven months after replacement of this device, the left ventricular pacing to right ventricular activation and the atrioventricular delay from automatic adjustments contributed to less functional mitral regurgitation. The findings from our case suggest that optimal CRT, by measuring intracardiac conduction parameters, is effective for functional mitral regurgitation.

Zusammenfassung. Der Linksschenkelblock (LSB) ist das elektrokardiografische Korrelat einer pathologischen Reizweiterleitung am Herzen, die zu einer dyssynchronen Erregung des Ventrikelmyokards und somit zu einer ineffizienten Kontraktion der Ventrikel führen kann. Meist ist der LSB assoziiert mit einer zugrundeliegenden Kardiopathie und stellt einen unabhängigen Risikofaktor der kardiovaskulären Mortalität dar, weswegen eine weitere Abklärung in jedem Fall indiziert ist. Neben der Behandlung einer möglichen Grunderkrankung steht im Falle einer bestehenden systolischen Herzinsuffizienz seit der Einführung der kardialen Resynchronisationstherapie (CRT) zudem eine spezifische elektrische Therapie zur Verfügung. Ein selteneres Phänomen ist der symptomatische und belastungsabhängige LSB bei strukturell gesundem Herzen.

Atrial fibrillation becomes a potentially lethal arrhythmia in the presence of preexcitation because the rapid ventricular activation can result in ventricular fibrillation. Fortunately, radiofrequency ablation is an effective treatment for these patients. Specific points of interest regarding this association are the mechanism of increased incidence of atrial fibrillation and the current management of patients presenting in atrial fibrillation. These are discussed in this editorial. Keywords: Atrial fibrillation, Preexcitation, Ablation

Aims The occurrence of left ventricular (LV) anodal activation during pacing with modern multipolar cardiac resynchronization therapy (CRT) systems has never been reported. The aim of our study was to demonstrate, by means of electrocardiogram (ECG) analysis, the occurrence of simultaneous cathodal–anodal LV capture with quadripolar LV leads. Methods and results We studied 10 first-time recipients of a CRT device equipped with a quadripolar LV lead. During follow-up, standard supine 12-lead ECGs were obtained in available cathode-to-anode LV pacing configurations with a pulse amplitude equal to twice the pacing threshold. The occurrence of simultaneous cathodal–anodal LV capture was defined as the presence of variations in electrocardiographic ventricular activation (EVA) when the distal tip (cathode)-to-device can (anode) pacing configuration was compared with the distal tip (cathode)-to-proximal ring (anode) configuration. In eight patients, we found differences in EVA when different LV sites were paced through the unipolar LV tip and unipolar LV ring configurations. In these patients, a difference in EVA was detected in 61.5% (59 of 96) of the ECG leads (marked difference in 31.3%, slight difference in 30.2%). Changes in EVA between unipolar tip-to-can and bipolar tip-to-ring pacing that were suggestive of cathodal–anodal LV capture were found in six patients. In these patients, a total of 30 (41.7%) ECG leads showed a difference in EVA (marked difference in 20.8%, slight difference in 20.8%). Conclusion In our experience, additional anodal capture by the proximal LV ring during LV pacing is provable in most recipients of a resynchronization device equipped with a multipolar LV lead.

Cardiac memory (CM) is identified as an altered T wave when normal ventricular activation resumes after an abnormal myocardial activation period. We present a case who initially underwent temporary right ventricular apex (RVA) pacing for one week which induced typical pseudo-primary T wave changes. The T wave inversion was observed after the end of RVA pacing when left bundle branch pacing (LBBP) was initiated, and the abnormal T waves gradually return to almost normal repolarization during LBBP 40 days later.

Introduction Cardiac resynchronisation therapy (CRT) corrects electrical dyssynchrony. However, the temporal changes in the electrical timing according to substrate are unclear. We used electrocardiographic imaging (ECGi) for serial non-invasive assessment of the underlying electrical substrate and its response to resynchronisation. Material and methods ECGi activation maps were constructed 1 day and 6 months post CRT implant. ECGi maps were analysed offline to determine the total ventricular activation time (TVaT) and the time for the bulk of ventricular activation (10th to 90th percentile activation; VaT10–90 Index). Statistical analysis was performed using repeated measures ANOVA with post-hoc pairwise comparisons using paired t-tests. The % relative change within each time point was also calculated and compared between the two time points. Results Eleven CRT patients were studied. Both total and bulk ventricular activation significantly decreased with CRT turned ON at day 1. Intrinsic (CRT OFF) TVaT and VaT10–90 Index at day 1 were 143 ± 23 and 84 ± 20 ms, respectively, and they significantly decreased post CRT to 115 ± 26 ms (P After 6 months, the relative decrease in TVaT with CRT ON remained stable (19% vs. 18% at day 1 and 6 months, respectively) whereas reduction the in VaT10–90 Index was decreased 39% vs. 26% at day 1 and 6 months, respectively. In non-ischaemic patients both total and bulk activation times reduced following CRT. Volumetric responders exhibited an electrical remodelling for bulk activation not apparent in Non-responders, after 6 months of CRT ON. Conclusions Intrinsic bulk myocardium activation becomes more rapid and synchronous with CRT. The bulk activation time is more susceptible to improvement by CRT in ischaemic patients and volumetric responders. These observations are consistent with CRT causing reverse electrophysiological remodelling in the bulk myocardium, but not in late-activating ischaemic or fibrotic regions.

BackgroundMechanisms of arrhythmogenicity in hypertrophic cardiomyopathy (HCM) are not well understood.ObjectiveTo characterize an electrophysiological substrate of HCM in comparison to ischemic cardiomyopathy (ICM), or healthy individuals.MethodsWe conducted a prospective case-control study. The study enrolled HCM patients at high risk for ventricular tachyarrhythmia (VT) (n=10; age 61±9 y; left ventricular ejection fraction (LVEF) 60±9%), and three comparison groups: healthy individuals (n=10; age 28±6 y; LVEF>70%), ICM patients with LV hypertrophy (LVH) and known VT (n=10; age 64±9 y; LVEF 31±15%), and ICM patients with LVH and no known VT (n=10; age 70±7y; LVEF 46±16%). All participants underwent 12-lead ECG, cardiac CT or MRI, and 128-electrode body surface mapping (BioSemi ActiveTwo, Netherlands). Non-invasive voltage and activation maps were reconstructed using the open-source SCIRun (University of Utah) inverse problem-solving environment.ResultsIn the epicardial basal anterior segment, HCM patients had the greatest ventricular activation dispersion [16.4±5.5 vs. 13.1±2.7 (ICM with VT) vs. 13.8±4.3 (ICM no VT) vs. 8.1±2.4 ms (Healthy); P=0.0007], the largest unipolar voltage [1094±211 vs. 934±189 (ICM with VT) vs. 898±358 (ICM no VT) vs. 842±90 µV (Healthy); P=0.023], and the greatest voltage dispersion [median(interquartile range) 215(161-281) vs. 189(143-208) (ICM with VT) vs. 158(109-236) (ICM no VT) vs. 110(106-168)µV (Healthy); P=0.041]. Differences were also observed in other endo-and epicardial basal and apical segments.ConclusionHCM is characterized by a greater activation dispersion in basal segments, a larger voltage, and a larger voltage dispersion through LV.

Background Despite the tremendous progress recently reported in ECG imaging (ECGI), some fundamental challenges are still hindering this non-invasive technology from meeting rising clinical expectations. In the present work, we address one of the major ECGI shortcomings in reconstruction of ventricular activation – the limited accuracy of endocardial and particularly septal mapping. Methods Ten CRT patients (five female, median (min-max) age – 61 (27–78) years) with previously implanted CRT devices underwent ECGI with isolated right ventricular (RV) pacing. In eight patients, the RV pacemaker lead was placed in the middle septal area of the posterior RV wall. Two subjects had a pacing lead in the anteroseptal apical segment, two at septal RVOT, two at septal junction with posterior wall and six in anterolateral segments. Lead positions were exactly known from CT scans, making the respective paced ECG sequences ideal for validation of ECGI endocardial accuracy. Non-invasive mapping was performed for single RV paced beats using original parameters of the CRT device. For non-invasive estimation of the focal origins, we considered the lead-field based fastest route algorithm (FRA) and its combination with the cardiac vector fit (FRA-V). Furthermore, we extended the resulting combined map by incorporating cardiac activation direction (FRA-V-D) provided by the cardiac dipole. Results The median (min-max) localization errors were 14 mm (7–27), 9 mm (7–28) and 11 mm (8–24) for FRA, FRA-V and FRA-V-D, respectively. Notably, in all cases at least one of the considered ECGI methods was able to correctly localize the found excitation origin on the endocardium. Conclusions This preliminary study investigates combination of the rule-based fastest route algorithm with cardiac vector fit and direction for non-invasive imaging of septal ventricular sources. The developed ECGI methodology delivers reasonable reconstruction accuracy with the 10 mm median localization error. These findings suggest potential use of ECGI for challenging clinical cases, where catheter access to the correct cardiac anatomical region plays a crucial role in the execution of the electrophysiological procedure.

Introduction Left bundle branch pacing (LBBP) has recently been reported to maintain left ventricular electrical synchrony with a low and stable threshold. However, the electrocardiogram (ECG) definitions of LBBP have not been well established. We report four cases to show the characteristics of the ECG and the intracardiac electrogram (EGM) in LBBP. Methods and results Four patients, two with an atrioventricular block (AVB) and two with left bundle branch block (LBBB), were included in the study. LBBP was performed and the ECGs and EGMs were collected and compared at different pacing outputs. Selective LBBP (S-LBBP) was defined as only capturing the LBB with a typical RBBB morphology and a discrete component between the pacing stimulus and ventricular activation in the EGMs. While nonselective LBBP (NS-LBBP) captured both the LBB and the local myocardium, resulting in a narrow right bundle branch block (RBBB) morphology without the discrete component. The left bundle branch (LBB) potential was recorded in two cases during narrow QRS complex or LBBB correction by selective His bundle pacing and SLBBP (n = 3) was achieved. A constant and shortest stimulus to left ventricular activation time (LVAT) in LBBP was obtained at different pacing outputs. Conclusion The ECG and EGM characteristics of LBBP can be summarized as: 1) RBBB pattern; 2) usually with the LBB potential; 3) SLBBP with specific ECG changes and a discrete component in EGM; and 4) with a constant and shortest stimulus to LVAT at different pacing outputs. Further studies are necessary to confirm these observations.

Various degree of ventricular activation by accessory pathway (AP) and normal conduction system in a patient with pre-excited atrial fibrillation (AF) may lead to ventricle dyssynchrony and cardiomyopathy.

The use of an electroanatomic navigation system in Cardiac Resynchronization Therapy (CRT) implantation is an increasingly used approach in the field of electrophysiology. The possibility to minimize X-ray exposure both for patients and for physicians is not the only most attractive aspect. Indeed it is feasible, safe, and allows to obtain more detailed information during the coronary sinus lead placement, in terms of both 3D anatomy and ventricular activation time. This procedure can improve the pacing site choice optimization, making CRT implantation an electrophysiological procedure.

Background His-bundle pacing (HBP) provides physiological ventricular activation. Observational studies have demonstrated the techniques' feasibility; however, data have come from a limited number of centers. Objectives We set out to explore the contemporary global practice in HBP focusing on the learning curve, procedural characteristics, and outcomes. Methods This is a retrospective, multicenter observational study of patients undergoing attempted HBP at seven centers. Pacing indication, fluoroscopy time, HBP thresholds, and lead reintervention and deactivation rates were recorded. Where centers had systematically recorded implant success rates from the outset, these were collated. Results A total of 529 patients underwent attempted HBP during the study period (2014-19) with a mean follow-up of 217 ± 303 days. Most implants were for bradycardia indications. In the three centers with the systematic collation of all attempts, the overall implant success rate was 81%, which improved to 87% after completion of 40 cases. All seven centers reported data on successful implants. The mean fluoroscopy time was 11.7 ± 12.0 minutes, the His-bundle capture threshold at implant was 1.4 ± 0.9 V at 0.8 ± 0.3 ms, and it was 1.3 ± 1.2 V at 0.9 ± 0.2 ms at last device check. HBP lead reintervention or deactivation (for lead displacement or rise in threshold) occurred in 7.5% of successful implants. There was evidence of a learning curve: fluoroscopy time and HBP capture threshold reduced with greater experience, plateauing after approximately 30-50 cases. Conclusion We found that it is feasible to establish a successful HBP program, using the currently available implantation tools. For physicians who are experienced at pacemaker implantation, the steepest part of the learning curve appears to be over the first 30-50 cases.

Cardiac resynchronization therapy (CRT) by the way of biventricular (BiV) pacing is an established component of heart failure treatment in selected patients and aims at reestablishing synchrony between right ventricular and left ventricular activation [1]. However, this form of cardiac excitation fails to emulate the multisite simultaneous endo- to epicardial activation resulting in torsional contraction, which is critical to achieve optimal cardiac output.

Electrocardiographic imaging has been shown to provide useful information for pre-procedure planning of catheter-ablation procedures. The methodology involves reconstruction of unipolar electrograms (EGMs) and isochronal maps on the epicardial surface from non-invasively acquired body-surface potentials. We have developed an algorithm for evaluating global myocardial activation times. First, the cross-correlation method determines the delay in local activation times among pairs of neighboring nodes. Next, a sparse linear system is constructed from known activation delays of neighboring nodes. To solve this system, we use a sparse Bayesian learning method to calculate the global myocardial activation times. The aim of this study was to assess the proposed method in both structurally normal and scarred ventricular myocardium. Isochronal maps of calculated activation times were compared with local activation times (LATs) derived from directly-measured epicardial EGMs obtained by electroanatomic contact mapping, for pacing delivered by an implantable cardioverter defibrillator (ICD) at the endocardial right-ventricular (RV) apex, and for catheter pacing at RV epicardial site. We found that even in the presence of infarct scar, isochronal maps calculated by the proposed method correlated closely with known LATs exported from an electroanatomic mapping system.

We present a case of sudden cardiac arrest 7 hours after radiofrequency ablation of the atrioventricular junction for symptomatic permanent atrial fibrillation unresponsive to medical therapy. The Holter monitoring revealed a progressive increasing of QT interval after the procedure, highlighting the repolarization instability after acute changes in heart rates associated with modification of ventricular activation, leading to occurrence of short coupling interval ventricular extra beats and finally to a "torsade de pointes." This illustration underlines the need to program a relatively rapid ventricular rate first weeks after junction ablation, especially in case of rapid ventricular rate prior to the procedure, as well as the role of continuous ECG and QT interval monitoring during hospital stay.

Left ventricular dysfunction and dilated cardiomyopathy (DCMP) are infrequently associated with sustained tachyarrhythmias in patients with Wolff-Parkinson-White (WPW) syndrome. DCMP has also been rarely reported (primarily in infants and children) in the absence of arrhythmia with a presumed

Cardiac resynchronization therapy (CRT) with biventricular pacing involves pacing of the left ventricle through a pacing lead in the coronary sinus (or epicardial or endocardial left ventricle) which mimics normal ventricular activation, but is not physiologic. His bundle pacing allows pacing

Heart failure is a complex clinical syndrome associated with a significant morbidity and mortality burden. Reductions in left ventricular (LV) function trigger adaptive mechanisms, leading to structural changes within the LV and the potential development of dyssynchronous ventricular activation. This is the substrate targeted during cardiac resynchronisation therapy (CRT); however, around 30–50% of patients do not experience benefit from this treatment. Non-response occurs as a result of pre-implant, peri-implant and post implant factors but the technical constraints of traditional, transvenous epicardial CRT mean they can be challenging to overcome. In an effort to improve response, novel alternative methods of CRT delivery have been developed and of these endocardial pacing, where the LV is stimulated from inside the LV cavity, appears the most promising.

It is now well over 100 years since Sunao Tawara clarified the location of the axis of the specialised myocardium responsible for producing coordinated ventricular activation. Prior to that stellar publication, controversies had raged as to how many bundles crossed the place of the atrioventricular insulation as found in mammalian hearts, as well as the very existence of the bundle initially described by Wilhelm His Junior. It is, perhaps surprising that controversies continue, despite the multiple investigations that have taken place since the publication of Tawara’s monograph. For example, we are still unsure as to the precise substrates for the so-called slow and fast pathways into the atrioventricular node. Much has been done, nonetheless, to characterise the molecular make-up of the specialised pathways, and to clarify their mechanisms of development. Of this work itself, a significant part has emanated from the laboratory coordinated for a quarter of a century by Antoon FM Moorman. In this review, which joins the others in recognising the value of his contributions and collaborations, we review our current understanding of the anatomy, development, and evolution of the atrioventricular conduction axis.

Background Cardiac resynchronization therapy (CRT) is now generally delivered via quadripolar leads. Assessment of the effect of different vector programs from quadripolar leads on ventricular activation can be now done using non-invasive electrocardiographic mapping (ECM). Material and methods In nineteen patients with quadripolar LV leads, activation maps were constructed. The total ventricular activation time (TVaT) and the time for the bulk of ventricular activation (VaT10–90) were calculated. Results CRT delivered via a quadripolar lead significantly reduced TVaT and VaT10–90 by a mean of 16 ms and 31 ms, respectively, compared to baseline. There was a marked reduction in ventricular activation between the most and least synchronous vectors: 28% difference in baseline TVaT and 37% difference in VaT10–90. Conclusion Changes in the configuration of an LV quadripolar lead significantly affected ventricular activation timings in both ischaemic and non-ischaemic subjects. This suggests that programming of the optimal pacing vector may need to be individually tailored.

From the atrioventricular node, electrical activation is propagated to both ventricles by a system of specialized conducting fibers, His Purkinje System (HPS), guaranteeing a fast, synchronous depolarization of both ventricles. From the predivisional common stem, a right and left branch separate, subdividing further in a fairly predictable fashion. Synchronous ventricular activation results in a QRS with specific characteristics and duration of less than 110 milliseconds. Block or delay in any part of the HPS changes the electrocardiographic (ECG) morphology. This article discusses the use and limitations of standard ECG in detecting abnormal ventricular propagation in specific areas of the HPS.

Background Catheter ablation of ventricular arrhythmias (VAs) originating from the para-Hisian region could be challenging because of a potential damage to atrioventricular conduction system. Objective The purpose of this study was to evaluate the safety and efficacy of catheter ablation of VAs originating from the para-Hisian region via a systematic direct approach from aortic sinus cusps (ASCs). Methods Twenty-one consecutive patients with VAs with para-Hisian origin were included. Electrophysiological mapping of the entire right ventricle was initially performed, and then retrograde ASC mapping was performed when the earliest ventricular activation was recorded in the His bundle region. Ablation was preferentially performed within ASCs in all patients. Results Radiofrequency energy delivery resulted in the elimination of VAs in 17 of 21 patients (81%). In the remaining 4 patients, radiofrequency application was initiated at the target site of the right ventricular septum around the His bundle region and clinical VAs were finally successfully eliminated without junctional rhythm in 2 of 4 patients. During a mean follow-up of 34.8 ± 11.3 months, 1 of the 19 acute successful patients had VA recurrence. No procedure-related complications occurred during ablation or follow-up. Conclusion Catheter ablation of VAs originating from the para-Hisian region via a direct approach from ASCs may be safe and effective in most unselected patients.

Background QRS narrowing following cardiac resynchronization therapy with biventricular (BiV) or left ventricular (LV) pacing is likely affected by patient‐specific conduction characteristics ( PR , qLV, LV ‐paced propagation interval), making a universal programming strategy likely ineffective. We tested these factors using a novel, device‐based algorithm (Sync AV ) that automatically adjusts paced atrioventricular delay (default or programmable offset) according to intrinsic atrioventricular conduction. Methods and Results Seventy‐five patients undergoing cardiac resynchronization therapy (age 66±11 years; 65% male; 32% with ischemic cardiomyopathy; LV ejection fraction 28±8%; QRS duration 162±16 ms) with intact atrioventricular conduction (PR interval 194±34, range 128–300 ms), left bundle branch block, and optimized LV lead position were studied at implant. QRS duration ( QRS d) reduction was compared for the following pacing configurations: nominal simultaneous BiV (Mode I: paced/sensed atrioventricular delay=140/110 ms), BiV+Sync AV with 50 ms offset (Mode II ), BiV+Sync AV with offset that minimized QRS d (Mode III ), or LV ‐only pacing+Sync AV with 50 ms offset (Mode IV ). The intrinsic QRS d (162±16 ms) was reduced to 142±17 ms (−11.8%) by Mode I, 136±14 ms (−15.6%) by Mode IV , and 132±13 ms (−17.8%) by Mode II . Mode III yielded the shortest overall QRS d (123±12 ms, −23.9% [ P QRS d prolongation in any patient. QRS narrowing occurred regardless of QRS d, PR , or LV ‐paced intervals, or underlying ischemic disease. Conclusions Post‐implant electrical optimization in already well‐selected patients with left bundle branch block and optimized LV lead position is facilitated by patient‐tailored BiV pacing adjusted to intrinsic atrioventricular timing using an automatic device–based algorithm.

Atrioventricular (AV) block has been extensively studied. However, conduction inside the myocardium in patients with AV block has not been reported. In this study, we aimed to demonstrate the presence of intramyocardial block in patients with AV block. Five consecutive patients with spontaneous high-grade AV block and Torsades de pointes (TdP) were prospectively studied with standard United States Catheter Instruments (USCI) endocardial temporary catheter located at the right ventricle (RV) apex. The morphology of endocardial potentials observed in the basic QRS complexes as well as during episodes of TdP was studied. The electrogram (EGM) of the basic rhythm showed a sharp deflection of high amplitude preceded and/or followed by a smooth potential of low amplitude interpreted as far-field potentials in all patients. The sharp potential can be observed at the beginning, in the middle or at the end of the smooth potential. All these potentials were reproduced from beat to beat and were falling inside the QRS complex of the surface ECG. Therefore, these aspects are zones of electrically depressed or silent myocardium larger than the interelectrode distance of 12 mm. This situation is in agreement with recent genetic factors. In this study, we demonstrated for the first time that patients with spontaneous AV block also have trouble in ventricular activation located on the AV conduction system and inside the myocardium. It is then possible to speculate that the presence of diffuse non-conducting myocardium explains why most TdPs do not degenerate into ventricular fibrillation (VF) and generally stop spontaneously.

We describe a neonate that developed alternating wide and narrow complex tachycardias following heart surgery for congenital heart defect. Although the etiology was sinus tachycardia, a premature atrial complex initiated aberrancy due to phase 3 block that was perpetuated due to 'linking' at similar or even slower heart rates. Similarly, there was abrupt transition from wide to narrow complex tachycardia following a premature ventricular complex without a change in subsequent heart rate. This was explained by interruption of linking phenomenon by premature ventricular activation. While the above mechanisms are described in the setting of a supraventricular tachyarrhythmia, this has not been reported during sinus tachycardia.

Background We aimed to analyze ventricular repolarization in neurocardiogenic syncope (NCS) patients by using T-peak-T-end interval, T-peak-T-end/QT ratio, T-peak-T-end/QTc ratio and corrected QT interval (QTc), QT dispersion (QTd), QT index (QTI) and corrected QT interval index (QTcI) comparing with the corrected JT dispersion (JTcd), and corrected JT (JTc) and the corrected JT interval index (JTcI), by inspecting ventricular activation until termination of repolarization. These parameters are used as an index of potential ventricular arrhythmogenesis. Methods We have studied patients with head-up tilt table test (HUTT) (+) (33 patients; mean age: 28 ± 11 years) and HUTT (–) as control group (33 patients; mean age: 30 ± 11 years). In all patients, T-peak-T-end interval, T-peak-T-end/QT ratio, T-peak-T-end/QTc ratio, QT, QTd, QTI, QTc, QTcI, JTd, JTc, and JTcI were measured on electrocardiogram. Results The following parameters were statistically significant between groups: QTd (22.72 ± 17.54 msn; 11.21 ± 13.40 msn; P = 0.004), QTc (424.27 ± 33.75 msn; 403.66 ± 38.08 msn; P = 0.023), QTcI (114.09 ± 14, 29%; 106.71 ± 15.33%, P = 0.047), and QTI (100.72 ± 7.19%; 97.14 ± 7.13%, P = 0.046). Furthermore, T-peak-T-end interval was significantly prolonged in the study group (93.78 ± 20.27 msn; 81.21 ± 11.66 msn; P = 0.003). T-peak-T-end/QT ratio was significantly higher in the study group (0.24 ± 0.04 msn; 0.22 ± 0.04 msn; P = 0.030). T-peak-T-end/QTc ratio was significantly higher in the study group (0.22 ± 0.04 msn; 0.20 ± 0.03 msn; P = 0.015). The JTc and JTd were also significantly higher in the study group ([103.00 ± 9, 72%; 95.44 ± 10.26%, P = 0.003], [27.57 ± 16.01 msn; 10.45 ± 16.08 msn; P < 0.001], respectively). Conclusions Electrocardiographic ventricular repolarization parameters including T-peak-T-end interval, T-peak-T-end/QT ratio, T-peak-T-end/QTc ratio, QTc, QTd, QTI, QTcI, JTc, JTd, and JTI are prolonged in NCS.

Background— Sudden infant death syndrome (SIDS) describes the sudden, unexplained death of a baby during its first year of age and is the third leading cause of infant mortality. It is assumed that ≤20% of all SIDS cases are because of cardiac arrhythmias resulting from mutations in ion channel proteins. Besides ion channels also cardiac gap junction channels are important for proper conduction of cardiac electric activation. In the mammalian heart Connexin43 (Cx43) is the major gap junction protein expressed in ventricular cardiomyocytes. Recently, a novel Connexin43 loss-of-function mutation (Cx43E42K) was identified in a 2-month-old SIDS victim. Methods and Results— We have generated Cx43E42K-expressing mice as a model for SIDS. Heterozygous cardiac-restricted Cx43E42K-mutated mice die neonatally without major cardiac morphological defects. Electrocardiographic recordings of embryonic Cx43+/E42K mice reveal severely disturbed ventricular activation, whereas immunohistochemical analyses show normal localization and expression patterns of gap junctional Connexin43 protein in the Cx43E42K-mutated newborn mouse heart. Conclusions— Because we did not find heterogeneous gap junction loss in Cx43E42K mouse hearts, we conclude that the Cx43E42K gap junction channel creates an arrhythmogenic substrate leading to lethal ventricular arrhythmias. The strong cardiac phenotype of Cx43E42K expressing mice supports the association between the human Cx43E42K mutation and SIDS and indicates that Connexin43 mutations should be considered in future studies when SIDS cases are to be molecularly explained.

Accessory Pathway Target in Ebstein's Anomaly Introduction Knowledge about local electrogram and atrial/ventricular electrogram amplitude ratio (A/V ratio) at the true atrioventricular ring for successful ablation of accessory pathways (APs) in patients with Ebstein's anomaly is limited. Methods Twenty-two adults with Ebstein's anomaly and APs were managed by 24 sessions of radiofrequency catheter ablation (RFCA). A right atrial/ventricular angiogram with or without 3-dimensional electroanatomic mapping was performed to delineate the true atrioventricular ring and atrialized right ventricle (ARV). Electrograms of successful targets were analyzed. For each right-sided AP target, 2 AP targets matched by location and conduction property from normal hearts were selected as controls, and their A/V ratios were compared. Results In 32 right-sided APs of all 22 patients, local ventricular activation at successful site presented as normal electrogram in 14, fractionated ventricular electrogram (FVE) in 16, and double ventricular potentials in 2. The bipolar voltage of ARV was markedly lower than in normal hearts. The A/V ratio at the successful target was significantly higher in APs with FVE than in control (1.64 ± 1.34 vs. 0.47 ± 0.19, P < 0.01), and was similar in APs with normal ventricular electrogram and in the control (0.38 ± 0.15 vs. 0.46 ± 0.15, P = 0.1726). The A/V ratio at the successful target with double ventricular potentials (after surgical correction) was 0.30 ± 0.20. All APs were successfully ablated without complications. Conclusions In patients with Ebstein's anomaly, FVE was found in 50% of the successful targets of APs. High A/V ratio at successful sites with FVE and normal A/V ratio at targets with normal ventricular electrogram can facilitate target recognition and ablation.

Electroanatomical mapping (EAM) systems are commonly used in clinical practice for guiding catheter ablation treatments of common arrhythmias. In focal tachycardias, the ablation target is defined by locating the earliest activation area determined by the joint analysis of electrogram (EGM) signals at different sites. However, this is currently a manual time-consuming and experience-dependent task performed during the intervention and thus prone to stress-related errors. In this paper, we present an automatic delineation strategy that combines electrocardiogram (ECG) information with the wavelet decomposition of the EGM signal envelope to identify the onset of each EGM signal for activation mapping. Fourteen electroanatomical maps corresponding to ten patients suffering from non-tolerated premature ventricular contraction (PVC) beats and admitted for ablation procedure were used for evaluation. We compared the results obtained automatically with two types of manual annotations: one during the intervention by an expert technician (on-procedure) and other after the intervention (off-procedure), free from time and procedural constraints, by two other technicians. The automatic annotations show a significant correlation (0.95, p

Cardiac memory is an electrocardiographic manifestation of transient T wave abnormalities, which is observed after abrupt interruption of abnormal ventricular activation. We report a case with preexisting complete left bundle branch block in whom cardiac memory was induced. This cardiac memory was induced by normalization of QRS morphology after development of complete atrioventricular block due to acute inferior myocardial infarction. Learning objective: Although T wave inversion can often be seen in acute coronary syndrome, cardiac memory might create unusual changes of T wave morphologies in the case with preexisting left bundle branch block. Premature beats arising from upstream of abnormal conduction site produced equalization of bi-ventricular activation in a case of preexisting complete left bundle branch block. This may cause normalization of the QRS complex and cardiac memory (T wave inversion).>