An electrocardiographic diagnostic model for differentiating right from left ventricular outflow tract arrythmias origin

Background/Introduction Several ECG signs have been proposed to discern the focal origin of ventricular outflow tract arrhythmias with a transition ≥V3. Their independent predictive value is unclear. Purpose The aim of the study is to establish a predictive model of independent ECG parameters to obtain an acute success in right-sided catheter ablation of isolated premature ventricular contractions (PVCs) or ventricular tachycardia (VT) from the ventricular outflow tract with a transition ≥V3. Methods We included 122 patients (62 women, mean age 54±16 years) with documented PVCs or VT showing a lower axis and predominantly negative QRS complexes in V1 and V2 who underwent ablation between January 2014 and June 2020. The achievement of acute ablation success from right endocardial positions was assessed. We performed a predictive model by multivariate logistic regression analysis including the following ECG variables associated with a right origin of the ventricular focus in previous studies: Transitional Zone (TZ) index, V2 transition ratio, V2S / V3R index, R-wave duration index, R/S-wave amplitude index in V2, variable coupling interval, and the presence of QS morphology in lead I. Results Two independent predictive ECG variables were identified: the V2S / V3R index (odds ratio 1.223; 95% CI, 1.024–1.460; p=0.026) and a coupling interval variability >60 ms (odds ratio 0.307; 95% CI, 0.129 - 0.731; p=0.008). The area under the curve of this model was 0.733 (Picture 1). Arrhythmias with transition in V3 present a greater electroanatomic overlap and, therefore, a higher probability of right failure (59.3% vs 73.5% in arrhythmias with transitions after V3). In these, the V2 transition ratio is useful to predict the origin of the ectopy. Conclusion Two easily identifiable ECG variables (the V2S / V3R index and coupling interval variability >60 ms) predict the acute success of a right-sided approach in the ablation of focal ventricular arrhythmias with predominantly negative QRS complexes in V1 and V2. FUNDunding Acknowledgement Type of funding sources: None. Predictive accuracy of the ECG model

Premature ventricular complexes and development of heart failure in a community-based population

ObjectiveA higher premature ventricular complex (PVC) frequency is associated with incident congestive heart failure (CHF) and death. While certain PVC characteristics may contribute to that risk, the current literature stems from patients in medical settings and is therefore prone to referral bias. This study aims to identify PVC characteristics associated with incident CHF in a community-based setting.MethodsThe Cardiovascular Health Study is a cohort of community-dwelling individuals who underwent prospective evaluation and follow-up. We analysed 24-hour Holter data to assess PVC characteristics and used multivariable logistic and Cox proportional hazards models to identify predictors of a left ventricular ejection fraction (LVEF) decline and incident CHF, respectively.ResultsOf 871 analysed participants, 316 participants exhibited at least 10 PVCs during the 24-hour recording. For participants with PVCs, the average age was 72±5 years, 41% were women and 93% were white. Over a median follow-up of 11 years, 34% developed CHF. After adjusting for demographics, cardiovascular comorbidities, antiarrhythmic drug use and PVC frequency, a greater heterogeneity of the PVC coupling interval was associated with an increased risk of LVEF decline and incident CHF. Of note, neither PVC duration nor coupling interval duration exhibited a statistically significant relationship with either outcome.ConclusionsIn this first community-based study to identify Holter-based features of PVCs that are associated with LVEF reduction and incident CHF, the fact that coupling interval heterogeneity was an independent risk factor suggests that the mechanism of PVC generation may influence the risk of heart failure.

Location and coupling interval of an ectopic excitation determine the initiation of atrial fibrillation from the pulmonary veins

Background and Objective: Ectopic beats originating from the pulmonary vein (PV) trigger atrial fibrillation (AF). The purpose of this study was to clarify the electrophysiological determinant of AF initiation from the PVs. Methods: Pacing studies were performed with a single extra stimulus mimicking an ectopic beat in the left superior pulmonary veins (LSPVs) in 62 patients undergoing AF ablation. Inducibility of AF, effective refractory period (ERP) and conduction properties within the PVs were analyzed. Results: A single extra stimulus in LSPV induced AF in 20 patients (32% of all patients) at the mean coupling interval (CI) of 172 ms. A CI-dependent anisotropic conduction at the AF onset was visualized in a 3D-mapping. Onset of AF was site-specific with reproducibility in each individual. Mean ERP in LSPV in the AF inducible group was shorter than that in the AF non-inducible group (182 ± 55 ms vs 254 ± 51 ms, P<0.0001). LSPV ERP dispersion was greater in the AF inducible group than in the AF non-inducible group (45 ± 28 ms vs 27 ± 19 ms, P<0.01). Circumferential intra-PV conduction time (IPVCT) exhibited decremental properties in response to shortening of CI, and the prolongation of IPVCT in the AF inducible site was greater than that in the AF non-inducible site (P<0.05) in each individual. Conclusions: Location and coupling interval of an ectopic excitation ultimately determine the initiation of AF from the PVs. ERP dispersion and circumferential conduction delay may lead to anisotropic conduction and reentry within the PVs that initiate AF.

Spatial Correction Improves Accuracy of Catheter Positioning During Ablation of Premature Ventricular Contractions: Differences Between Ventricular Outflow Tracts And Other Localizations.

1.1. PurposeHybrid activation mapping is a novel tool to correct for spatial displacement of the mapping catheter due to asymmetrical contraction of myocardium during premature ventricular contractions (PVC). The aim of this study is to describe the extent and cause of spatial displacement during PVC mapping and options for correction using hybrid activation mapping. 1.2. Methods and ResultsWe analyzed 5798 hybrid mapping points in 40 acquired hybrid maps of 22 consecutive patients (age 63±16 years, 45% female) treated for premature ventricular contractions (PVCs). Median PVC-coupling interval was 552 ms (IQR 83 ms). Spatial displacement was determined by measuring the dislocation of the catheter tip during PVC compared to the preceding sinus beat. Mean spatial displacement was 3.8±1.5 mm for all maps. The displacement was 1.3±0.4 mm larger for PVCs with non-outflow-tract origin compared to PVCs originating from the ventricular outflow tracts (RVOT/LVOT; p=0.028). Demographic parameters, PVC-coupling-interval and chamber of origin had no significant influence on the extent of spatial displacement. 1.3. ConclusionEctopic activation of the ventricular myocardium during PVCs results in spatial displacement of mapping points that is significantly larger for PVCs with non-outflow-tract origin. The correction for spatial displacement may improve accuracy of radiofrequency current (RFC)-application in catheter ablation of PVCs.

Noninvasive unipolar electrogram T-wave upslope is an accurate marker of local refractoriness in explanted hearts with drug-induced repolarization dispersion

Funding Acknowledgements Type of funding sources: Public grant(s) – National budget only. Main funding source(s): French National Research Agency Matthijs Cluitmans is supported by a Veni grant from the Netherlands Organization for Scientific Research Background The relationship between T-wave morphology in local unipolar electrograms (UEGs) as mapped with noninvasive electrocardiographic imaging (ECGI) and local repolarization time (RT) has not been validated in pronounced RT dispersion. Purpose To study the time of upslope of the T-wave (Tup) in epicardial UEGs mapped with ECGI as a marker of time of local refractoriness (trefr, a surrogate for RT) in intact hearts with RT dispersion. Methods Six pig hearts were Langendorff-perfused with selective perfusion of the LAD artery and submersed in a torso-shaped tank containing 256 electrodes on the torso surface (panel A). RT was prolonged in the non-LAD regions by infusing dofetilide (‘Dof’) and shortened in the LAD region using pinacidil (‘Pin’). Tup was determined in both invasive UEGs (recorded with epicardial electrodes) and in noninvasive UEGs (reconstructed with ECGI). Programmed stimulation was used to determine trefr, defined as the shortest coupling interval with capture. Both metrics were determined relative to the common pacing spike. Results In all six hearts, selective dofetilide and pinacidil infusion resulted in delayed trefr and Tup in the non-LAD region, and shortened invasive trefr and noninvasive Tup in the LAD region, respectively (panel B and C). Over all 59 observations, Tup showed high agreement with trefr (values close to line of identity, panel D) with strong correlation (r = 0.91). This finding was independent of T-wave polarity (positive, negative or biphasic). Conclusion The moment of steepest upslope of the T-wave in a noninvasively reconstructed UEG accurately reflects end of local refractoriness in intact hearts, in case of pronounced RT dispersion. Under these circumstances, when local RT is defined by moment of re-excitability (allowing to link it to conduction block and re-entry), ECGI T-wave upslope can be taken as a truthful marker for local RT. Abstract Figure. Results

Proarrhythmic Effect of RF ablation on the Right Ventricular Moderator Band

The right ventricular moderator band (MB) is increasingly being recognized as a source for PVCs and PVC-mediated ventricular fibrillation. Monomorphic PVCs, non-sustained monomorphic VT and ventricular fibrillation are all documented arrhythmias originating from the MB. The benign PVCs usually have a coupling interval in excess of 400 msec. When PVCs trigger VF, coupling intervals are typically short, less than 300 msec. We report here a case of long-standing frequent monomorphic PVCs with a coupling interval of > 400 msec from the right ventricular distal conduction system embedded in the moderator band that progressed to non-sustained ventricular tachycardia. Following suppression of the arrhythmia with RF ablation, the arrhythmia recurred with PVCs at a shorter coupling interval (<300 msec), with frequent repetitive non-sustained polymorphic VT and triggering of sustained ventricular fibrillation. The use of a cryoballoon to ablate over the course of the moderator band resulted in complete and durable suppression of ventricular arrhythmias.

Preliminary Study of Coupling Intervals of Premature Ventricular Complexes in Dogs With Different Cardiac Diseases

Coupling interval (CI), the time (ms) from the onset of a sinus QRS to the onset of the following premature ventricular complex (PVC), and their variability (CIV) might predict mortality and elucidate mechanisms of arrhythmogenesis. There has been limited investigation of CIV in dogs. Therefore, we determined CIV and prematurity index (PI) in three groups of dogs with ventricular arrhythmias that were subject to 24 hour ambulatory electrocardiographic (Holter) monitoring. Dogs in group 1 had presumptive arrhythmogenic right ventricular cardiomyopathy (ARVC), those in group 2 had structural heart disease in which patients with valvular heart disease predominated, and those in group 3 had a dilated cardiomyopathy (DCM) either phenotype or presumed familial cardiomyopathy. In this preliminary study, we did not find significant differences in indices of CIV between groups. Median PI was lower in dogs treated with antiarrhythmic therapy. Severity of cardiac remodeling, except for left atrial to aortic ratio, were not correlated with CIV. It was not possible to determine the mechanism of arrhythmias in ARVC, DCM phenotype or structural heart disease groups and re-entry, triggered activity, and abnormal automaticity are possible etiologies. The effect of antiarrhythmic therapy demonstrated potential drug effect on CIV. Risk for malignant arrhythmias and sudden cardiac death were not examined. A larger study would be needed to determine if differences exist; if present, this would give insight into possible mechanisms and optimal antiarrhythmic therapy.

Polymorphic ventricular tachycardia, ischaemic ventricular fibrillation, and torsade de pointes: importance of the QT and the coupling interval in the differential diagnosis

Aims Distinctive types of polymorphic ventricular tachycardia (VT) respond differently to different forms of therapy. We therefore performed the present study to define the electrocardiographic characteristics of different forms of polymorphic VT. Methods and results We studied 190 patients for whom the onset of 305 polymorphic VT events was available. The study group included 87 patients with coronary artery disease who had spontaneous polymorphic VT triggered by short-coupled extrasystoles in the absence of myocardial ischaemia. This group included 32 patients who had a long QT interval but nevertheless had their polymorphic VT triggered by ectopic beats with short coupling interval, a subcategory termed ‘pseudo-torsade de pointes] (TdP). For comparison, we included 50 patients who had ventricular fibrillation (VF) during acute myocardial infarction (‘ischaemic VF’ group) and 53 patients with drug-induced TdP (‘true TdP’ group). The QT of patients with pseudo-TdP was (by definition) longer than that of patients with polymorphic VT and normal QT (QTc 491.4 ± 25.2 ms vs. 447.3 ± 55.6 ms, P &lt; 0.001). However, their QT was significantly shorter than that of patients with true TdP (QTc 564.6 ± 75.6 ms, P &lt; 0.001). Importantly, the coupling interval of the ectopic beat triggering the arrhythmia was just as short during pseudo-TdP as during polymorphic VT with normal QT (359.1 ± 38.1 ms vs. 356.6 ± 39.4 ms, P = 0.467) but was much shorter than during true TdP (581.2 ± 95.3 ms, P &lt; 0.001). Conclusions The coupling interval helps discriminate between polymorphic VT that occurs despite a long QT interval (pseudo-TdP) and polymorphic arrhythmias striking because of a long QT (true TdP).