Endocardial repolarization dispersion in BrS: A novel automatic algorithm for mapping activation recovery interval.

INTRODUCTION: Repolarization dispersion in the right ventricular outflow tract (RVOT) contributes to the type-1 electrocardiographic (ECG) phenotype of Brugada syndrome (BrS), while data on the significance and feasibility of mapping repolarization dispersion in BrS patients are scarce. Moreover, the role of endocardial repolarization dispersion in BrS is poorly investigated. We aimed to assess endocardial repolarization patterns through an automated calculation of activation recovery interval (ARI) estimated on unipolar electrograms (UEGs) in spontaneous type-1 BrS patients and controls; we also investigated the relation between ARI and right ventricle activation time (RVAT), and T-wave peak-to-end interval (Tpe) in BrS patients. METHODS: Patients underwent endocardial high-density electroanatomical mapping (HDEAM); BrS showing an overt type-1 ECG were defined as OType1, while those without (latent type-1 ECG and LType1) received ajmaline infusion. BrS patients only underwent programmed ventricular stimulation (PVS). Data were elaborated to obtain ARI corrected with the Bazett formula (ARIc), while RVAT was derived from activation maps. RESULTS: 39 BrS subjects (24 OType1 and 15 LTtype1) and 4 controls were enrolled. OType1 and post-ajmaline LType1 showed longer mean ARIc than controls (306 ± 27.3 ms and 333.3 ± 16.3 ms vs. 281.7 ± 10.3 ms, p = .05 and p < .001, respectively). Ajmaline induced a significant prolongation of ARIc compared to pre-ajmaline LTtype1 (333.3 ± 16.3 vs. 303.4 ± 20.7 ms, p < .001) and OType1 (306 ± 27.3 ms, p < .001). In patients with type-1 ECG (OTtype1 and post-ajmaline LType1) ARIc correlated with RVAT (r = .34, p = .04) and Tpec (r = .60, p < .001), especially in OType1 subjects (r = .55, p = .008 and r = .65 p < .001, respectively). CONCLUSION: ARIc mapping demonstrates increased endocardial repolarization dispersion in RVOT in BrS. Endocardial ARIc positively correlates with RVAT and Tpec, especially in OType1.

Electrophysiological characteristics of epicardial to endocardial breakthrough in intractable cavotricuspid isthmus-dependent atrial flutter.

BACKGROUND: Epicardial to endocardial breakthrough (EEB) exists widely in atrial arrhythmia and is a cause for intractable cavotricuspid isthmus (CTI)-dependent atrial flutter (AFL). This study aimed to investigate the electrophysiological features of EEB in EEB-related CTI dependent AFL. METHODS: Six patients with EEB-related CTI-dependent AFL were identified among 142 consecutive patients who underwent CTI-dependent AFL catheter ablation with an ultra-high-density, high-resolution mapping system in three institutions. Activation maps and ablation procedure were analyzed. RESULTS: A total of seven EEBs were found in six patients. Four EEBs (including three at the right atrial septum and one in paraseptal isthmus) were recorded in three patients during tachycardia. The other three EEBs were identified at the inferolateral right atrium (RA) during pacing from the coronary sinus. The conduction characteristics through the EEB-mediated structures were evaluated in three patients. Two patients only showed unidirectional conduction. Activation maps indicated that CTI-dependent AFL with EEB at the atrial septum was actually bi-atrial macro-reentrant atrial tachycardia (BiAT). Intensive ablation at the central isthmus could block CTI bidirectionally in four cases. However, ablation targeted at the inferolateral RA EEB was required in two cases. Meanwhile, local potentials at the EEB location gradually split into two components with a change in activation sequence. CONCLUSIONS: EEB is an underlying cause for intractable CTI-dependent AFL. EEB-mediated structure might show unidirectional conduction. CTI-dependent AFL with EEB at the atrial septum may represent BiAT. Intensive ablation targeting the central isthmus or EEB at the inferolateral RA could block the CTI bidirectionally.

Fragmented endocardial signals and early afterdepolarizations during torsades de pointes tachycardia.

BACKGROUND: Bradycardia-induced torsade de pointes (TdP) tachycardia in patients with spontaneous high-degree atrioventricular block (AVB) is common. The aim of this study was to analyze endocardial recordings during TdP in spontaneous high-degree AVB in humans to better understand the electrophysiological mechanisms underlying this phenomenon. METHODS: The study group consisted of 5 patients with typical episodes of TdP during spontaneous high-degree AVB. A standard (USCI) temporary bipolar endocardial catheter positioned at the apex of the right ventricle (RV) and bipolar chest leads from two precordial leads V1 and V4 were used to record the tracings during TdP. RESULTS: The presence of a wide spectrum of fragmentations was noted on endocardial electrograms (EGMs), which were invisible on the surface electrocardiogram (ECG) tracing. Endocardial signals indicated that TdP started in the proximity of the RV apex, since the local EGM began prior to the QRS complex on the surface ECG. Early afterdepolarizations (EADs) were observed in 2 out of 5 cases confirming a common opinion about the mechanism of TdP. However, this phenomenon was not observed in 3 other patients suggesting that the arrhythmia was the result of a different mechanism originating in proximity to the RV apex. CONCLUSIONS: This work demonstrated early endocardial signals in the RV apex during TdP associated with high-degree AVB in humans, and exhibits a spectrum of fragmented signals in this area occurring on a single or multiple beats. These fragmentations indicate areas of poor conduction and various degrees of intramyocardial block, and therefore a new mechanism of TdP tachycardia in some patients with spontaneous high-degree AVB.

Endocardial contact mapping of the left atrial appendage in persistent atrial fibrillation.

INTRODUCTION: Isolation of the left atrial appendage (LAA) is often performed in persistent atrial fibrillation (AF). Propagation patterns in the LAA during AF remain to be elucidated. We sought to characterize propagation patterns in the LAA during AF in persistent AF. METHODS: Persistent AF patients undergoing catheter ablation were studied. Pulmonary vein isolation (PVI) was performed during continuous AF. If AF was not terminated by PVI, bi-atrial mapping was performed using a multi-electrode catheter during AF. Maps were collected at each site for 30 seconds and analyzed offline with a novel software, CARTOFINDER. This software made automatic determinations of whether activation was focal or rotational. The left atrium (LA) was divided into five regions, of which the LAA was one, and the right atrium (RA) into three. RESULTS: Eighty patients were studied (62 ± 10 years, 65 males). On average, 9.6 ± 2.2 and 4.1 ± 1.2 maps were created in the LA and RA, respectively. The LAA was mapped in 70 patients, resulting in 85 maps. In the LAA, activation was identified as focal more often than rotational (64 [91%] vs 10 [14%] patients, P < .001), seven patients displayed both. The number of focal activation events was greatest in the LAA (28.5 events/30 seconds [interquartile range, 15-54]) of the eight atrial regions. During focal activation, sites designated as earliest activation frequently covered a wide area, rather than being localized to a discrete site (5.4 ± 3.1 electrodes). CONCLUSIONS: The results of this study suggest that focal activation is a major mechanism underlying the arrhythmogenicity of the LAA in persistent AF.

High Frame Rate Ultrasound for Electromechanical Wave Imaging to Differentiate Endocardial From Epicardial Myocardial Activation.

Differentiation between epicardial and endocardial ventricular activation remains a challenge despite the latest technologies available. The aim of the present study was to develop a new tool method, based on electromechanical wave imaging (EWI), to improve arrhythmogenic substrate activation analysis. Experiments were conducted on left ventricles (LVs) of four isolated working mode swine hearts. The protocol aimed at demonstrating that different patterns of mechanical activation could be observed whether the ventricle was in sinus rhythm, paced from the epicardium or from the endocardium. A total of 72 EWI acquisitions were recorded on the anterior, lateral and posterior segments of the LV. A total of 54 loop records were blindly assigned to two readers. EWI sequences interpretations were correct in 89% of cases. The overall agreement rate between the two readers was 83%. When in a paced ventricle, the origin of the wave front was focal and originated from the endocardium or the epicardium. In sinus rhythm, wave front was global and activated within the entire endocardium toward the epicardium at a speed of 1.7 ± 0.28 m·s-1. Wave front speeds were respectively measured when the endocardium or the epicardium were paced at a speed of 1.1 ± 0.35 m·s-1 versus 1.3 ± 0.34 m·s-1 (p = NS). EWI activation mapping allows activation localization within the LV wall and calculation of the wave front propagation speed through the muscle. In the future, this technology could help localize activation within the LV thickness during complex ablation procedures.

New Adjusted Cutoffs for "Normal" Endocardial Voltages in Patients With Post-Infarct LV Remodeling.

OBJECTIVES: This study sought to determine new reference cutoffs for normal unipolar voltage (UV) and bipolar voltage (BV) that would be adjusted for the LV remodeling. BACKGROUND: The definition of "normal" left ventricular (LV) endocardial voltage in patients with post-infarct scar is still lacking. The reference voltage of the noninfarcted myocardium (NIM) may differ between patients depending on LV structural remodeling and the ensuing interstitial fibrosis. METHODS: Electroanatomic voltage mapping was integrated with isotropic late gadolinium-enhanced cardiac magnetic resonance in 15 patients with nonremodeled LV and 12 patients with remodeled LV (end-systolic volume index >50 ml/m2 with ejection fraction <47% assessed by cardiac magnetic resonance). Reference voltages (fifth percentile values) were determined from pooled NIM segments without late gadolinium enhancement. RESULTS: The cutoffs for normal BV and UV were ≥3.0 and ≥6.7 mV for nonremodeled LV and ≥2.1 and ≥6.4 mV for remodeled LV. Endocardial low-voltage area (LVA) defined by the adjusted cutoffs corresponded better to late gadolinium enhancement-detected scar than did LVA defined by uniform cutoffs. In 15 patients who underwent successful ablation of ventricular tachycardia, the LVA contained >97% of targeted evoked delayed potentials. Insights from whole-heart T1 mapping revealed more fibrotic NIM in patients with remodeled LV compared with nonremodeled LV. CONCLUSIONS: This study found substantial differences in endocardial voltage of NIM in post-infarct patients with remodeled versus nonremodeled LV. The new adjusted cutoffs for "normal" BV and UV enable a patient-tailored approach to electroanatomic voltage mapping of LV.

Multisize Electrodes for Substrate Identification in Ischemic Cardiomyopathy: Validation by Integration of Whole Heart Histology.

OBJECTIVES: This study sought to evaluate the value of combined electrogram (EGM) information provided by simultaneous mapping using micro- and conventional electrodes in the identification of post-myocardial infarction ventricular tachycardia substrate. BACKGROUND: Ventricular tachycardias after myocardial infarction are related to scars with complex geometry. Scar delineation and ventricular tachycardia substrate identification relies on bipolar voltages (BV) and EGM characteristics. Early reperfusion therapy results in small, nontransmural scars, the details of which may not be delineated using 3.5 mm tip catheters. METHODS: Nine swine with early reperfusion myocardial infarction were mapped using Biosense Webster's QDOT Micro catheter, incorporating 3 microelectrodes at the tip of the standard 3.5 mm electrode. Analysis of EGM during sinus rhythm, right ventricular pacing, and short-coupled right ventricular extrastimuli was performed. The swine were sacrificed and mapping data were projected onto the heart. Transmural biopsies (n = 196) corresponding to mapping points were obtained, allowing a head-to-head comparison of EGM recorded by micro- and conventional electrodes with histology. RESULTS: To identify scar areas using standard electrodes, unique cutoff values of unipolar voltage <5.44 mV, BV <1.27 mV (conventional), and BV <2.84 mV (microelectrode) were identified. Combining the information provided by unipolar voltage and BV mapping, the sensitivity of scar identification was increased to 93%. Micro-EGM were better able to distinguish small near-fields corresponding to a layer of viable subendocardium than conventional EGM were. CONCLUSIONS: The combined information provided by multisize electrode mapping increases the sensitivity with which areas of scar are identified. EGM from microelectrodes, with narrower spacing, allow identification of near-fields arising from thin subendocardial layer and layers activated with short delay obscured in EGM from conventional mapping catheter.

Mapping and Ablation of Ventricular Fibrillation Associated With Early Repolarization Syndrome.

BACKGROUND: We conducted a multicenter study to evaluate mapping and ablation of ventricular fibrillation (VF) substrates or VF triggers in early repolarization syndromes (ERS) or J-wave syndrome (JWS). METHODS: We studied 52 patients with ERS (4 women; median age, 35 years) with recurrent VF episodes. Body surface electrocardiographic imaging and endocardial and epicardial electroanatomical mapping of both ventricles were performed during sinus rhythm and VF for localization of triggers, substrates, and drivers. Ablations were performed on VF substrates, defined as areas that had late depolarization abnormalities characterized by low-voltage fractionated late potentials, and VF triggers. RESULTS: Fifty-one of the 52 patients had detailed mapping that revealed 2 phenotypes: group 1 had late depolarization abnormalities predominantly at the right ventricular (RV) epicardium (n=40), and group 2 had no depolarization abnormalities (n=11). Group 1 can be subcategorized into 2 groups: Group 1A included 33 patients with ERS with Brugada electrocardiographic pattern, and group 1B included 7 patients with ERS without Brugada electrocardiographic pattern. Late depolarization areas colocalize with VF driver areas. The anterior RV outflow tract/RV epicardium and the RV inferior epicardium are the major substrate sites for group 1. The Purkinje network is the leading underlying VF trigger in group 2 that had no substrates. Ablations were performed in 43 patients: 31 and 5 group 1 patients had only VF substrate ablation and VF substrates plus VF trigger, respectively (mean, 1.4±0.6 sessions); 6 group 2 patients and 1 patient without group classification had only Purkinje VF trigger ablation (mean, 1.2±0.4 sessions). Ablations were successful in reducing VF recurrences (P<0.0001). After follow-up of 31±26 months, 39 (91%) had no VF recurrences. CONCLUSIONS: There are 2 phenotypes of ERS/J-wave syndrome: one with late depolarization abnormality as the underlying mechanism of high-amplitude J-wave elevation that predominantly resides in the RV outflow tract and RV inferolateral epicardium, serving as an excellent target for ablation, and the other with pure ERS devoid of VF substrates but with VF triggers that are associated with Purkinje sites. Ablation is effective in treating symptomatic patients with ERS/J-wave syndrome with frequent VF episodes.

Usefulness of ICD electrograms analysis to distinguish endocardial vs epicardial ventricular tachycardia in arrhythmogenic right ventricular cardiomyopathy.

INTRODUCTION: Arrhythmogenic right ventricular cardiomyopathy (ARVC) is characterized by an epicardial (EPI) to endocardial (ENDO) fibrofatty infiltration of the RV predisposing to both EPI and ENDO ventricular tachycardia (VT). The relative timing between the VT QRS onset on the far-field ventricular electrogram (VEGM) to the local activation time recorded at the RV apex on the near-field VEGM from stored implantable cardioverter-defibrillator (ICD) events of VT can be helpful to discriminate ENDO from EPI VT in ARVC. METHODS AND RESULTS: We analyzed consecutive ARVC patients undergoing catheter ablation between 2006 and 2018. Only patients with retrievable ICD VEGMs of clinical VTs which could be matched with VTs induced at the time of ablation were included. A total of 26 VT events (16 ENDO, 10 EPI) from 19 ARVC patients were examined, yielding a mean far-field to near-field interval of 33 ± 15 ms for ENDO VTs and 52 ± 20 ms for EPI VTs (P = .020). At receiver-operating characteristic analysis, a far-field to a near-field interval of 60 ms or more ruled out ENDO VTs in 16 (100%) cases and identified EPI VTs with a positive predictive value (PPV) of 100% and a negative predictive value (NPV) of 73%. An interval of less than or equal to 30 ms ruled out EPI VTs in eight (80%) cases and diagnosed ENDO VTs with a PPV of 80% and an NPV of 50%. CONCLUSION: Far-field to near-field ICD VEGM timing may be used to predict ENDO vs EPI VT in ARVC before ablation, indicating an ENDO origin if the timing is less than or equal to 30 ms and an EPI origin if greater than or equal to 60 ms.

Conduction patterns of idiopathic arrhythmias from the endocardium and epicardium of outflow tracts: New insights with noninvasive electroanatomic mapping.

BACKGROUND: Idiopathic arrhythmias commonly arise from the septal right ventricular outflow tract (RVOT), sinuses of Valsalva (SoV), and great cardiac vein (GCV). Predicting the exact site of origin is important for preparation for catheter ablation. OBJECTIVE: The purpose of this study was to examine the diagnostic value of noninvasive electroanatomic mapping (NIEAM) to differentiate between septal RVOT, SoV, and GCV origin and compare it to that of 12-lead electrocardiography (ECG). METHODS: NIEAM maps (CardioInsight, Medtronic) were generated during spontaneous ventricular premature depolarizations (VPDs) and threshold pacing from septal RVOT, SoV, and GCV. Origin prediction using NIEAM was compared to algorithmic ECG criteria (maximal deflection index; V2 transition ratio) and subjective ECG evaluation. RESULTS: Sixty NIEAMs (18 spontaneous VPDs and 42 pace-maps) from 31 patients (age 56 ± 16 years) were analyzed. NIEAM showed distinct conduction patterns, best visualized at the base of the heart: septal RVOT VPDs propagate toward the tricuspid annulus, depolarizing the septum from inferior to superior; SoV VPDs engage the superior septum early; and GCV VPDs move laterally along the mitral annulus, depolarizing the heart from left to right. Activation of the lateral mitral annulus >60.50 ms and the superior basal septum <22.5 ms from onset predicts RVOT and SoV origin, respectively, in 100% of cases. NIEAM was superior to maximum deflection index in predicting GCV origin (100% vs 42.2% accuracy) and superior to V2 transition ratio in predicting SoV origin (100% vs 75.9% accuracy). CONCLUSION: Arrhythmias arising from the outflow tracts follow distinct propagation patterns depending on the origin. A 2-step algorithm using activation timing by NIEAM yields 100% diagnostic accuracy in predicting origin.

High-resolution noncontact charge-density mapping of endocardial activation.

BACKGROUND: Spatial resolution in cardiac activation maps based on voltage measurement is limited by far-field interference. Precise characterization of electrical sources would resolve this limitation; however, practical charge-based cardiac mapping has not been achieved. METHODS: A prototype algorithm, developed from first principles of electrostatic field theory, derives charge density (CD) as a spatial representation of the true sources of the cardiac field. The algorithm processes multiple, simultaneous, noncontact voltage measurements within the cardiac chamber to inversely derive the global distribution of CD sources across the endocardial surface. RESULTS: Comparison of CD to an established computer-simulated model of atrial conduction demonstrated feasibility in terms of spatial, temporal, and morphologic metrics. Inverse reconstruction matched simulation with median spatial errors of 1.73 mm and 2.41 mm for CD and voltage, respectively. Median temporal error was less than 0.96 ms and morphologic correlation was greater than 0.90 for both CD and voltage. Activation patterns observed in human atrial flutter reproduced those established through contact maps, with a 4-fold improvement in resolution noted for CD over voltage. Global activation maps (charge density-based) are reported in atrial fibrillation with confirmed reduction of far-field interference. Arrhythmia cycle-length slowing and termination achieved through ablation of critical points demonstrated in the maps indicates both mechanistic and pathophysiological relevance. CONCLUSION: Global maps of cardiac activation based on CD enable classification of conduction patterns and localized nonpulmonary vein therapeutic targets in atrial fibrillation. The measurement capabilities of the approach have roles spanning deep phenotyping to therapeutic application. TRIAL REGISTRATION: ClinicalTrials.gov NCT01875614. FUNDING: The National Institute for Health Research (NIHR) Translational Research Program at Royal Papworth Hospital and Acutus Medical.

Epicardial-endocardial breakthrough site ablation: Demonstration of alternative target for perimitral atrial tachycardia.

A 62-year-old man underwent the catheter ablation for persistent atrial tachycardia (AT) with a cycle length of 357 milliseconds. An ultrahigh resolution mapping revealed that this tachycardia was a clockwise perimitral AT despite the conduction was apparently blocked across the lateral mitral isthmus line both at the endocardium and within the coronary sinus. The AT was terminated by the single radiofrequency application at the site below the mitral isthmus line where the endocardial activation breakout was seen. This case suggests that the epicardial-endocardial conduction breakthrough site may be an alternative ablation target in a difficult ablation case of perimitral AT.

Three-dimensional myocardial scar characterization from the endocardium: Usefulness of endocardial unipolar electroanatomic mapping.

Epicardial ablation may be required to eliminate ventricular tachycardia (VT) in patients with underlying structural heart disease. The decision to gain epicardial access is frequently based on the suspicion of an epicardial origin for the VT and/or presence of an arrhythmogenic substrate. Epicardial pathology and VT is frequently present in patients with nonischemic right and/or left cardiomyopathies even in the setting of modest or no endocardial bipolar voltage substrate. In this setting, unipolar voltage mapping from the endocardium serves to help identify midmyocardial and/or epicardial VT substrate. The additional value of endocardial unipolar mapping includes its usefulness to predict the clinical outcome after VT ablation, to determine the irreversibility of myocardial disease, and to guide endomyocardial biopsy procedures to specific areas of intramural scarring. In this review, we aim to provide a guide to the use of endocardial unipolar mapping and its appropriate interpretation in a variety of clinical situations.

Prolonged action potential duration and dynamic transmural action potential duration heterogeneity underlie vulnerability to ventricular tachycardia in patients undergoing ventricular tachycardia ablation.

AIMS: Differences of action potential duration (APD) in regions of myocardial scar and their borderzones are poorly defined in the intact human heart. Heterogeneities in APD may play an important role in the generation of ventricular tachycardia (VT) by creating regions of functional block. We aimed to investigate the transmural and planar differences of APD in patients admitted for VT ablation. METHODS AND RESULTS: Six patients (median age 53 years, five male); (median ejection fraction 35%), were studied. Endocardial (Endo) and epicardial (Epi) 3D electroanatomic mapping was performed. A bipolar voltage of <0.5 mV was defined as dense scar, 0.5-1.5 mV as scar borderzone, and >1.5 mV as normal. Decapolar catheters were positioned transmurally across the scar borderzone to assess differences of APD and repolarization time (RT) during restitution pacing from Endo and Epi. Epi APD was 173 ms in normal tissue vs. 187 ms at scar borderzone and 210 ms in dense scar (P < 0.001). Endocardial APD was 210 ms in normal tissue vs. 222 ms in the scar borderzone and 238 ms in dense scar (P < 0.01). This resulted in significant transmural RT dispersion (ΔRT 22 ms across dense transmural scar vs. 5 ms in normal transmural tissue, P < 0.001), dependent on the scar characteristics in the Endo and Epi, and the pacing site. CONCLUSION: Areas of myocardial scar have prolonged APD compared with normal tissue. Heterogeneity of regional transmural and planar APD result in localized dispersion of repolarization, which may play an important role in initiating VT.

Epicardial connection between the right-sided pulmonary venous carina and the right atrium in patients with atrial fibrillation: A possible mechanism for preclusion of pulmonary vein isolation without carina ablation.

BACKGROUND: Ablation of the pulmonary venous carina is occasionally required for pulmonary vein isolation (PVI) despite its nonessential role in ipsilateral PVI from the anatomical (endocardial) viewpoint. Although the Bachmann bundle (BB) is a common and main interatrial band, local variations in small tongues of muscular fibers were frequently found in autopsy studies. OBJECTIVE: We sought to clarify the effect of the electrical conduction pattern from the right atrium (RA) to the left atrium (LA) during sinus rhythm on the necessity of performing right-sided pulmonary venous carina ablation to achieve PVI. METHODS: Study subjects comprised 37 consecutive patients undergoing initial catheter ablation of lone atrial fibrillation. During sinus rhythm, RA and LA activation maps were acquired using an electroanatomical mapping system. LA breakthroughs were classified into 3 sites: BB, fossa ovalis (FO), and right-sided pulmonary venous carina. Patients were divided into the carina-ABL (ablation) or non-carina-ABL group on the basis of the necessity of pulmonary venous carina ablation to achieve PVI. RESULTS: Patients were classified in the non-carina-ABL group (n = 26 [70%]) and carina-ABL group (n = 8 [22%]) after excluding 3 patients (8%) because of their complex ablation lesion sets. Breakthrough occurred in the BB (n = 21 patients [62%]), FO (n = 7 [21%]), carina (n = 1 [3%]), carina and BB (n = 3 [9%]), and carina and FO (n = 2 [6%]). Carina breakthrough occurred in 6 patients (75%) in the carina-ABL group but in no patients in the non-carina-ABL group (P < .0001). CONCLUSION: PVI was not achievable without carina ablation in one-fifth of patients, probably because of epicardial connections present between the right-sided pulmonary venous carina and the RA.

Utility of ripple mapping for identification of slow conduction channels during ventricular tachycardia ablation in the setting of arrhythmogenic right ventricular cardiomyopathy.

BACKGROUND: Ripple mapping displays every deflection of a bipolar electrogram and enables the visualization of conduction channels (RMCC) within postinfarction ventricular scar to guide ventricular tachycardia (VT) ablation. The utility of RMCC identification for facilitation of VT ablation in the setting of arrhythmogenic right ventricular cardiomyopathy (ARVC) has not been described. OBJECTIVE: We sought to (a) identify the slow conduction channels in the endocardial/epicardial scar by ripple mapping and (b) retrospectively analyze whether the elimination of RMCC is associated with improved VT-free survival, in ARVC patients. METHODS: High-density right ventricular endocardial and epicardial electrograms were collected using the CARTO 3 system in sinus rhythm or ventricular pacing and reviewed for RMCC. Low-voltage zones and abnormal myocardium in the epicardium were identified by using standardized late-gadolinium-enhanced (LGE) magnetic resonance imaging (MRI) signal intensity (SI) z-scores. RESULTS: A cohort of 20 ARVC patients that had undergone simultaneous high-density right ventricular endocardial and epicardial electrogram mapping was identified (age 44 ± 13 years). Epicardial scar, defined as bipolar voltage less than 1.0 mV, occupied 47.6% (interquartile range [IQR], 30.9-63.7) of the total epicardial surface area and was larger than endocardial scar, defined as bipolar voltage less than 1.5 mV, which occupied 11.2% (IQR, 4.2 ± 17.8) of the endocardium (P < 0.01). A median 1.5 RMCC, defined as continuous corridors of sequential late activation within scar, were identified per patient (IQR, 1-3), most of which were epicardial. The median ratio of RMCC ablated was 1 (IQR, 0.6-1). During a median follow-up of 44 months (IQR, 11-49), the ratio of RMCC ablated was associated with freedom from recurrent VT (hazard ratio, 0.01; P = 0.049). Among nine patients with adequate MRI, 73% of RMCC were localized in LGE regions, 24% were adjacent to an area with LGE, and 3% were in regions without LGE. CONCLUSION: Slow conduction channels within endocardial or epicardial ARVC scar were delineated clearly by ripple mapping and corresponded to critical isthmus sites during entrainment. Complete elimination of RMCC was associated with freedom from VT.

Simulated P wave morphology in the presence of endo-epicardial activation delay.

AIMS: Evidences of asynchrony between epicardial and endocardial activation in the atrial wall have been reported. We used a computer model of the atria and torso to investigate the consequences of such activation delay on P wave morphology, while controlling for P wave duration. METHODS AND RESULTS: We created 390 models of the atria based on the same geometry. These models differed by atrial wall thickness (from 2 to 3 mm), transmural coupling, and tissue conductivity in the endocardial and epicardial layers. Among them, 18 were in baseline, 186 had slower conduction in the epicardium layer and 186 in the endocardial layer. Conduction properties were adjusted in such a way that total activation time was the same in all models. P waves on a 16-lead system were simulated during sinus rhythm. Activation maps were similar in all cases. Endo-epicardial delay varied between -5.5 and 5.5 ms vs. 0 ± 0.5 ms in baseline. All P waves had the same duration but variability in their morphology was observed. With slower epicardial conduction, P wave amplitude was reduced by an average of 20% on leads V3-V5 and P wave area decreased by 50% on leads V1-V2 and by 40% on lead V3. Reversed, lower magnitude effects were observed with slower endocardial conduction. CONCLUSION: An endo-epicardial delay of a few milliseconds is sufficient to significantly alter P wave morphology, even if the activation map remains the same.