BACKGROUND:Targeting non-pulmonary vein triggers (NPVTs) after pulmonary vein isolation may reduce atrial fibrillation (AF) recurrence. Isoproterenol infusion and cardioversion of spontaneous or induced AF can provoke NPVTs but typically require vasopressor support and increased procedural time. OBJECTIVE:The purpose of this study was to identify risk factors for the presence of NPVTs and create a risk score to identify higher-risk subgroups. METHODS:Using the AF ablation registry at the Hospital of the University of Pennsylvania, we included consecutive patients who underwent AF ablation between January 2021 and December 2022. We excluded patients who did not receive NPVT provocation testing after failing to demonstrate spontaneous NPVTs. NPVTs were defined as non-pulmonary vein ectopic beats triggering AF or focal atrial tachycardia. We used risk factors associated with NPVTs with P <.1 in multivariable logistic regression model to create a risk score in a randomly split derivation set (80%) and tested its predictive accuracy in the validation set (20%). RESULTS:In 1530 AF ablations included, NPVTs were observed in 235 (15.4%). In the derivation set, female sex (odds ratio [OR] 1.40; 95% confidence interval [CI] 0.96-2.03; P = .080), sinus node dysfunction (OR 1.67; 95% CI 0.98-2.87; P = .060), previous AF ablation (OR 2.50; 95% CI 1.70-3.65; P <.001), and left atrial scar (OR 2.90; 95% CI 1.94-4.36; P <.001) were risk factors associated with NPVTs. The risk score created from these risk factors (PRE2SSS2 score; [PRE]vious ablation: 2 points, female [S]ex: 1 point, [S]inus node dysfunction: 1 point, left atrial [S]car: 2 points) had good predictive accuracy in the validation cohort (area under the receiver operating characteristic curve 0.728; 95% CI 0.648-0.807). CONCLUSION:A risk score incorporating predictors for NPVTs may allow provocation of triggers to be performed in patients with greatest expected yield.

BACKGROUND:Ventricular fibrillation (VF) can be initiated by ventricular premature depolarizations (VPDs) in the absence of obvious structural abnormalities. OBJECTIVE:The purpose of this study was to determine the prevalence of 12-lead electrocardiographic (ECG) sinus rhythm reduced QRS amplitude, QRS fractionation (QRSf), and early repolarization (ER) pattern, and the outcome of catheter ablation and VPD anatomic distribution in patients with VPDs initiating VF. METHODS:We compared a cohort with no apparent structural heart disease and VPDs initiating VF (group 1; n = 42) to a reference cohort (group 2; n = 61) of patients with no structural heart disease and symptomatic unifocal VPDs. RESULTS:A reduced QRS amplitude (<0.55 mV) in aVF (59% vs 10%; P <.001), QRSf in ≥2 contiguous leads (50% vs 16%; P <.001), and ER pattern (21.4% vs 1.6%; P = .01) were more common in group 1 than in group 2. At least 1 abnormal ECG finding was present in 34 group 1 patients (81%) vs 17 group 2 patients (28%) (P <.001). VPD origin included right ventricular and left ventricular distal Purkinje system and moderator band/papillary muscles in 83% of group 1 patients vs 18% of group 2 patients (P <.001). VF was eliminated with a single ablation procedure in 77% of group 1 patients with at least 2 years of follow-up. CONCLUSION:A reduced QRS amplitude (<0.55 mV) in aVF, QRSf in ≥2 contiguous leads, and/or an ER pattern are frequently observed in patients with VPDs initiating VF. VPDs initiating VF typically originate from the distal Purkinje system and papillary muscles and can be successfully eliminated with catheter ablation.

BACKGROUND Targeting nonpulmonary vein triggers (NPVTs) of atrial fibrillation (AF) after pulmonary vein isolation can be challenging. NPVTs are often single ectopic beats with a surface P-wave obscured by a QRS or T-wave.OBJECTIVES The goal of this study was to construct an algorithm to regionalize the site of origin of NPVTs using only intracardiac bipolar electrograms from 2 linear decapolar catheters positioned in the posterolateral right atrium (along the crista terminalis with the distal bipole pair in the superior vena cava) and in the proximal coronary sinus (CS).METHODS After pulmonary vein isolation in 42 patients with AF, pacing from 15 typical anatomic NPVT sites was conducted. For each pacing site, the electrogram activation sequence was analyzed from the CS catheter (simultaneous/ chevron/inverse chevron/distal-proximal/proximal-distal) and activation time (ie, CSCTAT) between the earliest electrograms from the 2 decapolar catheters was measured referencing the earliest CS electrogram; a negative CSCTAT value indicates the crista terminalis catheter electrogram was earlier, and a positive CSCTAT value indicates the CS catheter electrogram was earlier. A regionalization algorithm with high predictive value was defined and tested in a validation cohort with AF NPVTs localized with electroanatomic mapping.RESULTS In the study patient cohort (71% male; 43% with persistent AF, 52% with left atrial dilation), the algorithm grouped with high precision (positive predictive value 81%-99%, specificity 94%-100%, and sensitivity 30%-94%) the 15 distinct pacing sites into 9 clinically useful regions. Algorithm testing in a 98 patient validation cohort showed predictive accuracy of 91%.CONCLUSIONS An algorithm defined by the activation sequence and timing of electrograms from 2 linear multipolar catheters provided accurate regionalization of AF NPVTs to guide focused detailed mapping.

Introduction: Ablation of non-pulmonary vein triggers (NPVTs) after pulmonary vein isolation (PVI) may reduce atrial fibrillation (AF) recurrence. Localizing a trigger which initiates AF after a single atrial ectopic beat is challenging, especially in the scenario when the trigger P wave is obscured by preceding QRS-T complex. Aim: To evaluate the potential for noninvasive electrocardiographic imaging (ECGi) to localize NPVTs when the P wave morphology is superimposed on the T wave of the previous beat. Methods: We developed an algorithm which overlays and subtracts the preceding QRS-T wave complex from the QRS-T wave complex which is obscuring the P wave of interest, thus revealing the P wave morphology (Figure 1A). Resultant unobscured P waves (from multiple body surface electrodes) are then used for ECGi computation. In five patients undergoing AF ablation, after PVI, we paced from 15 atrial sites where NPVTs commonly arise, and evaluated the epicardial activation maps generated by ECGi both when pacing was timed to ensure an unobscured P wave and when timed to coincide with preceding QRS-T complex. Co-registration of CT-based ECGi activation maps with invasive electroanatomic map (EAM) allowed comparison of the earliest activation site on ECGi map from both the obscured P waves after QRS-T subtraction and unobscured P waves with true pacing locations on EAM (Figure 1B). Results: From 146 pacing sites in our patient cohort, for the unobscured P waves, median distance between earliest site on ECGi map and EAM pacing location was 16 mm (10-21 mm), and for obscured P waves after QRS-T subtraction, median distance was also 16 mm (12-23 mm) (Figure 1C). Conclusion: Using a QRS-T subtraction algorithm, ECGi can approximate origin of paced P waves whether P wave is unobscured or obscured by the preceding QRS-T complex. Spontaneous NPVT P waves are commonly obscured by the QRS-T wave and the ability to rapidly localize an early coupled P wave may facilitate NPVT mapping and ablation.

Targeting of non-pulmonary vein triggers (NPVTs) after pulmonary vein isolation (PVI) may reduce atrial fibrillation (AF) recurrence. Incrementally dosed isoproterenol infusion (up to 30mcg/min) and cardioversion of induced AF used to provoke NPVTs typically requires additional vasopressor support and increases procedure time.

BACKGROUND Intraprocedural identification of intramural septal substrate for ventricular tachycardia (ISS-VT) in nonischemic cardiomyopathy (NICM) is challenging. Delayed (>40 ms) transmural conduction time (DCT) with right ventricular basal septal pacing has been previously shown to identify ISS-VT.OBJECTIVES This study sought to determine whether substrate catheter ablation incorporating areas of DCT may improve acute and long-term outcomes.METHODS We included patients with NICM and ISS-VT referred for catheter ablation between 2016 and 2020. ISS-VT was defined by the following: 1) confluent septal areas of low unipolar voltage (<8.3 mV) in the presence of normal or minimal bipolar abnormalities; and 2) presence of abnormal electrograms in the septum. Substrate ablation was guided by the following: 1) activation and/or entrainment mapping for tolerated VT and pace mapping with ablation of abnormal septal electrograms for unmappable VTs (n = 57, Group 1); and 2) empirically extended to target areas of DCT during right ventricular basal septal pacing regardless of their participation in inducible VT(s) but sparing the conduction system when possible (n = 24, Group 2).RESULTS There were no significant baseline differences between Groups 1 and 2. Noninducibility of any VT programmed stimulation at the end of ablation was higher in Group 2 compared with Group 1 (80% vs 53%; P = 0.03). At 12-month follow-up, single-procedure VT-free survival was significantly higher (79% vs 46%; P = 0.006) and the time to VT recurrence was longer (mean 10 +/- 3 months vs 7 +/- 4 months; P = 0.02) in Group 2 compared with Group 1.CONCLUSIONS In patients with NICM and ISS-VT, a substrate ablation strategy that incorporates areas of DCT appears to improve freedom from recurrent VT.

Diffuse interstitial fibrosis (IF), which may be related to irreversibility of LV dysfunction (LVD), has been documented in animal models of PVC-induced cardiomyopathy (PIC) but has never been assessed in humans. In patients with suspected PIC, detection of IF with CMR-T1 mapping may improve risk stratification and predict response to catheter ablation

Introduction Targeting non-pulmonary vein triggers (NPVTs) after pulmonary vein isolation (PVI) reduces atrial fibrillation (AF) recurrence. However, NPVTs are often single atrial ectopic beats with surface P wave obscured, making regionalization a challenge. We aimed to construct an algorithm to regionalize the site of origin of NPVTs using exclusively intracardiac electrograms from two standardly positioned linear decapolar catheters positioned 1) in the postero-lateral right atrium, along crista terminalis (CT) with distal bipole pair extending into SVC, and 2) in the coronary sinus (CS), with proximal bipole pair at CS ostium. Methods In 42 patients with AF, after PVI, we paced at 15 sites where NPVTs commonly arise (Figure 1). For each pacing site we analyzed activation sequence of the CS catheter electrogram (simultaneous/chevron/inverse chevron/distal-proximal/proximal-distal) and the timing (CSCT time) between the earliest electrograms from the two decapolar catheters. Negative CSCT time indicates CT catheter electrogram is earliest, positive indicates CS catheter electrogram is earliest (Figure 2, lower right). Results In this patient cohort (71% male, 57% persistent AF, 52% left atrial dilation), our algorithm was able to group the 15 pacing sites, into 7 clinically useful and distinct regions with high precision (positive predictive value range 81-99%, Figure 2). Conclusions An algorithm defined by the activation sequence and timing of electrograms from two linear multipolar catheters allows for accurate regionalization of NPVTs. This may be used to expedite identification of a region of interest to guide further focused detailed mapping of AF NPVTs.

Introduction Ablation of non-pulmonary vein triggers (NPVTs) after pulmonary vein isolation (PVI) reduces atrial fibrillation (AF) recurrence, but localizing NPVTs can be challenging. We evaluated the potential for noninvasive electrocardiographic imaging (ECGi) to regionalize NPVTs and expedite more focused catheter-based mapping. ECGi combines measured body surface potentials with heart-torso geometry acquired from computed tomography (CT), to generate an activation map from a single recorded beat. Methods In 12 patients with AF undergoing first time AF ablation, the ECGi vest was fitted for preprocedural CT scan and then worn during procedure. Following completion of PVI, we paced from 15 atrial sites where NPVTs commonly arise (Figure 1), and evaluated the epicardial activation map generated by ECGi during steady state pacing at cycle length of 700-800 ms allowing an unobscured P wave. Merging of invasive anatomic map with CT-based ECGi map allowed comparison of ECGi activation map with true pacing location (Figure 2). Results From 180 pacing sites in our patient cohort (67% male, 58% persistent AF, 67% left atrial dilation), median distance between earliest activation site on ECGi map and pacing location was 16 mm (interquartile range, 11-22 mm), with 95% of sites within 30 mm (Figure 2). Septal pacing sites were measured to the epicardial aspect of the interatrial septum. Conclusions ECGi is able to consistently approximate the origin of paced beats from common NPVT sites and suggests the potential for rapid regionalization of NPVTs. The identified region can then be the focus of more detailed catheter-based mapping techniques to facilitate successful ablation of NPVTs.

Type of funding sources: None. HeartMate3TM (HM3) is a relatively new left ventricular assist device (LVAD) system. Its design and magnetically levitated pump may impact VTA. To describe clinical characteristics, procedural details, specific challenges and outcomes in patients with HM3 referred for ventricular tachycardia ablation (VTA). Data was collected from patients implanted with an HM3 system who underwent VTA in 7 tertiary centers. Data included baseline patient characteristics, procedural data, mortality, and arrhythmia-free survival.  The study cohort included 19 patients (18 male, aged 65 ± 7.8 years) with low left ventricular ejection fraction (LVEF, 17 ± 5%), presenting with VT (53% with storm VT).  VTs were induced in 89% of patients and a total of 41 VTs were observed.  Severe electromagnetic interference was present in the surface ECG (Figure A) but not on endocardial electrograms (Figure B). Hence, VT localization required analysis of intra-cardiac signals or the use of filter in the 40-20 Hz range. A total of 32 VTs were mapped and were successfully ablated (31% to the anterior wall, 38% to the septum, and only 9% to the inflow cannula region).  Notably, the large pump housing tends to obscure clear visualization of the apical region in fluoroscopy particularly in the LAO view (Figure C,D). Therefore, three-dimensional electro-anatomical mapping was aided by ICE or CARTOSound in 71% cases (Figure E). Non-inducibility of any VT was reached in 11 patients (58%). Over a follow up of 429 (IQR 101-692) days, 5 (26%) patients underwent a redo VT ablation due to recurrent VTA and 2 (11%) patients died. VT ablation in patients with HM3 is feasible and safe when done in the appropriate setup. Long-term arrhythmia free survival is acceptable but not well predicted by non-inducibility at the end of the procedure. Abstract Figure. HeartMate3 ablation Challenges

In patients presenting with repetitive ventricular arrhythmias (VAs), a specific pattern of left ventricular scar characterized by a subepicardial/midmyocardial ringlike distribution on cardiac magnetic resonance (CMR) has been recently associated with high risk of recurrent malignant VAs and sudden cardiac death (SCD). The genetic background and familial basis of ringlike left ventricular cardiomyopathy (RLCM) has not been previously investigated

Myocardial fibrosis and inflammation in patients with cardiac sarcoidosis (CS) may lead to sinus rhythm abnormalities such as, low QRS amplitude (QRSa), QRS fractionation (QRSf) and longer QRS duration (QRSd).

Frequent PVC can cause LV dysfunction, a condition known as PVC-induced cardiomyopathy (PIC). The predictors of PIC have been retrospectively investigated by comparing patients presenting with PIC to those with preserved LV function, but there are no longitudinal data evaluating the incidence and predictors of PIC

BACKGROUND: Ventricular tachycardia (VT) substrate in left ventricular (LV) nonischemic cardiomyopathy (NICM) consists of fibrosis with surviving myocardium. OBJECTIVE: The purpose of this study was to determine whether, in patients with LV NICM and sustained VT, reduced QRS amplitude and QRSf during sinus rhythm can identify the presence and location of abnormal septal (S-NICM) and/or free-wall (FW-NICM) VT substrate. METHODS: We compared patients with NICM and VT (group 1) with electroanatomic mapping septal (S-NICM; n = 21) or free-wall (FW-NICM; n = 20) VT substrate to a 38-patient reference cohort (group 2) with cardiac magnetic resonance imaging (cMRI) and NICM but no VT referred for primary prevention implantable cardioverter-defibrillator (26 [68.4%] with late gadolinium enhancement). RESULTS: Group 1 had lower QRS amplitude in leads II (0.60 +/- 0.22 vs 0.86 +/- 0.35, P <.001), aVR (0.60 +/- 0.24 vs 0.75 +/- 0.31, P = .002), aVF (0.48 +/- 0.20 vs 0.70 +/- 0.28, P <.001), and V2 (1.09 +/- 0.52 vs 1.38 +/- 0.55, P = .001) than group 2. QRS <0.55 mV in lead aVF identified VT and accompanying substrate with sensitivity 70% and specificity 71%. Most group 1 and group 2 patients had 12-lead ECG QRS fractionation (QRSf) in =2 contiguous leads (78% vs 63.2%, P = .14). Sensitivity and specificity for =2 QRSf leads identifying respective regional electroanatomic or cMRI abnormalities were 76% and 50% for inferior, 44% and 87% for lateral, and 21% and 89% for anterior leads. CONCLUSION: In LV NICM, low frontal plane QRS (<0.55 mV in aVF) is associated with VT substrate. Although multilead QRS fractionation is associated with the presence and location of VT substrate, it is frequently identified in patients without VT with cMRI abnormalities.

J wave syndrome with VF has been linked to epicardial (EPI) fragmented electrograms and myocardial fibrosis. We hypothesized that the EPI fibrotic process in LV non-ischemic cardiomyopathy (NICM) and VT should also be reflected by frequent J waves. Group 1 included patients (pts) with NICM and VT ablation with LV substrate mapping and VT localization to EPI or endocardium (ENDO). Group 2 included a reference cohort with NICM and no VT for primary prevention ICD. All pts had nonpaced rhythm. J waves were defined as a J point elevation with terminal QRS slurring or notching and ≥ 0.1mV concave upward ST-segment elevation. Patients were classified as having anterior (V1 to V4, avR), lateral (DI, aVL, V5, V6), inferior (DII, DIII and aVF). In Group 1, 45 pts (59.2%) had EPI and 31 pts (40.8%) ENDO LV bipolar low voltage and VT. J waves were more common if EPI substrate and VT than with ENDO VT substrate (57.7% vs 9.6%, p<0.001) and were most evident in lateral (EPI 46.6% vs ENDO 6.4%, p<0.001) and inferior (20% vs 3.2%, p=0.03) leads. Table 1. In Group II all 38 pts had magnetic resonance imaging (cMRI) and 26 (68.4%) had late gadolinium enhancement (LGE). Distribution of LGE was subendo to mid-myocardial septum and anterior LV, 15 pts (57%), mid-subepicardial inferior wall, 4 pts (15%) and other, 7pts. J waves were also more common in Group 1 with VT than Group 2 pts, 38 (50%) vs 9 (24%), P=0.007. There was a strong association between the presence of J waves and EPI substrate on voltage map or cMRI (Cramer's V=0.44, p<0.001). In pts with NICM and VT, J waves, commonly seen on 12-lead ECG in inferior or lateral leads, are strongly associated with EPI VT substrate.Tabled 1Table 1EPI substrate (n=45)ENDO substrate (n=31)P valueLGE (+)(n=26)LGE (-)(n=12)P valueJ wave in ≥1 lead/s33 (73.3%)5 (16.1%)p<0.0016(23.1%)3(25%)p=0.89J waves in ≥2 contiguous leads26 (57.7%)3 (9.6%)p<0.0015(19.2%)2(16.7%)p=0.85≥2 J waves in lead DII, DIII & aVF9 (20%)1 (3.2%)p=0.034(14.5%)1(8.3%)p=0.55≥2 J waves in lead DI, aVL, V5 & V621 (46.6%)2 (6.4%)p<0.0013(11.5%)1(8.3%)p=0.76≥2 J waves in lead V1 to V4 and aVR6 (13.3%)0 (0%)p=0.070(0%)0(0%)p=1 Open table in a new tab

LV endocardial(ENDO) unipolar(UNI) mapping (8.3mV cutoff) can identify the presence of epicardial(EPI) bipolar(BIP) scar in the setting of normal endo BIP voltage. Identification of EPI BIP scar may be influenced by intervening tissue characteristics and adjusting the UNI voltage color slider bar may more accurately identify the area of EPI BIP scar.

The term "nonischemic cardiomyopathy" (NICM) designates a myocardial disease characterized by mechanical and/or electrical dysfunction in the absence of significant coronary artery disease, valvular heart disease, hypertension, or congenital heart disease. Although sustained ventricular tachycardia (VT) occurs in only 5% of patients with NICM, it is an important cause of sudden cardiac death. In this review we summarize the current understanding of the anatomic and electrophysiologic substrates of VT in the different types of NICM. In addition, we discuss recent progress and experience with catheter ablation of VT in these patients.

Abstract Background Low QRS amplitude (QRSa), QRS fractionation (QRSf) and longer QRS duration (QRSd) are markers of myocardial fibrosis and inflammation in non-ischemic cardiomyopathy (NICM). Objective To determine if reduction of inflammation with treatment of cardiac sarcoidosis (CS) may reverse these 12 lead ECG parameter changes. Methods 21 patients (pts) with CS and VT ablation with a positive baseline positron emission tomographic (PET 1) scan were studied. All pts received prednisone ≥40 mg for 4 to 8 weeks followed by a taper and maintenance with methotrexate ± low-dose prednisone, <10 mg/day, until clinically stable and resolution of inflammation on PET 2 one year after initial. In addition, pts with low LV ejection fraction (13/21) received guideline directed medical therapy for heart failure. Pts at 1yr with positive PET2 (9) were compared to those with negative PET2 (12). Baseline and 1yr 12-lead ECGs were analyzed for QRSd, ≥2QRSf contiguous leads and QRSa in the limb leads. Results Pts in PET2(+) vs PET2(−) groups has similar gender (men 89% vs 100%, p=0.42), age (57±8 vs 56±10 years, p=0.8) and LV ejection fraction (41±11 vs 46±11, p=0.31). Baseline 12-lead ECGs showed similar QRSd, ≥2QRSf contiguous leads and QRSa for PET2(+) vs PET2(−); P all >0.15 (Table 1). At 1 yr there was a lower prevalence of ≥2QRSf contiguous leads and strong trend for shorter QRS duration and larger QRSa in lead DI if PET2(−) vs PET2(+). 4 pts demonstrated loss of QRSf 2 contiguous leads and/or increase in QRSa in DI by at least 0.15 mV from baseline if PET2(−) and none if PET2(+). Conclusions In pts with CS and VT, reversal of inflammation may result in a greater QRSa and reduction in QRSf. An increase in QRSa in lead 1 by >0.15mV and/or loss of QRSf identifies a clear positive response to treatment and negative PET at 1 year. Funding Acknowledgement Type of funding sources: Foundation. Main funding source(s): Richard T and Angela Clark Innovation Fund in Cardiovascular Medicine, the Mark S Marchlinski EP Research and Education Fund and the Winkelman Family Fund in Cardiovascular Innovation. Table 1

Background: The presence of epicardial connections (ECs) between pulmonary veins (PVs) and other anatomic structures may hinder PV isolation. In this study, we analyzed their prevalence, location, associated factors, and clinical implications. Methods: Five hundred thirty-four consecutive patients with atrial fibrillation undergoing radiofrequency ablation were included. We considered that an EC was present if: (1) the first pass around the PV antrum did not produce PV isolation and (2) subsequent atrial activation during PV pacing showed that the earliest site was located away from the ablation line and later activation sites were observed near the ablation line. Clinical and electrophysiological variables were collected from all patients. Patients were followed during 12.9±9.4 months, and any documented atrial tachyarrhythmia after the 3-month blanking period was classified as a recurrence. Results: Out of the 534 patients included, 72 (13.5%) were found to have 81 ECs. There was a significant association between the presence of ECs and structural heart disease (15.3% in patients without ECs versus 36.5% in patient with ECs; P <0.001) and patent foramen ovale (4.6% versus 13.5%; P =0.002). The presence of a left common trunk was significantly associated with the absence of ECs (29.6% in patients without ECs versus 16.2% in patients with ECs; P =0.014). Patients with ECs had lower acute success in PV isolation compared with patients without ECs (99.1% versus 86.1%; P <0.001). After adjusting for age, sex, type of atrial fibrillation, left atrium area, hypertension, structural heart disease, presence of left common trunk, patent foramen ovale, and time for atrial fibrillation diagnosis to the ablation, we found a significantly higher risk of atrial tachyarrhythmia recurrences in patients with ECs compared with patients without ECs (hazard ratio, 1.7 [95% CI, 1.1–2.9]; P =0.04). Conclusions: ECs between PVs and other adjacent structures are frequent in patient with atrial fibrillation (prevalence: 13.5%). Structural heart disease and a patent foramen ovale are strongly associated with the presence of ECs. ECs reduce the acute and chronic success of PV isolation.

When pacing trains with a constant cycle length (CL) but increasing number of beats are introduced during a macroreentrant atrial tachycardia (MAT), the postpacing interval (PPI) is expected to increase if entrainment does not occur but could be stable if entrainment occurs. We tested the ability of PPI analysis to detect entrainment.