BACKGROUND:The subcutaneous implantable cardioverter defibrillator (S-ICD) offers protection from sudden cardiac death without transvenous leads. Although contemporary techniques and programming have reduced inappropriate shocks, high rates persist in certain populations. The objective of this study was to evaluate the impact of a novel quantitative vector screening (QVS) protocol on the incidence of sensing-related complications and inappropriate shocks in patients undergoing S-ICD implantation. METHODS:We analyzed 223 consecutive patients who underwent S-ICD implantation at the Hospital of the University of Pennsylvania from December 2018 to July 2025. Traditional vector screening was used before 2023. In 2023, we implemented QVS, which incorporated quantitative sensing scores for each candidate and raised the threshold for S-ICD implantation. The primary end point was time to first inappropriate shock or under-sensed ventricular arrhythmia. Secondary outcomes included SMART Pass deactivation and need for device revision. Outcomes were reported as survival analyses. RESULTS:During preimplant screening, the QVS protocol reduced patient eligibility from 96% to 83%. The median follow-up after implant was 42 months (interquartile range, 48) in the traditional vector screening arm and 18 months (interquartile range, 15) in the QVS arm. The primary end point of time to first inappropriate shock or under-sensed ventricular arrhythmia was longer in the QVS arm (log-rank, P=0.02). There were 23 primary end point events among 145 patients in the traditional vector screening arm (5.2 per 100 patient-years [95% CI, 3.1-7.4]) and 2 primary end point events among 78 patients in the QVS arm (1.8 per 100 patient-years [95% CI, 0.01-4.38]). CONCLUSIONS:Implementation of a novel S-ICD screening protocol with stricter eligibility thresholds reduced sensing-related complications, particularly inappropriate shocks.
BACKGROUNDClinical recognition of multifocal premature ventricular complexes (PVCs) poses diagnostic and therapeutic challenges. Despite their morphological diversity, these arrhythmias may originate from a confined anatomical region, allowing a systematic mapping and ablation strategy.OBJECTIVETo describe clinical characteristics and propose a stepwise approach to mapping and ablation of multifocal PVCs originating from the basal septal LV ostium.METHODSPatients with multifocal septal PVCs, who underwent coronary venous mapping (CVM), were included. Ablation targeted the basal LV septum from the anterolateral LV ostium to the posterior LV process.RESULTSTwenty-four patients (mean age 64.5±9.2 years; 92% male) were included. Baseline electrocardiogram (ECG) showed PR prolongation >200 ms in 50%, QRS>100 ms in 75%, absent septal r waves in 63% and QRS fractionation in inferior leads in 38%. Left ventricular ejection fraction (LVEF) was preserved or mildly reduced (median 45%). Cardiac magnetic resonance (CMR) showed delayed gadolinium enhancement in 71%, intracardiac echocardiography revealed septal abnormalities in 83%. Intramural CVM was feasible in 75%, revealing fractionated electrograms; intramural activation preceded endocardial activation by 10 ms(p<0.01). Thirteen patients (54%) received implantable cardioverter-defibrillator (ICD). PVC burden decreased from 18.7% to 2.8%(p<0.01), with ≥80% reduction in 83%. During 1.7 years of follow-up, 4 patients (31%) received appropriate therapies.CONCLUSIONSMultifocal septal PVCs are consistently associated with abnormalities on ECG, CMR and/or intramural septal electrograms. A stepwise ablation approach substantially reduces PVC burden, although damage to the conduction system remains clinically relevant. The risk of malignant ventricular arrhythmias remains high despite preserved or mildly reduced LVEF.
Background Intramyocardial mapping of left ventricular outflow tract (LVOT) premature ventricular complexes (PVCs) via septal coronary venous branches is helpful to define the site of origin (SOO) and guide ablation. The limitation of unipolar far-field signals with wire mapping can be obviated through the use of a multipolar mapping catheter. Objectives This study reports our mapping and ablation experience of suspected LVOT PVCs using intraseptal mapping with multipolar catheters. Methods Patients with suspected LVOT PVCs in whom intraseptal mapping was attempted using multipolar catheters were included. The V2 S-wave and R-wave pattern break (PB) ratios were calculated using the S-wave or R-wave amplitudes in lead V2 divided by the sum of the S-wave or R-wave amplitudes in leads V1 and V3, respectively. Endocardial, intramyocardial, or epicardial SOO was based on activation pattern. Results Of 86 patients, multipolar intraseptal mapping was successfully performed in 60 (70%; 30% female, 53% with prior ablation). PVCs were most commonly mapped to an intramyocardial source and least commonly to the epicardium. For left bundle branch block PVCs, a V2 S-wave PB ratio >2.7 ruled in an intramyocardial or epicardial source, whereas a ratio <1.2 ruled out an endocardial source. For right bundle branch block morphology PVCs, a V2 R-wave PB ratio <1.0 ruled out an endocardial source. Acute ablation success was achieved in 98% and freedom from recurrence was 93% at a median follow-up of 12.4 months. Recording of intraseptal late potentials with reversal during PVC was observed in 25 (42%) patients and was associated with long-term success. Conclusions Ablation of LVOT PVCs guided by intraseptal mapping using multipolar catheters is feasible and highly effective. Electrocardiogram predictors of SOO identify patients in whom intraseptal mapping may be useful. Reversal of late potentials with PVCs may represent abnormal substrate in idiopathic PVCs in ostensibly structurally normal hearts.
Background Inherited cardiomyopathies cause ventricular tachycardia (VT) and heart failure, yet genotype‐based substrate characterization is limited. Methods Patients with inherited cardiomyopathy undergoing VT (n=80) or premature ventricular complex (n=25) ablation between 2010 and 2024 were evaluated for arrhythmia substrate, ablation, and heart failure outcomes. Results Among 105 patients, the median age was 51 years, 72% were men, and the cohort comprised desmosomal (desmoplakin [DSP], 11%; non‐DSP, 24%), titin (22%), lamin A/C (LMNA; 20%), sarcomeric (14%), ion‐channel (5%), and cytoskeletal/Z‐disk (4%) genotype groups. In the VT cohort, low‐voltage substrate was predominantly septal in the LMNA (55%), titin (67%), and sarcomeric (75%) groups; both septal (75%) and lateral left ventricle (75%) in the cytoskeletal/Z‐disk group; perimitral (71%) and lateral left ventricle (57%) in the DSP desmosomal group; and right ventricular free wall (91%) in the non‐DSP desmosomal group. Ablation eliminated clinical VT in 90%, with noninducibility of any VT in 52 of 80 (65%) cases. VT‐free survival was 51% during 3 years (1.8–6.3 years). Among recurrences, 11 of 39 (28%) patients had a single VT episode. VT‐free survival was highest in the non‐DSP desmosomal group and lowest in the LMNA group (66% versus 20%, P=0.03). Residual VT inducibility (hazard ratio [HR], 2 [95% CI, 1.05–3.77]) and LMNA variant (HR, 2.25 [95% CI, 1.1–4.57]) predicted recurrence. In the premature ventricular complex cohort, the burden decreased from 12% (interquartile range [IQR]=Q3–Q1, 21–8) to 3.75% (IQR 3–1, 6–1), and 17 of 25 (68%) had ≤5% burden. End‐stage heart failure outcome (left ventricular assist device, transplant, or death) occurred in 29% overall and 52% in the LMNA group. Conclusions Genotype correlates with VT substrate. Ablation successfully reduced VT and premature ventricular complex burden; however, long‐term VT recurrence was common except in non‐DSP desmosomal variants. LMNA variants portend worse outcomes.
INTRODUCTION:Mobile ambulatory cardiac telemetry (MCOT) use has increased over time; however, data on the prevalence and the impact of emergent arrhythmia notifications with MCOT remains unclear. We sought to determine the prevalence and clinical impact of emergent arrhythmia events in patients undergoing MCOT monitoring. We also analyzed the efficiency of the emergent notification process. METHODS:We analyzed 8404 consecutive patients from two centers who were prescribed Philips MCOT (K153473) over a 28-month period (September 2018-January 2021). Participants meeting emergent notification criteria were included. The primary outcome was any unscheduled provider intervention after the emergent notification. We also analyzed several time domains of the provider notification process. RESULTS:A total of 122 patients (1.45%) satisfied emergent notification criteria during the study period. The median notification time from arrhythmia onset to provider notification was 42 min. Physician review of the arrhythmia notifications showed agreement with the monitoring technician diagnosis in 102/122 (83.6%). An emergent notification resulted in an unscheduled follow-up visit in 104/122 (85.2%) patients. Time from arrhythmia event to unscheduled follow up visit was < 24 h in 88/104 (84.6%), 24-72 h in 9/104 (8.7%) and > 72 h in 7/104 (6.7%). In 33 patients (27%), emergent notifications resulted in unscheduled interventions including: device implantation (24), ablation (8), and electrical cardioversion (4). CONCLUSIONS:Emergent arrhythmias events recorded during ambulatory telemetry monitoring resulted in unscheduled patient contact in 85% of cases and procedures in 27% of cases. The monitoring notification process was efficient, with median time from arrhythmia onset to provider notification of 42 min.
Background Pulmonary veins (PVs) are major sources of atrial fibrillation (AF) triggers, but patients may also have non-PV (NPV) triggers. Data on the impact of targeting NPV triggers on AF ablation outcomes are limited. Objectives This study aimed to assess the outcome of patients undergoing AF ablation based on their NPV trigger status. Methods Patients undergoing first-time AF ablation using radiofrequency energy between 2018 and 2023 who received trigger provocative maneuvers were included. The provocative maneuvers consisted of cardioversion of AF, incremental isoproterenol infusion (3, 6, 12, and 20-30 μg/min) and/or an atrial burst pacing protocol. NPV triggers were defined as ectopic foci initiating AF, sustained focal atrial tachycardia (AT), or atrioventricular nodal reentrant tachycardia. Recurrence was defined as AF/AT >30 seconds after a 90-day blanking period. Results Of 2,315 patients included, 2,046 (88.4%) did not have NPV triggers, 233 (10.1%) had NPV triggers that were ablated, and 36 (1.6%) had NPV triggers that were not targeted or failed localization/ablation attempts. One-year recurrence rate was 29.5% in patients without NPV triggers, 38.2% in those with ablated NPV triggers (adjusted HR: 1.35; 95% CI: 1.08-1.69), and 72.2% in those with untreated NPV triggers (adjusted HR: 3.71; 95% CI: 2.48-5.54). This response pattern remained consistent regardless of NPV trigger subtype (AF vs focal AT) or provocation method (spontaneous vs induced triggers). Conclusions Failure to ablate induced NPV triggers is associated with a high risk of recurrence. Although the ablation of NPV triggers reduces recurrence rates to levels approaching those without such triggers, their presence indicates a modestly worse prognosis.
BACKGROUND:Clinical recognition of multifocal premature ventricular complexes (PVCs) poses diagnostic and therapeutic challenges. Despite their morphological diversity, these arrhythmias may originate from a confined anatomical region, allowing a systematic mapping and ablation strategy. OBJECTIVE:To describe clinical characteristics and propose a stepwise approach to mapping and ablation of multifocal PVCs originating from the basal septal left ventricular (LV) ostium. METHODS:Patients with multifocal septal PVCs who underwent coronary venous mapping were included. Ablation targeted the basal LV septum from the anterolateral LV ostium to the posterior LV process. RESULTS:Twenty-four patients (mean age, 64.5 ± 9.2 years; 92% male) were included. Baseline electrocardiogram showed PR prolongation of >200 ms in 50%, QRS of >100 ms in 75%, absent septal R waves in 63%, and QRS fractionation in inferior leads in 38%. LV ejection fraction was preserved or mildly reduced (median, 45%). Cardiac magnetic resonance showed delayed gadolinium enhancement in 71%, and intracardiac echocardiography revealed septal abnormalities in 83%. Intramural coronary venous mapping was feasible in 75%, revealing fractionated electrograms; intramural activation preceded endocardial activation by 10 ms (P < .01). Thirteen patients (54%) received an implantable cardioverter-defibrillator. PVC burden decreased from 18.7% to 2.8% (P < .01), with ≥80% reduction in 83%. During 1.7 years of follow-up, 4 patients (31%) received appropriate therapies. CONCLUSION:Multifocal septal PVCs are consistently associated with abnormalities on electrocardiogram, cardiac magnetic resonance and/or intramural septal electrograms. A stepwise ablation approach substantially reduces PVC burden, although damage to the conduction system remains clinically relevant. The risk of malignant ventricular arrhythmias remains high despite preserved or mildly reduced LV ejection fraction.