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Aims Wearable devices are transforming the electrocardiogram (ECG) into a ubiquitous medical test. This study assesses the association between premature ventricular and atrial contractions (PVCs and PACs) detected on wearable-format ECGs (15 s single lead) and cardiovascular outcomes in individuals without cardiovascular disease (CVD). Methods and results Premature atrial contractions and PVCs were identified in 15 s single-lead ECGs from N = 54 016 UK Biobank participants (median age, interquartile range, age 58, 50–63 years, 54% female). Cox regression models adjusted for traditional risk factors were used to determine associations with atrial fibrillation (AF), heart failure (HF), myocardial infarction (MI), stroke, life-threatening ventricular arrhythmias (LTVAs), and mortality over a period of 11.5 (11.4–11.7) years. The strongest associations were found between PVCs (prevalence 2.2%) and HF (hazard ratio, HR, 95% confidence interval = 2.09, 1.58–2.78) and between PACs (prevalence 1.9%) and AF (HR = 2.52, 2.11–3.01), with shorter prematurity further increasing risk. Premature ventricular contractions and PACs were also associated with LTVA (P < 0.05). Associations with MI, stroke, and mortality were significant only in unadjusted models. In a separate UK Biobank sub-study sample [UKB-2, N = 29,324, age 64, 58–60 years, 54% female, follow-up 3.5 (2.6–4.8) years] used for independent validation, after adjusting for risk factors, PACs were associated with AF (HR = 1.80, 1.12–2.89) and PVCs with HF (HR = 2.32, 1.28–4.22). Conclusion In middle-aged individuals without CVD, premature contractions identified in 15 s single-lead ECGs are strongly associated with an increased risk of AF and HF. These data warrant further investigation to assess the role of wearable ECGs for early cardiovascular risk stratification.

AimsCardiac resynchronization therapy programmed to dynamically fuse pacing with intrinsic conduction using atrioventricular (AV) timing algorithms (e.g. SyncAV) has shown promise; however, mechanistic data are lacking. This study assessed the impact of SyncAV on electrical dyssynchrony across various pacing modalities using non-invasive epicardial electrocardiographic imaging (ECGi).Methods and resultsTwenty-five patients with left bundle-branch block (median QRS duration (QRSd) 162.7 ms) and intact AV conduction (PR interval 174.0 ms) were prospectively enrolled. ECGi was performed acutely during biventricular pacing with fixed nominal AV delays (BiV) and using SyncAV (optimized for the narrowest QRSd) during: BiV + SyncAV, LV-only single-site (LVSS + SyncAV), MultiPoint pacing (MPP + SyncAV), and LV-only MPP (LVMPP + SyncAV). Dyssynchrony was quantified via ECGi (LV activation time, LVAT; RV activation time, RVAT; LV electrical dispersion index, LVEDi; ventricular electrical uncoupling index, VEU; and biventricular total activation time, VVtat). Intrinsic conduction LVAT (124 ms) was significantly reduced by BiV pacing (109 ms) (P = 0.001) and further reduced by LVSS + SyncAV (103 ms), BiV + SyncAV (103 ms), LVMPP + SyncAV (95 ms), and MPP + SyncAV (90 ms). Intrinsic RVAT (93 ms), VVtat (130 ms), LVEDi (36 ms), VEU (50 ms), and QRSd (163 ms) were reduced by SyncAV across all pacing modes. More patients exhibited minimal LVAT, VVtat, LVEDi, and QRSd with MPP + SyncAV than any other modality.ConclusionDynamic AV delay programming targeting fusion with intrinsic conduction significantly reduced dyssynchrony, as quantified by ECGi and QRSd for all evaluated pacing modes. MPP + SyncAV achieved the greatest synchrony overall but not for all patients, highlighting the value of pacing mode individualization during fusion optimization.

Aims The SMART Pass™ (SP) algorithm is a high-pass filter that aims to reduce inappropriate therapy (IT) in subcutaneous internal cardiac defibrillator (S-ICD), but SP can deactivate due to low amplitude sensed R waves or asystole. The association between IT and SP deactivation and management strategies were evaluated, hypothesizing SP deactivation increases the risk of IT and device re-programming, or lead/generator re-positioning could reduce this risk. Methods and results Retrospective single-centre audit of Emblem™ S-ICD devices implanted 2016 to 2020 utilizing health records and remote monitoring data. Cox regression models evaluated associations between SP deactivation and IT. A total of 348 patients (27 ± 16.6 months follow-up) were studied: 73% primary prevention. Thirty-eight patients (11.8%) received 83 shocks with 27 patients (7.8%) receiving a total of 44 IT. Causes of IT were oversensing (98%) and aberrantly conducted atrial fibrillation (2%). SP deactivation occurred in 32 of 348 patients (9%) and was significantly associated with increased risk of IT (hazard ratio 5.36, 95% CI 2.37-12.13). SP deactivation was due to low amplitude R waves (94%), associated with a higher defibrillation threshold at implant and presence of arrhythmogenic right ventricular cardiomyopathy. No further IT occurred 16 ± 15.5 months after corrective interventions, with changing the sensing vector being successful in 59% of cases. Conclusion To reduce the risk of IT, the cause of the SP deactivation should be investigated, and appropriate reprogramming, device, or lead modifications made. Utilizing the alert for SP deactivation and electrograms could pro-actively prevent IT.

Background Radiofrequency catheter ablation (CA) can reduce ventricular tachycardia (VT) burden and registry data suggests an improvement in mortality. However, there is significant heterogeneity in patient morbidity and VT phenotype. A risk prediction model derived from observational data has suggested pre-procedural left ventricular (LV) function, age and underlying ischaemic cardiomyopathy are associated with greater post-procedural mortality. Validation of proposed factors in clinical practice is required to facilitate comprehensive pre-procedural risk stratification and inform decision making. Purpose To determine whether proposed pre-procedural predictors of mortality after VTCA are valid in a UK population and explore any association with other predictors. Method Patients undergoing VTCA at a tertiary electrophysiology centre between 06/07/16 and 31/07/19 were included. Pre-specified characteristics and mortality follow-up data were analysed from electronic health records. Cox regression analysis was undertaken to determine association with mortality. Results 161 patients with mean age of 63 ±15.9 years underwent VTCA of whom 133 (83%) were male. During the follow-up period (16 months, 13-24; median, 1st-3rd quartile) 16 patients died. No deaths occured in the 27 (16%) patients with structurally normal hearts. Chronic kidney disease (CKD) stage III-IV (HR 14.73 [4.9-44.4]), LV ejection fraction Conclusion Proposed risk stratifying factors are validated in our UK centre’s experience. Additionally, CKD and baseline LVID appear to be associated with mortality in our population and warrant further study. Risk factor Hazard ratio Lower confidence interval Upper confidence interval P-value Atrial fibrillation (yes/no) 0.14 0.02 1.11 0.06 Age (years) 1.08 1.02 1.14 Abstract Figure 1: Kaplan-Meier survival curves

Funding Acknowledgements National Institute for Health Research; British Heart Foundation; and The Wellcome Trust and Engineering and Physical Sciences Research Council. Background Accurate identification of targets for catheter ablation therapy of ventricular tachycardias (VTs) in the postinfarction heart remains a significant challenge. Identification of such targets often requires VT-induction to delineate the entry/exit points of the reentrant circuit sustaining the VT. However, inducibility may not be possible due to hemodynamic instability. In this scenario, substrate ablation strategies can still be performed to uncover the arrhythmogenic substrate during sinus or paced rhythm. However, substrate mapping may fail to accurately delineate the reentrant circuit resulting in VT recurrence after the procedure. Purpose To use computer simulations to compare the ability of different electroanatomical maps constructed following typical substrate ablation strategies to identify the VT exit site. Methods An image-based computational model of the porcine post-infarction left ventricle was constructed to simulate VT and paced rhythm. Electroanatomical maps were constructed based on the following features extracted from electrograms computed on the endocardial surface: activation time (AT), bipolar electrogram amplitude, signal fractionation and the reentry vulnerability index (RVI - a metric combining activation and repolarization timings to identify tissue susceptibility to reentry). Potential ablation targets during substrate mapping were compared for: highest 5% AT gradient; lowest 5% bipolar signal amplitudes; areas with fragmented signals (more than one peak); and lowest 5% RVI. The minimum distance, d, between the manually identified VT exit site and the targets was measured. Results The RVI performed better than the other metrics at detecting the VT exit site (see Figure). The minimum distance between sites of lowest RVI and the exit site was 3.2mm compared to 13.1mm and 15.9mm in traditional AT and voltage maps, respectively. As the scar was not transmural, parameters derived from all electrograms (including those located on dense scar regions) were used to construct the electroanatomical maps. This improved the performance of the RVI significantly, making it more specific than the other metrics as can be seen in the Figure. Conclusions Among all metrics investigated here, the RVI identified the vulnerable region closest to VT exit site. This finding suggests that activation-repolarization metrics may improve the detection of pro-arrhythmic regions without having to induce VT. Moreover, the RVI may be particularly well suited for detecting vulnerable regions within non-transmural scars. Abstract Figure. VT and Substrate Mapping