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Background: Premature ventricular contraction (PVC) burden is a risk factor for heart failure and cardiovascular death in patients with structural heart disease. Long-term electrocardiographic monitoring can have a significant impact on PVC burden evaluation by further defining PVC distribution patterns., Objective: This study aimed to ascertain the optimal duration of electrocardiographic monitoring to characterize PVC burden and to understand clinical characteristics associated with frequent PVCs and nonsustained ventricular tachycardia in a large US cohort., Methods: Commercial data (iRhythm's Zio patch) from June 2011 to April 2022 were analyzed. Inclusion criteria were age >18 years, PVC burden ≥5%, and wear period ≥13 days. PVC burden cutoffs were determined on the basis of AHA/ACC/HRS guidelines for very frequent PVCs (10,000-20,000 during 24 hours). Patients were assigned to categories by PVC densities: low, <10%; moderate, 10% to <20%; and high, ≥20%. Mean measured error was assessed at baseline and daily until the wear period's end for overall PVC burden and different PVC densities., Results: Analysis of 106,705 patch monitors revealed a study population with mean age of 70.6 ± 14.6 years (33.6% female). PVC burden was higher in male patients and those >65 years of age. PVC burden mean error decreased from 2.9% at 24 hours to 1.3% at 7 days and 0.7% at 10 days. Number of ventricular tachycardia episodes per patient increased with increasing PVC burden (P < .0001)., Conclusion: Extending ambulatory monitoring beyond 24 hours to 7 days or more improves accuracy of assessing PVC burden. Ventricular tachycardia frequency and duration vary by initial PVC density, highlighting the need for prolonged cardiac monitoring., Competing Interests: Disclosures Luigi DiBiase is a consultant for Biosense Webster, Boston Scientific, Stereotaxis, and St Jude Medical and has received speaker honoraria from Medtronic, AtriCure, EPiEP, and Biotronik. Edward Gerstenfeld has served on advisory boards for Biosense Webster, Adagio Medical, and Boston Scientific; has received lecture honoraria from Medtronic, Biosense Webster, Abbott, and Boston Scientific; and has received a research grant from Abbott. Timm Dickfeld has served on advisory boards for Biosense Webster and InHeart and has received consulting honoraria from Impulse Dynamics. Nishant Verma has received speaker’s fees from Medtronic, Boston Scientific, Abbott, and Zoll. Ardit Kacorri, Lori Crosson, and Alan Wilk are employees of iRhythm Technologies. The other authors have no conflicts of interest to disclose., (Copyright © 2024 Heart Rhythm Society. Published by Elsevier Inc. All rights reserved.)

Background: Cardioneuroablation has been emerging as a potential treatment alternative in appropriately selected patients with cardioinhibitory vasovagal syncope (VVS) and functional AV block (AVB). However the majority of available evidence has been derived from retrospective cohort studies performed by experienced operators., Methods: The Cardioneuroablation for the Management of Patients with Recurrent Vasovagal Syncope and Symptomatic Bradyarrhythmias (CNA-FWRD) Registry is a multicenter prospective registry with cross-over design evaluating acute and long-term outcomes of VVS and AVB patients treated by conservative therapy and CNA., Results: The study is a prospective observational registry with cross-over design for analysis of outcomes between a control group (i.e., behavioral and medical therapy only) and intervention group (Cardioneuroablation). Primary and secondary outcomes will only be assessed after enrollment in the registry. The follow-up period will be 3 years after enrollment., Conclusions: There remains a lack of prospective multicentered data for long-term outcomes comparing conservative therapy to radiofrequency CNA procedures particularly for key outcomes including recurrence of syncope, AV block, durable impact of disruption of the autonomic nervous system, and long-term complications after CNA. The CNA-FWRD registry has the potential to help fill this information gap., (© 2024. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

In light of the adverse prognosis related to severe mitral regurgitation, heart failure, or sudden cardiac death in a subset of patients with mitral valve prolapse (MVP), identifying those at higher risk is key. For the first time in decades, researchers have the means to rapidly advance discovery in the field of MVP thanks to state-of-the-art imaging techniques, novel omics methodologies, and the potential for large-scale collaborations using web-based platforms. The National Heart, Lung, and Blood Institute recently initiated a webinar-based workshop to identify contemporary research opportunities in the treatment of MVP. This report summarizes 3 specific areas in the treatment of MVP that were the focus of the workshop: 1) improving management of degenerative mitral regurgitation and associated left ventricular systolic dysfunction; 2) preventing sudden cardiac death in MVP; and 3) understanding the mechanisms and progression of MVP through genetic studies and small and large animal models, with the potential of developing medical therapies., Competing Interests: Funding Support and Author Disclosures Dr Delling is supported by the UCSF Resource Allocation Program 7501268 and by National Institutes of Health (NIH) research grant R01HL153447. Dr Noseworthy has received research funding from the NIH, including the National Heart, Lung, and Blood Institute (R21AG 62580-1, R01HL 131535-4, R01HL 143070-2), the National Institute on Aging (R01AG 062436-1), Agency for Healthcare Research and Quality (R01HS 25402-3), Food and Drug Administration (FD 06292), and the American Heart Association (18SFRN34230146; has filed patents related to the application of artificial intelligence to the ECG for diagnosis and risk stratification and has licensed several A-ECG algorithms to Anumana; is involved in potential equity/royalty relationship with AliveCor; is a study investigator in an ablation trial sponsored by Medtronic; and has served on an expert advisory panel for OptumLabs. Dr Adams’s institution, the Icahn School of Medicine at Mount Sinai, receives royalties for mitral and tricuspid valve repair prostheses related to his intellectual property from Edwards Lifesciences and Medtronic. Dr Borger’s institution receives speakers’ honoraria and/or consulting fees on his behalf from Edwards Lifesciences, Medtronic, Abbott, and CryoLife. Dr Elmariah has received research funding from the NIH (R01HL 151838) and the American Heart Association (19TPA34910170); has received research grants from Edwards Lifesciences, Medtronic, and Abbott Vascular; and is a consultant for Edwards Lifesciences. Dr Gerstenfeld has received lecture honoraria from Medtronic, Boston Scientific, and Abbott; has received research funding from, is on the scientific advisory board, and has received compensation from Biosense Webster; is on the scientific advisory board for and is PI of a clinical ablation trial sponsored by Farapulse; and is on the Data and Safety Monitoring Board for trials sponsored by Thermedical Inc and Abbott. Dr Norris has received research funding from the NIH (HL131546, GM103444, HL149696, HL122906), and the American Heart Association (19TPA34850095, 20SRG35540029, 19TPA34900016, 17CSA33590067). Dr Padala is supported by the National Heart, Lung, and Blood Institute (R01HL135145, R01HL140325, R01HL133667, R01HL144714, R01HL135505) and by the National Institute of Biomedical Imaging and Bioengineering (R01EB031101); has significant stock ownership and a role as a director in Nyra Medical; and has received consulting fees from Heart Repair Technologies Inc in the last 12 months. Dr Weinsaft is supported by NIH research grants R01HL128278 and R01HL151686. Dr Enriquez-Sarano has served as a consultant for Edwards, Cryolife, ChemImage, and HighLife. Dr Levine is supported by NIH research grants R01HL128099 and R01HL141917, American Heart Association 963793/Levine/2022, and funding of the Ellison Foundation. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose., (Copyright © 2022 The Authors. Published by Elsevier Inc. All rights reserved.)

Premature ventricular complexes (PVCs) are increasingly recognized, as the use of ECG wearables becomes more widespread. In particular, PVCs arising from both the right ventricular outflow tract (RVOT) and left ventricular outflow tract (LVOT) comprise the majority of these arrhythmias and form a significant component of an electrophysiology practice. A keen understanding of the correlative anatomy of the outflow tracts, in addition to recognizing key ECG indices illustrating PVC sites of origin, are fundamental in preparing for a successful ablation. Patient selection, incorporating symptomatology, structural disease, and PVC burden can pose a challenge, though tools such as the ABC-VT risk score may help identify those patients with a higher risk of clinical deterioration. Utilizing intracardiac echocardiography to highlight salient anatomic features not visible with fluoroscopy allows for a more precise and safer ablation. Interpretation of intracardiac EGMs, and the careful examination for low amplitude highly fractionated pre-potentials, enhanced by the advent of new developed mapping/ablation catheters, remains crucial. Utilizing these tools will guide the electrophysiologist to an efficient and effective outflow tract PVC ablation., (© 2021 Wiley Periodicals LLC.)

Background: Survival after sudden cardiac arrest is limited by postarrest myocardial dysfunction, but understanding of this phenomenon is constrained by a lack of data from a physiological model of disease. In this study, we established an in vivo model of cardiac arrest and resuscitation, characterized the biology of the associated myocardial dysfunction, and tested novel therapeutic strategies., Methods: We developed rodent models of in vivo postarrest myocardial dysfunction using extracorporeal membrane oxygenation resuscitation followed by invasive hemodynamics measurement. In postarrest isolated cardiomyocytes, we assessed mechanical load and Ca(2) (+)-induced Ca(2+) release (CICR) simultaneously using the microcarbon fiber technique and observed reduced function and myofilament calcium sensitivity. We used a novel fiberoptic catheter imaging system and a genetically encoded calcium sensor, GCaMP6f, to image CICR in vivo., Results: We found potentiation of CICR in isolated cells from this extracorporeal membrane oxygenation model and in cells isolated from an ischemia/reperfusion Langendorff model perfused with oxygenated blood from an arrested animal but not when reperfused in saline. We established that CICR potentiation begins in vivo. The augmented CICR observed after arrest was mediated by the activation of Ca(2+)/calmodulin-dependent protein kinase II (CaMKII). Increased phosphorylation of CaMKII, phospholamban, and ryanodine receptor 2 was detected in the postarrest period. Exogenous adrenergic activation in vivo recapitulated Ca(2+) potentiation but was associated with lesser CaMKII activation. Because oxidative stress and aldehydic adduct formation were high after arrest, we tested a small-molecule activator of aldehyde dehydrogenase type 2, Alda-1, which reduced oxidative stress, restored calcium and CaMKII homeostasis, and improved cardiac function and postarrest outcome in vivo., Conclusions: Cardiac arrest and reperfusion lead to CaMKII activation and calcium long-term potentiation, which support cardiomyocyte contractility in the face of impaired postarrest myofilament calcium sensitivity. Alda-1 mitigates these effects, normalizes calcium cycling, and improves outcome., (© 2016 American Heart Association, Inc.)

Introduction: Catheter ablation is an effective treatment of scar-related ventricular tachycardia (VT), but the overall complexity of the procedure has precluded its widespread use. Remote magnetic navigation (RMN) has been shown to facilitate cardiac mapping and ablation of VT in a retrospective series. STOP-VT is the first multicenter, prospective, single-arm and single-procedure study evaluating RMN-based mapping and ablation of post-infarction VT., Methods: Patients with documented VT and prior MI, in whom an ICD was implanted either for primary or secondary prevention, were recruited from four EU and US centers. Either a transseptal (48 patients) or transaortic (5 patients) approach was employed to gain access for ventricular endocardial mapping/ablation during VT (entrainment mapping, activation mapping) and/or substrate mapping in sinus rhythm (elimination of fractionated/late potentials, variable extent of substrate modification) with RMN and irrigated RF ablation. The primary endpoints were as follows: (i) non-inducibility of the target VT or any other sustained VT; (ii) elimination of sustained VT/VF during ICD follow-up of up to 12 months., Results: The cohort included 53 consecutive patients (median age 67 years, 49 men, median LVEF 31%). One hemodynamically unstable patient was excluded at the onset of mapping. Inducibility of sustained VT was achieved an average of 2.2 times per patient (1-8), with mean tachycardia cycle length (TCL) 374 milliseconds (179-510). Mean total procedure and fluoroscopy times were 223 minutes and 8.7 minutes, respectively; mean cumulative fluoroscopy time during mapping and ablation was 0.95 minutes; maximum power averaged 42.3 W with nominal saline 30 cc/min irrigation; mean cumulative RF time was 38 minutes. Non-inducibility of the target VT was achieved in 49/52 patients (94.2%) and non-inducibility of any VT was achieved in 38/52 patients (73.1%). A combination of RMN and manual ablation was performed in two patients, rendering one non-inducible. During the 12-month ICD follow-up period, freedom from any sustained VT/VF was observed in 30 patients (62%), of which 19 (63%) were off antiarrhythmic medications. Five patients expired during follow-up: one presented with a VT storm, but for the others, death was not related to VT/VF (MI-cardiogenic shock, pulmonary embolism, bronchogenic carcinoma, end stage heart failure). No procedural complications were reported., Conclusions: This first prospective, single-procedure, multicenter study indicates that remote magnetic navigation is a safe and effective method for catheter ablation of post-infarction VT., (© 2016 Wiley Periodicals, Inc.)

The heritable cardiovascular disorder long QT syndrome (LQTS), characterized by prolongation of the QT interval on electrocardiogram, carries a high risk of sudden cardiac death. We sought to add new data to the existing knowledge of genetic mutations contributing to LQTS to both expand our understanding of its genetic basis and assess the value of genetic testing in clinical decision-making. Direct sequencing of the five major contributing genes, KCNQ1, KCNH2, SCN5A, KCNE1, and KCNE2, was performed in a cohort of 115 non-related LQTS patients. Pathogenicity of the variants was analyzed using family segregation, allele frequency from public databases, conservation analysis, and Condel and Provean in silico predictors. Phenotype-genotype correlations were analyzed statistically. Sequencing identified 36 previously described and 18 novel mutations. In 51.3% of the index cases, mutations were found, mostly in KCNQ1, KCNH2, and SCN5A; 5.2% of cases had multiple mutations. Pathogenicity analysis revealed 39 mutations as likely pathogenic, 12 as VUS, and 3 as non-pathogenic. Clinical analysis revealed that 75.6% of patients with QTc≥500 ms were genetically confirmed. Our results support the use of genetic testing of KCNQ1, KCNH2, and SCN5A as part of the diagnosis of LQTS and to help identify relatives at risk of SCD. Further, the genetic tools appear more valuable as disease severity increases. However, the identification of genetic variations in the clinical investigation of single patients using bioinformatic tools can produce erroneous conclusions regarding pathogenicity. Therefore segregation studies are key to determining causality.