Leadless pacing is a safe and effective alternative to transvenous pacing for bradycardia. Micra AV is a leadless, single-device solution that provides atrioventricular synchronous ventricular pacing therapy. Early results from the Micra AV CED study showed reductions in short-term complications associated with the Micra AV leadless pacemaker among US Medicare patients. The objective of this study is to compare chronic complications, re-interventions, and all-cause mortality at 2 years between patients implanted with a Micra AV leadless pacemaker and a traditional dual-chamber transvenous (DC-TV) pacemaker.

The co-ordinated electrical activity of ∼2 billion cardiac cells ensures stability of the heartbeat. Indeed, the remarkably low incidence (<1%) of ventricular arrhythmias in the healthy heart is only possible when the electrical event across this syncytium is closely controlled. In contrast, the diseased myocardium is associated with increased electrophysiological heterogeneity, unstable rhythm, and increased incidence of lethal arrhythmias. But what is the link between cellular and tissue level heterogeneity? Recent research has shown the existence of considerable cellular heterogeneity even in the healthy heart, suggesting that cell-to-cell variability in electrical (e.g. action potential duration) and mechanical performance (e.g. twitch amplitude) is a normal property. This observation has been previously unappreciated because the aggregated function in the form of QT-interval and cardiac output varies <1% on a beat-to-beat basis. This article describes the underlying cellular variability that is tolerated-and perhaps needed-by different regions of the heart for normal function and indicates why this variability is not apparent in function at the chamber and organ level. Thus, in contrast to the current dominant view, this article postulates that heterogeneity is normal and potentially endows various functional benefits. This new view of how the component parts of the heart come together to function also suggests novel mechanisms for cardiac pathologies, namely that dysfunction may emerge from changes in the extent and/or nature of heterogeneity. Once understood, restoring normal forms of heterogeneity could be a novel approach to treatment.

Catheter ablation (CA) of idiopathic ventricular arrhythmias (VAs) from the epicardial left ventricular summit is challenging. The endocardial approach targets two sites: the endocardial closest site (ECS) to the epicardial earliest activation site (epi-EAS) and the endocardial earliest activation site (endo-EAS). We aimed to differentiate between cases where CA at the ECS was effective and where CA at the endo-EAS yielded success.

Despite increasing evidence demonstrating the safety of magnetic resonance imaging (MRI) in patients with cardiac implantable electronic devices (CIEDs), this procedure is often neglected in this population. This Spanish registry aimed to determine the proportion of MRI referrals and performance among patients with pacemakers (PMs) or implantable cardioverter defibrillators (ICDs).

We aimed to investigate the risk of sinus node dysfunction (SND) indicating cardiac pacing and mortality in first-degree relatives to patients with a pacemaker implanted on this indication and assess the effect of onset-age on disease risk.

The third-generation laser balloon (LB3) is an established ablation device for pulmonary vein isolation (PVI) that allows direct visualization of the anatomical target. Equipped with an automatic circumferential laser delivery modality, it aims at continuous circumferential PVI, improving both acute and clinical outcomes. We sought to evaluate the clinical efficacy of LB3 ablation using an anatomical-based approach without verifying electrical isolation.

Temperature-controlled high-power short-duration (HPSD) radiofrequency catheter ablation for pulmonary vein isolation (PVI) utilizing a novel ablation catheter (QDOT Micro) with real-time assessment of catheter tip temperature aims for safer, more effective and faster procedures.

Structural and fibrotic remodelling is a well-known contributor to the atrial fibrillation (AF) substrate. Epicardial adipose tissue (EAT) is increasingly recognized as a contributor through electrical remodelling in the atria. We aimed to assess the association of LA fibrosis and EAT with LA strain and function using cardiac magnetic resonance (CMR) imaging in patients with AF.

The CHA2DS2VASc score is recommended for stroke risk stratification in patients with atrial fibrillation (AF). This score assigns one extra point to female sex based on evidence from the early 2000s, suggesting higher thromboembolic risk in women. This incremental risk of thromboembolism in women has decreased over time between 2007 and 2018, becoming non-significant in recent years. The objective of this study was to assess the impact of removing the sex category (Sc) from the CHA2DS2VASc score, thus validating a non-sex CHA2DS2VASc (i.e. CHA2DS2VA) score.

Little is known about the distribution and clinical course of patients with inherited arrhythmia syndrome (IAS) and concomitant atrial arrhythmias (AAs).

Catheter ablation is an effective treatment method for recurrent ventricular tachycardias (VTs). However, at least in part, procedural and clinical outcomes are limited by challenges in generating an adequate lesion size in the ventricular myocardium. We investigated procedural and clinical outcomes of VT ablation using a novel 'large-footprint' catheter that allows the creation of larger lesions either by radiofrequency (RF) or by pulsed field (PF) energy.

Athletes are predisposed to atrial arrhythmias but the association between intense endurance exercise training, ventricular arrhythmias (VAs) and sudden cardiac death is less well established. Thus, it is unclear whether the 'athlete's heart' promotes specific arrhythmias or whether it represents a more general pro-arrhythmogenic phenotype. Whilst direct causality has not been established, it appears possible that repeated exposure to high-intensity endurance exercise in some athletes contributes to formation of pro-arrhythmic cardiac phenotypes that underlie VAs. Theories regarding potential mechanisms for exercise-induced VAs include repeated bouts of myocardial inflammation and stretch-induced cellular remodelling. Small animal models provide some insights, but larger animal and human data are sparse. The current clinical approach to VAs in athletes is to differentiate those with and without structural or electrical heart disease. However, if the athlete's heart involves a degree of pro-arrhythmogenic remodelling, then this may not be such a simple dichotomy. Questions are posed by athletes with VAs in combination with extreme remodelling. Some markers, such as scar on magnetic resonance imaging, may point toward a less benign phenotype but are also quite common in ostensibly healthy athletes. Other clinical and invasive electrophysiology features may be helpful in identifying the at-risk athlete. This review seeks to discuss the association between athletic training and VAs. We will discuss the potential mechanisms, clinical significance and approach to the management of athletes with VAs.

Atrial fibrillation (AF) is the most common sustained arrhythmia among patients with hypertrophic cardiomyopathy (HCM), increasing symptom burden and stroke risk. We aimed to construct a plasma proteomics-based model to predict new-onset AF in patients with HCM and determine dysregulated signalling pathways.

A novel three-dimensional mapping platform combined with a lattice-tip catheter that can toggle between monopolar pulsed field ablation (PFA) and radiofrequency energy delivery was recently launched. So far, the system was predominantly applied in general anaesthesia (GA), not in deep sedation.

Left ventricular assist devices (LVADs) are an increasingly used strategy for the management of patients with advanced heart failure. Although these devices effectively improve survival, atrial and ventricular arrhythmias are common with a prevalence of 20-50% at one year after LVAD implantation. Arrhythmias predispose these patients to additional risk and are associated with considerable morbidity from recurrent implantable cardioverter-defibrillator shocks, progressive failure of the unsupported right ventricle, and herald an increased risk of mortality. Management of patients with arrhythmias and LVAD differs in many aspects from the general population heart failure patients. These include ruling out the reversible causes of arrhythmias that in LVAD patients may include mechanical irritation from the inflow cannula and suction events. For patients with symptomatic arrhythmias refractory to medical treatment, catheter ablation might be relevant. There are specific technical and procedural challenges perceived to be unique to LVAD-related ventricular tachycardia (VT) ablation such as vascular and LV access, signal filtering, catheter manoeuvrability within decompressed chambers, and electroanatomic mapping system interference. In some patients, the arrhythmogenic substrate might not be readily accessible by catheter ablation after LVAD implantation. In this regard, the peri-implantation period offers a unique opportunity to surgically address arrhythmogenic substrate and suppress future VT recurrences. This document aims to address specific aspects of the management of arrhythmias in LVAD patients focusing on anti-arrhythmic drug therapy and ablations.

The use of ultrasound (US)-guided venous puncture for cardiac pacing/defibrillation lead placement may minimize the risk of periprocedural complications and radiation exposure. However, none of the published studies have been sufficiently powered to recommend this approach as the standard of care. We compare the safety and efficacy of ultrasound-guided axillary venous puncture (US-AVP) vs. fluoroscopy-guided access for cardiac implantable electronic devices (CIEDs) by performing an individual patient data meta-analysis based on previously published studies.

Alterations in repolarisation gradients and increased heterogeneity are key electrophysiological determinants of ventricular arrhythmogenesis across a variety of aetiologies with and without structural heart disease. High-density repolarisation mapping to localise these repolarisation abnormalities could improve characterisation of the individual arrhythmogenic substrate and inform more targeted ablation. Yet, due to challenges posed by intrinsic features of human cardiac repolarisation itself as well as technical and practical limitations, they are not routinely assessed, and traditional substrate mapping techniques remain strictly limited to determining conduction abnormalities. Here, we provide an overview of the mechanistic role of repolarisation alterations in ventricular re-entry arrhythmias followed by a description of a clinical workflow that enables high-density repolarisation mapping during VT ablations using existing clinical tools. We describe step-by-step guidance of how-to set-up and generate repolarisation maps illustrating the approach in case examples of structural normal and abnormal hearts. Furthermore, we discuss how repolarisation mapping could be combined with existing substrate mapping approaches, including isochronal late activation mapping, to delineate sites of increased re-entry vulnerability, that may represent targets for ablation without the requirement for VT induction. Finally, we review challenges and pitfalls and ongoing controversies in relation to repolarisation mapping and discuss the need for future technical and analytical improvements in repolarisation mapping to integrate into ventricular substrate mapping strategies. Repolarisation mapping remains investigational and future research efforts need to be focused on prospective trials to establish the additional diagnostic value and its role in clinical ablation procedures.