Arrhythmia & Electrophysiology Review最新文献

During His-Purkinje conduction system (HPS) pacing, it is crucial to confirm capture of the His bundle or left bundle branch versus myocardialonly capture. For this, several methods and criteria for differentiation between non-selective (ns) capture - capture of the HPS and the adjacent myocardium - and myocardial-only capture were developed. HPS capture results in faster and more homogenous depolarisation of the left ventricle than right ventricular septal (RVS) myocardial-only capture. Specifically, the depolarisation of the left ventricle (LV) does not require slow cell-to-cell spread of activation from the right side to the left side of the interventricular septum but begins simultaneously with QRS onset as in native depolarisation. These phenomena greatly influence QRS complex morphology and form the basis of electrocardiographic differentiation between HPS and myocardial paced QRS. Moreover, the HPS and the working myocardium are different tissues within the heart muscle that vary not only in conduction velocities but also in refractoriness and capture thresholds. These last two differences can be exploited for the diagnosis of HPS capture using dynamic pacing manoeuvres, namely differential output pacing, programmed stimulation and burst pacing. This review summarises current knowledge of this subject.

Extensive knowledge of the anatomy of the atrioventricular conduction axis, and its branches, is key to the success of permanent physiological pacing, either by capturing the His bundle, the left bundle branch or the adjacent septal regions. The inter-individual variability of the axis plays an important role in underscoring the technical difficulties known to exist in achieving a stable position of the stimulating leads. In this review, the key anatomical features of the location of the axis relative to the triangle of Koch, the aortic root, the inferior pyramidal space and the inferoseptal recess are summarised. In keeping with the increasing number of implants aimed at targeting the environs of the left bundle branch, an extensive review of the known variability in the pattern of ramification of the left bundle branch from the axis is included. This permits the authors to summarise in a pragmatic fashion the most relevant aspects to be taken into account when seeking to successfully deploy a permanent pacing lead.

Successful translation of research focussing on atrial arrhythmogenic mechanisms has potential to provide a mechanism-tailored classification and to support personalised treatment approaches in patients with AF. The clinical uptake and clinical implementation of new diagnostic techniques and treatment strategies require translational research approaches on various levels. Diagnostic translation involves the development of clinical diagnostic tools. Additionally, multidisciplinary teams are required for collaborative translation to describe genetic mechanisms, molecular pathways, electrophysiological characteristics and concomitant risk factors. In this article, current approaches for AF substrate characterisation, analysis of genes potentially involved in AF and strategies for AF risk factor assessment are summarised. The authors discuss challenges and obstacles to clinical translation and implementation into clinical practice.

Left ventricular septal pacing (LVSP) and left bundle branch pacing (LBBP) have been introduced to maintain or correct interventricular and intraventricular (dys)synchrony. LVSP is hypothesised to produce a fairly physiological sequence of activation, since in the left ventricle (LV) the working myocardium is activated first at the LV endocardium in the low septal and anterior free-wall regions. Animal studies as well as patient studies have demonstrated that LV function is maintained during LVSP at levels comparable to sinus rhythm with normal conduction. Left ventricular activation is more synchronous during LBBP than LVSP, but LBBP produces a higher level of intraventricular dyssynchrony compared to LVSP. While LVSP is fairly straightforward to perform, targeting the left bundle branch area may be more challenging. Long-term effects of LVSP and LBBP are yet to be determined. This review focuses on the physiology and practicality of LVSP and provides a guide for permanent LVSP implantation.

The His-Purkinje system is a network of bundles and fibres comprised of specialised cells that allow for coordinated, synchronous activation of the ventricles. Although the histology and physiology of the His-Purkinje system have been studied for more than a century, its role in ventricular arrhythmias has recently been discovered with the ongoing elucidation of the mechanisms leading to both benign and life-threatening arrhythmias. Studies of Purkinje-cell electrophysiology show multiple mechanisms responsible for ventricular arrhythmias, including enhanced automaticity, triggered activity and reentry. The variation in functional properties of Purkinje cells in different areas of the His-Purkinje system underlie the propensity for reentry within Purkinje fibres in structurally normal and abnormal hearts. Catheter ablation is an effective therapy in nearly all forms of reentrant arrhythmias involving Purkinje tissue. However, identifying those at risk of developing fascicular arrhythmias is not yet possible. Future research is needed to understand the precise molecular and functional changes resulting in these arrhythmias.

Conduction system pacing (CSP) comprises His bundle pacing and left bundle branch area pacing and is rapidly gaining widespread adoption. Effective CSP not only depends on successful system implantation but also on proper device programming. Current implantable impulse generators are not specifically designed for CSP. Either single chamber, dual chamber or CRT devices can be used for CSP depending on the underlying heart rhythm (sinus rhythm or permanent atrial arrhythmia) and the aim of pacing. Different programming issues may arise depending on the device configuration. This article aims to provide an update on practical considerations for His bundle and left bundle branch area pacing programming and follow-up.

Despite a century of research, the mechanisms of AF remain unresolved. A universal motif within AF research has been unstable re-entry, but this remains poorly characterised, with competing key conceptual paradigms of multiple wavelets and more driving rotors. Understanding the mechanisms of AF is clinically relevant, especially with regard to treatment and ablation of the more persistent forms of AF. Here, the authors outline the surprising but reproducible finding that unstable re-entrant circuits are born and destroyed at quasi-stationary rates, a finding based on a branch of mathematics known as renewal theory. Renewal theory may be a way to potentially unify the multiple wavelet and rotor theories. The renewal rate constants are potentially attractive because they are temporally stable parameters of a defined probability distribution (the exponential distribution) and can be estimated with precision and accuracy due to the principles of renewal theory. In this perspective review, this new representational architecture for AF is explained and placed into context, and the clinical and mechanistic implications are discussed.

Despite advances in the field of cardiac resynchronisation therapy (CRT), response rates and durability of therapy remain relatively static. Optimising device timing intervals may be the most common modifiable factor influencing CRT efficacy after implantation. This review addresses the concept of fusion pacing as a method for improving patient outcomes with CRT. Fusion pacing describes the delivery of CRT pacing with a programming strategy to preserve intrinsic atrioventricular (AV) conduction and ventricular activation via the right bundle branch. Several methods have been assessed to achieve fusion pacing. QRS complex duration (QRSd) shortening with CRT is associated with improved clinical response. Dynamic algorithm-based optimisation targeting narrowest QRSd in patients with intact AV conduction has shown promise in people with heart failure with left bundle branch block. Individualised dynamic programming achieving fusion may achieve the greatest magnitude of electrical synchrony, measured by QRSd narrowing.