Non-Pharmacological Therapy for Atrial Fibrillation: Managing the Left Atrial Appendage

The prevalence of atrial fibrillation (AF) is increasing in parallel with an ageing population leading to increased morbidity and mortality. The most feared complication of AF is stroke, with the arrhythmia being responsible for up to 20% of all ischemic strokes. An important contributor to this increased risk of stroke is the left atrial appendage (LAA). A combination of the LAA's unique geometry and atrial fibrillation leads to low blood flow velocity and stasis, which are precursors to thrombus formation. It has been hypothesized for over half a century that excision of the LAA would lead to a reduction in the incidence of stroke. It has only been in the last 20–25 years that the knowledge and technology has been available to safely carry out such a procedure. We now have a number of viable techniques, both surgical and percutaneous, which will be covered in this paper

2019 HRS/EHRA/APHRS/LAHRS expert consensus statement on catheter ablation of ventricular arrhythmias: Executive summary

Ventricular arrhythmias are an important cause of morbidity and mortality and come in a variety of forms, from single premature ventricular complexes to sustained ventricular tachycardia and fibrillation. Rapid developments have taken place over the past decade in our understanding of these arrhythmias and in our ability to diagnose and treat them. The field of catheter ablation has progressed with the development of new methods and tools, and with the publication of large clinical trials. Therefore, global cardiac electrophysiology professional societies undertook to outline recommendations and best practices for these procedures in a document that will update and replace the 2009 EHRA/HRS Expert Consensus on Catheter Ablation of Ventricular Arrhythmias. An expert writing group, after reviewing and discussing the literature, including a systematic review and meta-analysis published in conjunction with this document, and drawing on their own experience, drafted and voted on recommendations and summarized current knowledge and practice in the field. Each recommendation is presented in knowledge byte format and is accompanied by supportive text and references. Further sections provide a practical synopsis of the various techniques and of the specific ventricular arrhythmia sites and substrates encountered in the electrophysiology lab. The purpose of this document is to help electrophysiologists around the world to appropriately select patients for catheter ablation, to perform procedures in a safe and efficacious manner, and to provide follow-up and adjunctive care in order to obtain the best possible outcomes for patients with ventricular arrhythmias

A clinically relevant sheep model of orthotopic heart transplantation 24 h after donor brainstem death

BACKGROUND: Heart transplantation (HTx) from brainstem dead (BSD) donors is the gold-standard therapy for severe/end-stage cardiac disease, but is limited by a global donor heart shortage. Consequently, innovative solutions to increase donor heart availability and utilisation are rapidly expanding. Clinically relevant preclinical models are essential for evaluating interventions for human translation, yet few exist that accurately mimic all key HTx components, incorporating injuries beginning in the donor, through to the recipient. To enable future assessment of novel perfusion technologies in our research program, we thus aimed to develop a clinically relevant sheep model of HTx following 24 h of donor BSD. METHODS: BSD donors (vs. sham neurological injury, 4/group) were hemodynamically supported and monitored for 24 h, followed by heart preservation with cold static storage. Bicaval orthotopic HTx was performed in matched recipients, who were weaned from cardiopulmonary bypass (CPB), and monitored for 6 h. Donor and recipient blood were assayed for inflammatory and cardiac injury markers, and cardiac function was assessed using echocardiography. Repeated measurements between the two different groups during the study observation period were assessed by mixed ANOVA for repeated measures. RESULTS: Brainstem death caused an immediate catecholaminergic hemodynamic response (mean arterial pressure, p = 0.09), systemic inflammation (IL-6 - p = 0.025, IL-8 - p = 0.002) and cardiac injury (cardiac troponin I, p = 0.048), requiring vasopressor support (vasopressor dependency index, VDI, p = 0.023), with normalisation of biomarkers and physiology over 24 h. All hearts were weaned from CPB and monitored for 6 h post-HTx, except one (sham) recipient that died 2 h post-HTx. Hemodynamic (VDI - p = 0.592, heart rate - p = 0.747) and metabolic (blood lactate, p = 0.546) parameters post-HTx were comparable between groups, despite the observed physiological perturbations that occurred during donor BSD. All p values denote interaction among groups and time in the ANOVA for repeated measures. CONCLUSIONS: We have successfully developed an ovine HTx model following 24 h of donor BSD. After 6 h of critical care management post-HTx, there were no differences between groups, despite evident hemodynamic perturbations, systemic inflammation, and cardiac injury observed during donor BSD. This preclinical model provides a platform for critical assessment of injury development pre- and post-HTx, and novel therapeutic evaluation. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s40635-021-00425-4

Mechanisms and mapping of ventricular arrhythmias in cardiomyopathy

© 2009 Dr. Haris M. HaqqaniHeart failure due to ischemic and dilated cardiomyopathy is a large and expanding public health problem, and ventricular arrhythmias are a common and potentially fatal complication of this condition. Despite extensive investigation, the mechanisms of ventricular arrhythmias in cardiomyopathy remain incompletely understood. This thesis examines these mechanisms, particularly with reference to the potential role of the underlying electrophysiologic substrate. It also evaluates the validity and utility of some of the tools commonly used to assist in the mapping and catheter ablation of ventricular arrhythmias. The central rationale of this thesis is that the mechanisms of ventricular arrhythmogenesis in cardiomyopathy are optimally studied by comparing ischemic and dilated cardiomyopathy patients with spontaneous (rather than inducible) ventricular tachycardia to otherwise similar heart failure patients who have never developed clinical arrhythmias. This has been done in the two largest projects herein. In the setting of ischemic cardiomyopathy, it is demonstrated that there are large differences in the electrophysiologic substrate between the groups such that patients with clinical ventricular tachycardia have substantially greater endocardial scarring as inferred by the presence of low-voltage zones and scar-related electrograms compared to control cardiomyopathy patients with no spontaneous arrhythmias. Furthermore, there appear to be fundamental differences in the nature of the scarring process with ventricular tachycardia patients having more abnormal electrograms per unit area of low-voltage and more scar-related putative conducting channels (which may form critical diastolic isthmuses in tachycardia). This was accompanied by a lower rate of ventricular tachycardia inducibility in the control patients. Taken together these findings point to a major role for the electrophysiologic substrate in ventricular arrhythmogenesis in the setting of ischemic cardiomyopathy. The situation in dilated cardiomyopathy is more complicated and although significant endocardial substrate differences were again seen in this context, there was marked heterogeneity in the group with ventricular tachycardia with some patients having extensive low-voltage zones and others having normal endocardial voltage. As the pericardium could not be accessed for ethical reasons in control patients with no clinical arrhythmia, the precise role of an abnormal epicardial substrate was not able to be defined in this study. Another project in this thesis examines potential improvements (in the form of a multielectrode mapping catheter) to a widely used electroanatomic mapping system that can assist in mapping ventricular tachycardia circuits and the substrates underlying them. A further project compares magnetic resonance imaging and electroanatomic substrate mapping in defining ventricular scarring in the context of cardiomyopathy. And finally, electroanatomic mapping is used to look at endocardial activation patterns and electrical dyssynchrony in cardiomyopathy patients with and without left bundle branch block. The demonstrated variability in these factors may underlie the significant non-response rates to cardiac resynchronization therapy. In summary, it is apparent from this work that the electrophysiologic substrate plays a crucial role in mechanism of the ventricular arrhythmias seen in heart failure patients with ischemic and dilated cardiomyopathy. An improved understanding of these mechanisms may in turn lead to better diagnosis, risk stratification and ultimately management of heart failure patients suffering from, or at risk of developing these potentially lethal arrhythmias

The electrocardiographic footprints of atrial ectopy

Atrial ectopics, also known as a premature atrial complexes (PAC)or atrial premature depolarisations (APD), are supraventricular beats arising from a focus other than the sinus node. Because the various foci provide an array of electrocardiographic (ECG)appearances, an extensive, but confusing nomenclature has developed. Atrial ectopics are a very common finding on Holter ECG monitoring at all ages, the incidence increasing in frequency with age. In the otherwise normal heart, they are generally infrequent and an innocent finding, but in patients with heart disease, they may be a harbinger to more serious atrial tachyarrhythmias. In this review, the ECG footprints of atrial ectopy will be defined. These footprints include prematurity and P wave morphology. The associated features of variable atrioventricular (AV)conduction, variable post-ectopic pauses and variable QRS morphology due to aberrancy will also be discussed. Each of these features will be explained in detail with ECG examples

The footprints of electrocardiographic interference: fact or artefact

Corporeal and particularly extra-corporeal interference is a very common problem encountered with both resting electrocardiograph (ECG) tracings and ambulatory recordings. The interference may be either electrical or mechanical and if severe, may affect the interpretation of the tracings. The interference, seen as artefact, can be divided into obvious, subtle or complicated. Obvious artefact may result from poor electrode attachment or body motion, whereas electrical interference is predominantly 50 or 60 Hz alternating current or radiofrequency waves from power lines, electrical equipment, mobile phones, fluorescent lights and electrical diathermy. Careful attention to the application of electrodes and finding the best environment for performing a 12-lead ECG will eradicate most interference. When subtle, the artefact can mimic cardiac arrhythmias, leading to incorrect interpretation of the tracings. There is also a complicated interference group, usually due to implanted cardiac electronic pacing devices and neurostimulators. These create persistent artefact, which may result in repeated unsuccessful attempts at procuring an artefact free tracing. This manuscript will describe the genesis of interference, how an ECG machine or monitor deals with interference and will discuss the common causes of interference. The characteristic patterns will be described and clues provided on how to differentiate subtle artefact from cardiac arrhythmias