Epicardial Box Lesion Using Bipolar Biparietal Radiofrequency and Multimodality Scar Evaluation - a case series

Background Surgical epicardial AF ablation can be performed as a stand-alone (thoracoscopic) procedure or concomitant to other cardiac surgery. In hybrid AF ablation thoracoscopic surgical epicardial ablation is combined with a percutaneous endocardial ablation. The Medtronic Gemini-S clamp is a surgical tool that uses irrigated bipolar biparietal RF energy applied with two clamp lesions that overlap to create one epicardial box lesion including the posterior LA wall and the pulmonary veins. Case summary We describe three patients with therapy-refractory persistent AF and different stages of atrial remodelling in whom the Medtronic Cardioblate Gemini-S Irrigated RF Surgical Ablation System was used for hybrid AF ablation. Acute endocardial validation at the end of the hybrid ablation revealed a complete box lesion in all three cases. At 2-year follow-up, two out of three patients had recurrence of atrial arrhythmias. Invasive electro-anatomical mapping confirmed persistence of the box lesion, and the mechanism of arrhythmia recurrence in both patients was unrelated to posterior left atrium or the pulmonary veins. The third patient has been without arrhythmia symptoms since the ablation procedure. A 3D late gadolinium enhancement (LGE) magnetic resonance imaging (MRI) illustrates the ablation scar non-invasively in two cases. Discussion Thoracoscopic biparietal RF AF ablation with the Medtronic Cardioblate Gemini-S Irrigated RF Surgical Ablation System results in permanent transmural scar formation, irrespective of the stage of atrial remodelling, as shown in this small population by means of multimodality scar evaluation.

Atrial Fibrosis, Ischaemic Stroke and Atrial Fibrillation

Atrial fibrosis is an important component of the arrhythmic substrate in AF. Evidence suggests that atrial fibrosis also plays a role in increasing the risk of stroke in patients with the arrhythmia. Patients with embolic stroke of undetermined source (ESUS), who are suspected to have AF but are rarely shown to have it, frequently demonstrate evidence of atrial fibrosis; measured using late-gadolinium enhancement MRI, this manifests as atrial remodelling encompassing structural, functional and electrical properties. In this review, the authors discuss the available evidence linking atrial disease, including fibrosis, with the risk of ischaemic stroke in AF, as well as in the ESUS population, in whom it has been linked to recurrent stroke and new-onset AF. They also discuss the implications of this association on future research that may elucidate the mechanism of stroke and stroke prevention strategies in the AF and ESUS populations.

New Strategies for the Treatment of Atrial Fibrillation

Atrial fibrillation (AF) is the most prevalent cardiac arrhythmia in the clinical practice. It significantly contributes to the morbidity and mortality of the elderly population. Over the past 25–30 years intense effort in basic research has advanced the understanding of the relationship between the pathophysiology of AF and atrial remodelling. Nowadays it is clear that the various forms of atrial remodelling (electrical, contractile and structural) play crucial role in initiating and maintaining the persistent and permanent types of AF. Unlike in ventricular fibrillation, in AF rapid ectopic firing originating from pulmonary veins and re-entry mechanism may induce and maintain (due to atrial remodelling) this complex cardiac arrhythmia. The present review presents and discusses in detail the latest knowledge on the role of remodelling in AF. Special attention is paid to novel concepts and pharmacological targets presumably relevant to the drug treatment of atrial fibrillation.

A case report: cardiac dysphagia — a ghost of the past?

Background Rheumatic heart disease has become rare in developed countries and physicians have grown unfamiliar with the disease and its clinical course. The mitral valve is most commonly affected leading to mitral regurgitation and/or stenosis. The chronic volume and/or pressure overload leads to atrial remodelling and enlargement, driving the development of atrial fibrillation and thromboembolic events. Case Summary A 87-year-old patient with a history of rheumatic mitral stenosis and mitral valve replacement was admitted to the neurology department for vertigo. A stroke was suspected and she underwent a transoesophageal echocardiogram which was complicated by dysphagia. Oesophageal manometry and CT revealed oesophagogastric junction outflow obstruction due to extrinsic compression by a giant left atrium. Discussion Dysphagia due to a giant left atrium is rare. Various diagnostic criteria exist and the prevalence thus depends on which criterium is used. It is mostly encountered in rheumatic mitral disease, although there are reports of non-rheumatic etiology. When the left atrium assumes giant proportions it can compress adjacent intrathoracic structures. Compression of the oesophagus can lead to dysphagia, as in our case. A transoesophageal echocardiogram in these cases is relatively contraindicated and should only be performed if there is considerable reason to believe that it may change patient management.

Implications of SGLT Inhibition on Redox Signalling in Atrial Fibrillation

Atrial fibrillation (AF) is the most common sustained (atrial) arrhythmia, a considerable global health burden and often associated with heart failure. Perturbations of redox signalling in cardiomyocytes provide a cellular substrate for the manifestation and maintenance of atrial arrhythmias. Several clinical trials have shown that treatment with sodium-glucose linked transporter inhibitors (SGLTi) improves mortality and hospitalisation in heart failure patients independent of the presence of diabetes. Post hoc analysis of the DECLARE-TIMI 58 trial showed a 19% reduction in AF in patients with diabetes mellitus (hazard ratio, 0.81 (95% confidence interval: 0.68–0.95), n = 17.160) upon treatment with SGLTi, regardless of pre-existing AF or heart failure and independent from blood pressure or renal function. Accordingly, ongoing experimental work suggests that SGLTi not only positively impact heart failure but also counteract cellular ROS production in cardiomyocytes, thereby potentially altering atrial remodelling and reducing AF burden. In this article, we review recent studies investigating the effect of SGLTi on cellular processes closely interlinked with redox balance and their potential effects on the onset and progression of AF. Despite promising insight into SGLTi effect on Ca2+ cycling, Na+ balance, inflammatory and fibrotic signalling, mitochondrial function and energy balance and their potential effect on AF, the data are not yet conclusive and the importance of individual pathways for human AF remains to be established. Lastly, an overview of clinical studies investigating SGLTi in the context of AF is provided.

Ganoderma lucidum Polysaccharide Peptide Reduce Inflammation and Oxidative Stress in Patient with Atrial Fibrillation

BACKGROUND: Atrial fibrillation (AF) could be triggered by inflammation and oxidative stress. Ganoderma lucidum has an active substance in the form of β-glucan that can reduce inflammatory process and oxidative stress in rats. The objective of this study was to evaluate the effect of Ganoderma lucidum polysaccharide peptide (GLPP) in paroxysmal AF subjects with parameters of anti-inflammatory antioxidant, electrocardiography and health-related quality of life (HRQoL).METHODS: A randomized closed-label clinical trial with pre- and post-test design was conducted. After AF subjects selection, the subjects were randomized, interviewed and veni-punctured to isolate blood plasma. AF Subjects were then treated with placebo or GLPP for 90 days. Post-test blood plasma was collected on the following day after the 90th day. Then anti-inflammatory and antioxidant parameters were measured. After that, echocardiographic and HRQoL assessments were performed.RESULTS: A total of 38 subjects, 11 males and 27 females, completed the study with no significant changes in diets, physical activities, or medications. Comparing to control, the 90-days GLPP-treated subject characteristics were significant difference in systolic blood pressure, heart rate, malondialdehyde, high-sensitivity C-reactive protein, tumor necrosis factor-a, interleukin (IL)-1b, IL-6, primary (P)-wave dispersion, P-max, physical functioning, limitation to physical health, energy/fatigue, pain, and physical limitation.CONCLUSION: GLPP has several potential effects in AF subjects, including anti-inflammatory, antioxidant, and atrial remodelling, so that HRQoL of AF subjects could be improved. Hence, GLPP could suggested as a potential supplementing agent for AF management.KEYWORDS: atrial fibrillation, Ganoderma lucidum, inflammation, antioxidant, atrial remodelling, quality of life

Transcriptome and proteome mapping in the sheep atria reveal molecular features of atrial fibrillation progression

Aims Atrial fibrillation (AF) is a progressive cardiac arrhythmia that increases the risk of hospitalization and adverse cardiovascular events. There is a clear demand for more inclusive and large-scale approaches to understand the molecular drivers responsible for AF, as well as the fundamental mechanisms governing the transition from paroxysmal to persistent and permanent forms. In this study, we aimed to create a molecular map of AF and find the distinct molecular programs underlying cell type-specific atrial remodelling and AF progression. Methods and Results We used a sheep model of long-standing, tachypacing-induced AF, sampled right and left atrial tissue and isolated cardiomyocytes from control, intermediate (transition) and late time points during AF progression, and performed transcriptomic and proteome profiling. We have merged all these layers of information into a meaningful 3-component space in which we explored the genes and proteins detected and their common patterns of expression. Our data-driven analysis points at extracellular matrix remodelling, inflammation, ion channel, myofibril structure, mitochondrial complexes, chromatin remodelling, and genes related to neural function, as well as critical regulators of cell proliferation as hallmarks of AF progression. Most important, we prove that these changes occur at early transitional stages of the disease, but not at later stages, and that the left atrium undergoes significantly more profound changes than the right atrium in its expression program. The pattern of dynamic changes in gene and protein expression replicate the electrical and structural remodelling demonstrated previously in the sheep and in humans, and uncover novel mechanisms potentially relevant for disease treatment. Conclusions Transcriptomic and proteomic analysis of AF progression in a large animal model shows that significant changes occur at early stages, and that among others involve previously undescribed increase in mitochondria, changes to the chromatin of atrial cardiomyocytes, and genes related to neural function and cell proliferation. Translational Perspective We have generated a detailed molecular map of AF progression in a clinically relevant large-animal model. Such data would be very difficult if not impossible to obtain from patients. Our results provide a framework for a comprehensive molecular analysis of the disease, pointing to novel avenues of research toward identifying early events that can lead to therapeutically targets to prevent AF-induced atrial remodelling.

Atrial Tachycardias After Atrial Fibrillation Ablation: How to Manage?

With catheter ablation becoming effective for non-pharmacological management of AF, many cases of atrial tachycardia (AT) after AF ablation have been reported in the past decade. These arrhythmias are often symptomatic and respond poorly to medical therapy. Post-AF-ablation ATs can be classified into the following three categories: focal, macroreentrant and microreentrant ATs. Mapping these ATs is challenging because of atrial remodelling and its complex mechanisms, such as double ATs and multiple-loop ATs. High-density mapping can achieve precise identification of the circuits and critical isthmuses of ATs and improve the efficacy of catheter ablation. The purpose of this article is to review the mechanisms, mapping and ablation strategy, and outcome of ATs after AF ablation.