Catheter ablation in rate-controlled atrial fibrillation with severely reduced ejection fraction: intervention for irregularity-mediated cardiomyopathy.

Background: Recent evidence suggests atrial fibrillation (AF) causes cardiomyopathy due to remodeling driven by both irregular rate and rhythm. Atrial fibrillation (AF) ablation in patients with reduced ejection fraction (EF) ≤ 35% has been shown to improve EF and mortality. It is unknown whether the benefits of AF ablation among patients with reduced EF are affected by the degree of pre-ablation rate control.

Conduction velocity is reduced in the posterior wall of hypertrophic cardiomyopathy patients with normal bipolar voltage undergoing ablation for paroxysmal atrial fibrillation.

Objectives: We investigated characteristics of left atrial conduction in patients with HCM, paroxysmal AF and normal bipolar voltage.

Background: Patients with hypertrophic cardiomyopathy (HCM) exhibit abnormal cardiac tissue arrangement. The incidence of atrial fibrillation (AF) is increased fourfold in patients with HCM and confers a fourfold increased risk of death.

Comparison of combined substrate-based mapping techniques to identify critical sites for ventricular tachycardia ablation.

Background: Established electroanatomic mapping techniques for substrate mapping for ventricular tachycardia (VT) ablation includes voltage mapping, isochronal late activation mapping (ILAM), and fractionation mapping. Omnipolar mapping (Abbott Medical, Inc.) is a novel optimized bipolar electrogram creation technique with integrated local conduction velocity annotation.

Catheter ablation of atrioventricular nodal reentrant tachycardia with an irrigated contact-force sensing radiofrequency ablation catheter.

Introduction: Radiofrequency ablation (RFA) slow pathway modification for catheter ablation of atrioventricular nodal reentrant tachycardia (AVNRT) is traditionally performed using a 4-mm nonirrigated (NI) RF ablation catheter. Slow pathway modification using irrigated, contact-force sensing (ICFS) RFA catheters has been described in case reports, but the outcomes have not been systematically evaluated.

Methods: Acute procedural outcomes of 200 consecutive patients undergoing slow pathway modification for AVNRT were analyzed.

Elevated Left Atrial Volume Index Predicts Incident Atrial Fibrillation After Typical Right Atrial Flutter Ablation.

Purpose: Incident atrial fibrillation (AF) is common after cavotricuspid isthmus (CTI) dependent atrial flutter (AFL) ablation. Risk factors for the development of AF post ablation are not well understood. The purpose of this study was to identify patients undergoing CTI ablation for AFL most likely to develop AF.

Genetically engineered SCN5A mutant pig hearts exhibit conduction defects and arrhythmias.

SCN5A encodes the α subunit of the major cardiac sodium channel Na(V)1.5. Mutations in SCN5A are associated with conduction disease and ventricular fibrillation (VF); however, the mechanisms that link loss of sodium channel function to arrhythmic instability remain unresolved.

Spinal cord stimulation protects against atrial fibrillation induced by tachypacing.

Background: Spinal cord stimulation (SCS) has been shown to modulate atrial electrophysiology and confer protection against ischemia and ventricular arrhythmias in animal models.

Objective: To determine whether SCS reduces the susceptibility to atrial fibrillation (AF) induced by tachypacing (TP).

Methods: In 21 canines, upper thoracic SCS systems and custom cardiac pacing systems were implanted.

Spatiotemporal electrophysiological changes in a murine ablation model.

Aims: High recurrence rates after complex radiofrequency ablation procedures, such as for atrial fibrillation, remain a major clinical problem. Local electrophysiological changes that occur following cardiac ablation therapy are incompletely described in the literature. The purpose of this study was to determine whether alterations in conduction velocity, action potential duration (APD), and effective refractory period resolve dynamically following cardiac ablation.

Reversibility of PRKAG2 glycogen-storage cardiomyopathy and electrophysiological manifestations.

Background: PRKAG2 mutations cause glycogen-storage cardiomyopathy, ventricular preexcitation, and conduction system degeneration. A genetic approach that utilizes a binary inducible transgenic system was used to investigate the disease mechanism and to assess preventability and reversibility of disease features in a mouse model of glycogen-storage cardiomyopathy.

Methods And Results: Transgenic (Tg) mice expressing a human N488I PRKAG2 cDNA under control of the tetracycline-repressible alpha-myosin heavy chain promoter underwent echocardiography, ECG, and in vivo electrophysiology studies.

Gap junctions and propagation of the cardiac action potential.

Pacemaker cells in the heart generate periodic electrical signals that are conducted to the working myocardium via the specialized conduction system. Effective cell-to-cell communication is critical for rapid, uniform conduction of cardiac action potentials-- a prerequisite for effective, synchronized cardiac contraction. Local circuit currents form the basis of the depolarization wave front in the working myocardium.

Somatic events modify hypertrophic cardiomyopathy pathology and link hypertrophy to arrhythmia.

Sarcomere protein gene mutations cause hypertrophic cardiomyopathy (HCM), a disease with distinctive histopathology and increased susceptibility to cardiac arrhythmias and risk for sudden death. Myocyte disarray (disorganized cell-cell contact) and cardiac fibrosis, the prototypic but protean features of HCM histopathology, are presumed triggers for ventricular arrhythmias that precipitate sudden death events. To assess relationships between arrhythmias and HCM pathology without confounding human variables, such as genetic heterogeneity of disease-causing mutations, background genotypes, and lifestyles, we studied cardiac electrophysiology, hypertrophy, and histopathology in mice engineered to carry an HCM mutation.