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Aims Atrial septal defects (ASD) are associated with atrial arrhythmias, but the arrhythmia substrate in these patients is poorly defined. We hypothesized that bi-atrial fibrosis is present and that right atrial fibrosis is associated with atrial arrhythmias in ASD patients. We aimed to evaluate the extent of bi-atrial fibrosis in ASD patients and to investigate the relationships between bi-atrial fibrosis, atrial arrhythmias, shunt fraction, and age. Methods and results Patients with uncorrected secundum ASDs (n  = 36; 50.4 ± 13.6 years) underwent cardiac magnetic resonance imaging with atrial late gadolinium enhancement. Comparison was made to non-congenital heart disease patients (n  = 36; 60.3 ± 10.5 years) with paroxysmal atrial fibrillation (AF). Cardiac magnetic resonance parameters associated with atrial arrhythmias were identified and the relationship between bi-atrial structure, age, and shunt fraction studied. Bi-atrial fibrosis burden was greater in ASD patients than paroxysmal AF patients (20.7 ± 14% vs. 10.1 ± 8.6% and 14.8 ± 8.5% vs. 8.6 ± 6.1% for right and left atria respectively, P  = 0.001 for both). In ASD patients, right atrial fibrosis burden was greater in those with than without atrial arrhythmias (33.4 ± 18.7% vs. 16.8 ± 10.3%, P  = 0.034). On receiver operating characteristic analysis, a right atrial fibrosis burden of 32% had a 92% specificity and 71% sensitivity for predicting the presence of atrial arrhythmias. Neither age nor shunt fraction was associated with bi-atrial fibrosis burden. Conclusion Bi-atrial fibrosis burden is greater in ASD patients than non-congenital heart disease patients with paroxysmal AF. Right atrial fibrosis is associated with the presence of atrial arrhythmias in ASD patients. These findings highlight the importance of right atrial fibrosis to atrial arrhythmogenesis in ASD patients. [ABSTRACT FROM AUTHOR]

Objective: Local activation time (LAT) mapping of the atria is important for targeted treatment of atrial arrhythmias, but current methods do not interpolate on the atrial manifold and neglect uncertainties associated with LAT observations. In this paper, we describe novel methods to, first, quantify uncertainties in LAT arising from bipolar electrogram analysis and assignment of electrode recordings to the anatomical mesh, second, interpolate uncertain LAT measurements directly on left atrial manifolds to obtain complete probabilistic activation maps, and finally, interpolate LAT jointly across both the manifold and different S1–S2 pacing protocols. Methods: A modified center of mass approach was used to process bipolar electrograms, yielding a LAT estimate and error distribution from the electrogram morphology. An error distribution for assigning measurements to the anatomical mesh was estimated. Probabilistic LAT maps were produced by interpolating on a left atrial manifold using Gaussian Markov random fields, taking into account observation errors and characterizing LAT predictions by their mean and standard deviation. This approach was extended to interpolate across S1–S2 pacing protocols. Results: We evaluated our approach using recordings from three patients undergoing atrial ablation. Cross-validation showed consistent and accurate prediction of LAT observations both at different locations on the left atrium and for different S1–S2 intervals. Significance: Interpolation of scalar and vector fields across anatomical structures from point measurements is a challenging problem in biomedical engineering, compounded by uncertainties in measurements and meshes. New methods and approaches are required, and in this paper, we have demonstrated an effective method for probabilistic interpolation of uncertain LAT. [ABSTRACT FROM AUTHOR]

Aims: Local activation time (LAT) mapping forms the cornerstone of atrial tachycardia diagnosis. Although anatomic and positional accuracy of electroanatomic mapping (EAM) systems have been validated, the effect of electrode sampling density on LAT map reconstruction is not known. Here, we study the effect of chamber geometry and activation complexity on optimal LAT sampling density using a combined in silico and in vivo approach.Methods and results: In vivo 21 atrial tachycardia maps were studied in three groups: (1) focal activation, (2) macro-re-entry, and (3) localized re-entry. In silico activation was simulated on a 4×4cm atrial monolayer, sampled randomly at 0.25-10 points/cm2 and used to re-interpolate LAT maps. Activation patterns were studied in the geometrically simple porcine right atrium (RA) and complex human left atrium (LA). Activation complexity was introduced into the porcine RA by incomplete inter-caval linear ablation. In all cases, optimal sampling density was defined as the highest density resulting in minimal further error reduction in the re-interpolated maps. Optimal sampling densities for LA tachycardias were 0.67 ± 0.17 points/cm2 (focal activation), 1.05 ± 0.32 points/cm2 (macro-re-entry) and 1.23 ± 0.26 points/cm2 (localized re-entry), P = 0.0031. Increasing activation complexity was associated with increased optimal sampling density both in silico (focal activation 1.09 ± 0.14 points/cm2; re-entry 1.44 ± 0.49 points/cm2; spiral-wave 1.50 ± 0.34 points/cm2, P < 0.0001) and in vivo (porcine RA pre-ablation 0.45 ± 0.13 vs. post-ablation 0.78 ± 0.17 points/cm2, P = 0.0008). Increasing chamber geometry was also associated with increased optimal sampling density (0.61 ± 0.22 points/cm2 vs. 1.0 ± 0.34 points/cm2, P = 0.0015).Conclusion: Optimal sampling densities can be identified to maximize diagnostic yield of LAT maps. Greater sampling density is required to correctly reveal complex activation and represent activation across complex geometries. Overall, the optimal sampling density for LAT map interpolation defined in this study was ∼1.0-1.5 points/cm2. [ABSTRACT FROM AUTHOR]

The article discusses a study which investigated the hypothesis that acute pulmonary vein isolation (PVI) results from a combination of irreversible and reversible atrial injury. The study used cardiac magnetic resonance imaging (CMRI) after radiofrequency ablation and involved 25 paroxysmal atrial fibrillation (AF) patients. The study found the higher T2 signal on acute scans. Greater decline in delayed enhancement (DE) on chronic imaging in patients with recurrences is also observed.

Introduction: A patent foramen ovale (PFO) is located at the anterior and superior part of the anatomical interatrial septum, the area that is targeted during transseptal puncture. This study sought to investigate the impact of accessing the left atrium via a PFO on paroxysmal AF ablation. Methods: From March 2004, 203 patients (55 ± 11 years) underwent catheter ablation for paroxysmal AF (80 ± 71 months), with the endpoint being electrical isolation of all pulmonary veins (PV) and AF noninducibility. The presence of a PFO was determined by both transesophageal echocardiography and catheter probing. Procedural difficulty was evaluated by radiofrequency (RF), procedural, and fluoroscopic durations. Clinical follow-up was also investigated. Results: A PFO was detected in 27 patients (13%) by transesophageal echocardiography and in 22 additional patients (total 49 patients, 24%), by catheter probing (P < 0.001). A PFO was associated with longer total RF applications (57 ± 19 vs 51 ± 18 min, P = 0.04) and RF applications to isolate the PVs (42 ± 16 vs 35 ± 12 min, P = 0.001). Procedural and fluoroscopic times were unaffected. Seventy-three patients (36%) required a second procedure; there was no difference in the number of PV reconnections (1.3 vs 1.8 veins, P = NS). After a mean follow-up of 19 ± 9 months, 194/203 patients (96%) were free of AF, with no difference in patients in whom a PFO had been used. Conclusion: Although isolation of PVs is longer, overall procedural duration and success is not affected when using a PFO compared with a transseptal puncture. The presence of a PFO is underestimated by transesophageal echocardiography with brachial injection when compared with catheter probing. [ABSTRACT FROM AUTHOR]

Objectives: This study evaluated the impact of catheter ablation of the coronary sinus (CS) region during paroxysmal and persistent atrial fibrillation (AF). Background: The CS musculature and connections have been implicated in the genesis of atrial arrhythmias. Methods: Forty-five patients undergoing catheter ablation of AF were studied. The CS was targeted if AF persisted after ablation of pulmonary veins and selected left atrial tissue. CS ablation was commenced endocardially by dragging along the inferior paramitral left atrium. Ablation was continued from within the vessel (epicardial) if CS electrograms had cycle lengths shorter than that of the left atrial appendage. RF energy was limited to 35 W endocardially and 25 W epicardially. The impact of ablation was evaluated on CS electrogram cycle length (CSCL) and activation sequence, atrial fibrillatory cycle length measured in the left atrial appendage (AFCL) and on perpetuation of AF. Results: Endocardial ablation significantly prolonged CSCL by 17 ± 5 msec and organized the CS activation sequence (from 13% of patients before to 51% after ablation); subsequent epicardial ablation further increased local CSCL by 32 ± 27 msec (P < 0.001). AFCL prolonged significantly both during endocardial and epicardial ablation (median: 152 to 167 msec P = 0.03) and was associated with AF termination in 16 (35%) patients (46% of paroxysmal and 30% of persistent AF). AFCL prolongation ≥5 msec and/or AF termination was associated with more rapid activity in the CS region originally: P ≤ 0.04. Conclusion: Catheter ablation targeting both the endocardial and epicardial aspects of the CS region significantly prolongs fibrillatory cycle length and terminates AF persisting after PV isolation in 35% of patients. [ABSTRACT FROM AUTHOR]

Background: Left atrial (LA) linear lesions are effective in substrate modification for atrial fibrillation (AF). However, achievement of complete conduction block remains challenging and conduction recovery is commonly observed. The aim of the study was to investigate the localization of gap sites of recovered LA linear lesions. Methods and Results: Forty-eight patients with paroxysmal (n = 26) and persistent/permanent (n = 22) AF underwent repeat ablation after pulmonary vein (PV) isolation and LA linear ablation at the LA roof and/or mitral isthmus due to recurrences of AF or flutter. In 35 patients, conduction through the mitral isthmus line (ML) had recovered whereas roof-line recovery was observed in 30 patients. The gaps within the ML were distributed to the junction between left inferior PV and left atrial appendage in 66%, the middle part of the ML in 20%, and in 8% to the endocardial aspect of the ML while only 6% of lines showed an epicardial site of recovery. The RL predominantly recovered close to the right superior PV (54%) and less frequently in the mid roof or close to the left PV (both 23%). Reablation of lines required significantly shorter RF durations (ML: 7.24 ± 5.55 minutes vs 24.08 ± 9.38 minutes, RL: 4.24 ± 2.34 minutes vs 11.54 ± 6.49 minutes; P = 0.0001). Patients with persistent/permanent AF demonstrated a significantly longer conduction delay circumventing the complete lines than patients with paroxysmal AF (228 ± 77 ms vs 164 ± 36 ms, P = 0.001). Conclusions: Gaps in recovered LA lines were predominantly located close to the PVs where catheter stability is often difficult to achieve. Shorter RF durations are required for reablation of recovered linear lesions. Conduction times around complete LA lines are significantly longer in patients with persistent/permanent AF as compared to patients with paroxysmal AF. [ABSTRACT FROM AUTHOR]

The article presents a medical case of a 62-year-old man who developed atrial arrhythmia following first atrial fibrillation (AF) ablation, which carried for five years persistent for at least five months. At electrophysiological study, ablation was performed during AF with amiodarone continued to the time of the procedure. Two days after the ablation, he developed an atrial arrhythmia, which was considered as AF with relatively organized atrial activity in V1.

The article presents a case of a 38-year-old patient with documented pre-excited atrial fibrillation (AF). The patient was injected with adenosine following ablation. It is stated that the noncontact virtual electrogram data showed fractionation throughout the atrium during the phase of ultra rapid activity.

Atrial arrhythmias are common in patients with atrial septal defects (ASD) but the effects of percutaneous closure on atrial arrhythmia prevalence is unclear. We investigated the effects of ASD device closure and the impact of age at time of closure on prevalent atrial arrythmia. Meta-analysis of studies reporting atrial arrhythmia prevalence in adult patients before and after percutaneous closure was performed. Primary outcomes were prevalence of 'all atrial arrhythmia' and atrial fibrillation alone post closure. Sub-group analysis examined the effects of closure according to age in patients; <40 years, ≥40 and ≥ 60 years. 25 studies were included. Meta-analysis of all studies demonstrated no reduction in all atrial arrhythmia or atrial fibrillation prevalence post-closure (OR 0.855, 95% CI 0.672 to 1.087, P =.201 and OR 0.818, 95% CI 0.645 to 1.038, P =.099, respectively). A weak reduction in all atrial arrhythmia and atrial fibrillation was seen in patients ≥40 years (OR 0.77, 95% CI 0.616 to 0.979, P =.032 and OR 0.760, 95% CI 0.6 to 0.964, P =.024, respectively) but not ≥60 years (OR 0.822, 95% CI 0.593 to 1.141, P =.242 and OR 0.83, 95% CI 0.598 to 1.152, P =.266, respectively). No data were available in patients <40 years. This, and other limitations, prevents conclusive assessment of the effect of age on arrhythmia prevalence. Overall, percutaneous ASD closure is not associated with a reduction in atrial arrhythmia prevalence in this meta-analysis. A weak benefit is seen in patients ≥40 years of age, not present in patients ≥60 years. • Atrial arrhythmias are common in adults with atrial septal defects. • The effect of percutaneous ASD closure on atrial arrhythmia prevalence is unclear. • This meta-analysis showed no effect on atrial arrhythmias with device closure. • A weak beneficial effect was seen in those ≥40 years, but not in those ≥60 years. • Atrial ablation at time of closure may be of benefit in selected patients. [ABSTRACT FROM AUTHOR]