Noninvasive Assessment of Atrial Fibrillation Complexity in Relation to Ablation Characteristics and Outcome

Background: The use of surface recordings to assess atrial fibrillation (AF) complexity is still limited in clinical practice. We propose a noninvasive tool to quantify AF complexity from body surface potential maps (BSPMs) that could be used to choose patients who are eligible for AF ablation and assess therapy impact.Methods: BSPMs (mean duration: 7 ± 4 s) were recorded with a 252-lead vest in 97 persistent AF patients (80 male, 64 ± 11 years, duration 9.6 ± 10.4 months) before undergoing catheter ablation. Baseline cycle length (CL) was measured in the left atrial appendage. The procedural endpoint was AF termination. The ablation strategy impact was defined in terms of number of regions ablated, radiofrequency delivery time to achieve AF termination, and acute outcome. The atrial fibrillatory wave signal extracted from BSPMs was divided in 0.5-s consecutive segments, each projected on a 3D subspace determined through principal component analysis (PCA) in the current frame. We introduced the nondipolar component index (NDI) that quantifies the fraction of energy retained after subtracting an equivalent PCA dipolar approximation of heart electrical activity. AF complexity was assessed by the NDI averaged over the entire recording and compared to ablation strategy.Results: AF terminated in 77 patients (79%), whose baseline AF CL was 177 ± 40 ms, whereas it was 157 ± 26 ms in patients with unsuccessful ablation outcome (p = 0.0586). Mean radiofrequency emission duration was 35 ± 21 min; 4 ± 2 regions were targeted. Long-lasting AF patients (≥12 months) exhibited higher complexity, with higher NDI values (≥12 months: 0.12 ± 0.04 vs. <12 months: 0.09 ± 0.03, p < 0.01) and short CLs (<160 ms: 0.12 ± 0.03 vs. between 160 and 180 ms: 0.10 ± 0.03 vs. >180 ms: 0.09 ± 0.03, p < 0.01). More organized AF as measured by lower NDI was associated with successful ablation outcome (termination: 0.10 ± 0.03 vs. no termination: 0.12 ± 0.04, p < 0.01), shorter procedures (<30 min: 0.09 ± 0.04 vs. ≥30 min: 0.11 ± 0.03, p < 0.001) and fewer ablation targets (<4: 0.09 ± 0.03 vs. ≥4: 0.11 ± 0.04, p < 0.01).Conclusions: AF complexity can be noninvasively quantified by PCA in BSPMs and correlates with ablation outcome and AF pathophysiology

Early Repolarization Syndrome: Diagnostic and Therapeutic Approach

An early repolarization pattern can be observed in 1% up to 13% of the overall population. Whereas, this pattern was associated with a benign outcome for many years, several more recent studies demonstrated an association between early repolarization and sudden cardiac death, so-called early repolarization syndrome. In early repolarization syndrome patients, current imbalances between epi- and endo-cardial layers result in dispersion of de- and repolarization. As a consequence, J waves or ST segment elevations can be observed on these patients' surface ECGs as manifestations of those current imbalances. Whereas, an early repolarization pattern is relatively frequently found on surface ECGs in the overall population, the majority of individuals presenting with an early repolarization pattern will remain asymptomatic and the isolated presence of an early repolarization pattern does not require further intervention. The mismatch between frequently found early repolarization patterns in the overall population, low incidences of sudden cardiac deaths related to early repolarization syndrome, but fatal, grave consequences in affected patients remains a clinical challenge. More precise tools for risk stratification and identification of this minority of patients, who will experience events, remain a clinical need. This review summarizes the epidemiologic, pathophysiologic and diagnostic background and presents therapeutic options of early repolarization syndrome

Atrial Fibrillation Mechanisms and Implications for Catheter Ablation

AF is a heterogeneous rhythm disorder that is related to a wide spectrum of etiologies and has broad clinical presentations. Mechanisms underlying AF are complex and remain incompletely understood despite extensive research. They associate interactions between triggers, substrate and modulators including ionic and anatomic remodeling, genetic predisposition and neuro-humoral contributors. The pulmonary veins play a key role in the pathogenesis of AF and their isolation is associated to high rates of AF freedom in patients with paroxysmal AF. However, ablation of persistent AF remains less effective, mainly limited by the difficulty to identify the sources sustaining AF. Many theories were advanced to explain the perpetuation of this form of AF, ranging from a single localized focal and reentrant source to diffuse bi-atrial multiple wavelets. Translating these mechanisms to the clinical practice remains challenging and limited by the spatio-temporal resolution of the mapping techniques. AF is driven by focal or reentrant activities that are initially clustered in a relatively limited atrial surface then disseminate everywhere in both atria. Evidence for structural remodeling, mainly represented by atrial fibrosis suggests that reentrant activities using anatomical substrate are the key mechanism sustaining AF. These reentries can be endocardial, epicardial, and intramural which makes them less accessible for mapping and for ablation. Subsequently, early interventions before irreversible remodeling are of major importance. Circumferential pulmonary vein isolation remains the cornerstone of the treatment of AF, regardless of the AF form and of the AF duration. No ablation strategy consistently demonstrated superiority to pulmonary vein isolation in preventing long term recurrences of atrial arrhythmias. Further research that allows accurate identification of the mechanisms underlying AF and efficient ablation should improve the results of PsAF ablation

Myotonic dystrophy type 1 mimics and exacerbates Brugada phenotype induced by Nav1.5 sodium channel loss of function mutation.

International audienceBACKGROUND: Myotonic dystrophy type 1 (DM1), a muscular dystrophy due to CTG-expansion in the DMPK gene, can cause cardiac conduction disorders and sudden death. These cardiac manifestations are similar to those observed in loss-of-function SCN5A mutations, which are also responsible for Brugada syndrome (BrS). OBJECTIVE: To investigate DM1 effects on the clinical expression of a loss-of-function SCN5A mutation causing BrS. METHODS: We performed complete clinical evaluation, including ajmaline test, in one family combining DM1 and BrS. We screened the known BrS susceptibility genes. We characterized an SCN5A mutation using whole-cell patch-clamp experiments associated to cell surface biotinylation. RESULTS: The proband, a 15-year old female, was a survivor of out-of-hospital cardiac arrest with ventricular fibrillation. She combined a DMPK CTG-expansion from the father's side and an SCN5A mutation (S910L) from the mother's side. S910L is a trafficking defective mutant inducing a dominant negative effect when transfected with wild-type Nav1.5. This loss-of-function SCN5A mutation caused a Brugada phenotype during the mother's ajmaline test. Surprisingly in the father, a DM1 patient without SCN5A mutation, ajmaline also unmasked a Brugada phenotype. Furthermore, association of both genetic abnormalities in the proband exacerbated the response to ajmaline with a massive conduction defect. CONCLUSIONS: Our study is the first to describe the deleterious effect of DM1 on the clinical expression of a loss-of-function SCN5A mutation and to show a provoked BrS phenotype in a DM1 patient. The modification of the electrocardiographic pattern by ajmaline supports the hypothesis of a link between DM1 and Nav1.5 loss-of-function

The Spectrum of Idiopathic Ventricular Fibrillation and J-Wave Syndromes: Novel Mapping Insights

KEY POINTS Idiopathic ventricular fibrillation (IVF) is defined as unexplained sudden cardiac death due to ven-tricular fibrillation (VF) without any identifiable structural or electrical cause after extensive investigations (no phenotype). Recent data show that the use of high-density electrophysiologic mapping may ultimately offer sub-clinical diagnoses of cardiac disease in about 90% of individuals with IVF. Two major conditions underlie the occurrence of VF: the presence of either depolarization abnormalities due to micro-structural myocardial alteration or Purkinje abnormalities manifesting as triggering ectopy or reentry in the peripheral network. J-wave syndromes are defined as a distinct electrocardiographic phenotype (slurring/notch) affecting the junction between the QRS complex and the ST segment in inferolateral leads. Recent data provide evidence for heterogeneous substrates, related to either delayed depolarization due to microstructural alterations or early repolarization abnormalities. IVF and J-wave syndromes are the result of a wide spectrum of pathophysiologic processes. The individual phenotypic characterization is essential given its implications in therapy, genetic testing, and risk stratification

Contact-force guided single-catheter approach for pulmonary vein isolation: Feasibility, outcomes, and cost-effectiveness

Background: For conventional ablation of paroxysmal atrial fibrillation (AF), an ablation catheter in conjunction with a circular mapping catheter (CMC) is typically used for pulmonary vein isolation (PVI). Objective: The purpose of this study was to evaluate an approach for PVI with a single contact-force (CF) ablation catheter in terms of procedural reliability, outcomes, and cost-effectiveness. Methods: One hundred consecutive patients with paroxysmal AF were included in the study. Fifty patients (study group) underwent a CF-guided single-catheter approach, whereby PVI was demonstrated when sequential pacing at 9 equidistant points within the lesion set (carina included) failed to capture the left atrium. For confirmation, PVI was verified with a CMC. In comparison, 50 patients (control group) underwent a conventional PVI ablation guided by a CMC. Results: Procedure time (101 ± 17 minutes vs 107 ± 15 minutes, P = .11), ablation time (24.2 ± 7.1 minutes vs 22.6 ± 8.8 minutes, P = .37), fluoroscopy time (5.6 ± 2.2 minutes vs 8.3 ± 3.4 minutes, P = .09), and applied CF (17.8 ± 2.6 g vs 18 ± 2.8 g, P = .72) did not reach statistical difference between the study and control groups. CF-guided single-catheter ablation achieved successful PVI in 98% of the study group and a 31% reduction in cost. At 1-year follow-up, sinus rhythm maintenance rate was similar in both groups (86% vs 84%, P = .78). Conclusion: In paroxysmal AF, a CF-guided single-catheter technique is an effective method for PVI, yielding substantial cost savings and clinical results similar to a conventional approach