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Clinical treatment of cardiac arrhythmia by radiofrequency ablation (RFA) currently lacks quantitative and precise visualization of lesion formation in the myocardium during the procedure. This study aims at evaluating thermal dose (TD) imaging obtained from real-time magnetic resonance (MR) thermometry on the heart as a relevant indicator of the thermal lesion extent. MR temperature mapping based on the Proton Resonance Frequency Shift (PRFS) method was performed at 1.5 T on the heart, with 4 to 5 slices acquired per heartbeat. Respiratory motion was compensated using navigator-based slice tracking. Residual in-plane motion and related magnetic susceptibility artifacts were corrected online. The standard deviation of temperature was measured on healthy volunteers (N = 5) in both ventricles. On animals, the MR-compatible catheter was positioned and visualized in the left ventricle (LV) using a bSSFP pulse sequence with active catheter tracking. Twelve MR-guided RFA were performed on three sheep in vivo at various locations in left ventricle (LV). The dimensions of the thermal lesions measured on thermal dose images, on 3D T1-weighted (T1-w) images acquired immediately after the ablation and at gross pathology were correlated. MR thermometry uncertainty was 1.5 °C on average over more than 96% of the pixels covering the left and right ventricles, on each volunteer. On animals, catheter repositioning in the LV with active slice tracking was successfully performed and each ablation could be monitored in real-time by MR thermometry and thermal dosimetry. Thermal lesion dimensions on TD maps were found to be highly correlated with those observed on post-ablation T1-w images (R = 0.87) that also correlated (R = 0.89) with measurements at gross pathology. Quantitative TD mapping from real-time rapid CMR thermometry during catheter-based RFA is feasible. It provides a direct assessment of the lesion extent in the myocardium with precision in the range of one millimeter. Real-time MR thermometry and thermal dosimetry may improve safety and efficacy of the RFA procedure by offering a reliable indicator of therapy outcome during the procedure.

Prevalence and prognostic value of conduction disturbances in patients with the Brugada syndrome (BrS) remains poorly known. Electrocardiograms (ECGs) from 325 patients with BrS (47 ± 13 years, 258 men) with spontaneous (n = 143) or drug-induced (n = 182) type 1 ECG were retrospectively reviewed. Two hundred twenty-six patients (70%) were asymptomatic, 73 patients (22%) presented with unexplained syncope, and 26 patients (8%) presented with sudden death or implantable cardioverter-defibrillator appropriated therapies at diagnosis or during a mean follow-up of 48 ± 34 months. P-wave duration of ≥120 ms was present in 129 patients (40%), first degree atrioventricular block (AVB) in 113 (35%), right bundle branch block (BBB) in 90 (28%), and fascicular block in 52 (16%). Increased P-wave duration, first degree AVB, and right BBB were more often present in patients after drug challenge than in patients with spontaneous type 1 ST elevation. Left BBB was present in 3 patients. SCN5A mutation carriers had longer P-wave duration and longer PR and HV intervals. In multivariate analysis, first degree AVB was independently associated with sudden death or implantable cardioverter-defibrillator appropriated therapies (odds ratio 2.41, 95% confidence interval 1.01 to 5.73, p = 0.046) together with the presence of syncope and spontaneous type 1 ST elevation. In conclusion, conduction disturbances are frequent and sometimes diffuse in patients with BrS. First degree AVB is independently linked to outcome and may be proposed to be used for individual risk stratification.

Purpose of Review Imaging plays a crucial role in the therapy of ventricular tachycardia (VT). We offer an overview of the different methods and provide information on their use in a clinical setting. Recent Findings The use of imaging in VT has progressed recently. Intracardiac echography facilitates catheter navigation and the targeting of moving intracardiac structures. Integration of pre-procedural CT or MRI allows for targeting the VT substrate, with major expected impact on VT ablation efficacy and efficiency. Advances in computational modeling may further enhance the performance of imaging, giving access to pre-operative simulation of VT. These advances in non-invasive diagnosis are increasingly being coupled with non-invasive approaches for therapy delivery. Summary This review highlights the latest research on the use of imaging in VT procedures. Image-based strategies are progressively shifting from using images as an adjunct tool to electrophysiological techniques, to an integration of imaging as a central element of the treatment strategy.

Currently, pulmonary vein isolation (PVI) is the gold standard in catheter ablation for atrial fibrillation (AF). However, PVI alone may be insufficient in the management of persistent AF, and complementary methods are being explored. One such method takes an anatomical approach—improving both its success rate and lesion durability may lead to improved treatment outcomes. An additional approach complementary to the anatomical one is also attracting attention, one that focuses on epicardial conduction. This involves ethanol ablation of the vein of Marshall (VOM) and can be very effective in blocking epicardial conduction related to Marshall structure; it is becoming incorporated into standard treatment. However, the pitfall of this “Marshall-PLAN”, a method that combines an anatomical approach with ethanol infusion within the VOM (Et-VOM), is that Et-VOM and other line creations are not always successfully completed. This has led to cases of AF and/or atrial tachycardia (AT) recurrence even after completing this lesion set. Investigating effective adjunctive methods will enable us to complete the lesion set with the aim to lower the rates of recurrence of AF and/or AT in the future.

Treatment options for atrial fibrillation (AF) have evolved from simple, fluoroscopy-guided pulmonary vein isolation for those patients with paroxysmal AF to complex, multi-modality procedures targeting not only anatomic structures but also electrophysiologic phenomena including complex fractionated electrograms, sites of dominant frequency and local non-venous drivers in patients with persistent and permanent AF. The stepwise ablation approach is a novel technique whereby structures contributing to initiation and maintenance of AF are sequentially targeted by radiofrequency ablation. Broadly divided into pulmonary veins, left atrial (LA) roof, left atrium (incorporating all anatomic regions of the chamber), mitral isthmus and non-LA structures, each region is targeted in sequence and the impact of ablation upon the global fibrillatory process assessed by measurement of AF cycle length (AFCL) at a site remote from the ablation target. In addition to pulmonary vein electrical disconnection and demonstrable complete conduction block across the roof and mitral isthmus lines (when performed), ablation is performed at those sites displaying continuous electrical and complex fractionated activity, with the endpoint of local organization, as well as at sites displaying electrograms consistent with focal sources driving AF. Ablation is accompanied by a cumulative increase in the AFCL prior to termination of AF by conversion either directly to sinus rhythm or to an atrial tachycardia which is then mapped conventionally and ablated. There is a ceiling of ablation within the LA beyond which further ablation is unlikely to result in a clinical benefit and should prompt evaluation of the contribution of the right atrium to maintenance of AF. The stepwise approach benefits from the integration of anatomic and electrophysiologic information to achieve a high level of success in termination of chronic AF by catheter ablation.

Early repolarization pattern (ERP) has recently been associated with idiopathic ventricular fibrillation and with cardiovascular mortality in the general population. We aimed to identify electrocardiographic tools to differentiate the “malignant” form of ERP from benign ERP in a population-based study. We retrospectively assessed the prevalence of ERP by recording electrocardiograms in 1,161 southwestern French subjects 35 to 64 years old. ERP was defined by an elevation of the J point ≥1 mm in 2 consecutive leads excluding leads V1 through V3. We categorized ERP as notching or slurring pattern as located in inferior and/or lateral leads and measured the J-point elevation amplitude. ST segment after ERP was categorized as ascendant or horizontal/nonascendant and T waves as negative or positive. Association of ERP with all-cause and cardiovascular mortalities was assessed by adjusted Cox proportional hazard models. ERP was found in 157 subjects (13.3%). During a mean follow-up of 14.2 ± 2 years, 77 subjects died (6.6%), of whom 24 (2.1%) died from cardiovascular causes. Subjects with ERP had an increased hazard ratios for all-cause mortality (2.45, 95% confidence interval [CI] 1.44 to 4.15, p = 0.001) and cardiovascular mortality (5.60, 95% CI 2.27 to 11.8, p = 0.001). The highest risk was found for notching ERP and ERP with a nonascendant/horizontal ST segment, yielding when associated increased hazard ratios of 3.84 (95% CI 2.14 to 6.92, p = 0.001) and 8.75 (95% CI 3.48 to 22.0, p = 0.001) for all-cause and cardiovascular mortalities, respectively. Conversely, a slurring ERP or ascendant ST segment was not associated with increased mortality. ERP localization, J-point elevation amplitude, or T-wave morphology did not distinguish benign from malignant forms of ERP. In conclusion, ERP with notching pattern and horizontal/descendant ST segments was associated with the highest risk of all-cause and cardiovascular deaths. These electrocardiographic patterns may be used for risk stratification in subjects with ERP.

In patients with heart failure, atrial fibrillation may exacerbate ventricular dysfunction and symptoms. In this study, catheter ablation was performed to restore sinus rhythm in patients with heart failure and refractory atrial fibrillation. The results show improvement in the left ventricular ejection fraction, symptoms, exercise capacity, and quality of life. Catheter ablation was performed to restore sinus rhythm in patients with heart failure and refractory atrial fibrillation. There was improvement in the ejection fraction, exercise capacity, and quality of life. Congestive heart failure and atrial fibrillation, the two “epidemics” of cardiovascular disease, 1 are major health problems. They often coexist, and the intersection of the two conditions creates a vicious circle, with congestive heart failure promoting the development of atrial fibrillation and vice versa. 2 , 3 In addition, each increases the morbidity and mortality associated with the other. 4 , 5 Among patients with congestive heart failure, maintaining sinus rhythm with the use of antiarrhythmic drugs is challenging, owing to the limited efficacy and potentially deleterious effects of the drugs. 6 – 10 This finding has led to renewed interest in rate control, stimulated by reports . . .

While pulmonary vein isolation for paroxysmal atrial fibrillation (AF) is highly effective, catheter ablation for persistent AF remains a challenge with varying clinical success reported. Several ablation techniques have been proposed to target persistent AF, with the additional ablation of complex fractionated electrograms and linear lesions shown to provide incremental success to pulmonary vein isolation alone. Recently, several studies have suggested the presence of localized drivers (re-entrant or focal) in AF. By targeting these drivers, clinical outcomes may be maintained while minimizing the extent of ablation. This article will focus on the conventional stepwise ablation approach for persistent AF versus driver-guided ablation with the use of newer mapping technologies.

SCN5A Mutations and the Role of Genetic Background in the Pathophysiology of Brugada Syndrome Vincent Probst, MD, PhD ; Arthur A.M. Wilde, MD, PhD ; Julien Barc, MS ; Frederic Sacher, MD ; Dominique Babuty, MD ; Philippe Mabo, MD ; Jacques Mansourati, MD ; Solena Le Scouarnec, PhD ; Florence Kyndt, PharmD, PhD ; Cedric Le Caignec, MD, PhD ; Pascale Guicheney, PhD ; Laetitia Gouas, PhD ; Juliette Albuisson, MD ; Paola G. Meregalli, MD ; Hervé Le Marec, MD, PhD ; Hanno L. Tan, MD, PhD and Jean-Jacques Schott, PhD From the INSERM (V.P., J.B., S.L.S., F.K., H.L.M., J.J.S.), UMR915; CNRS (V.P., J.B., S.L.S., F.K., H.L.M., J.J.S.), ERL3147; Université de Nantes (V.P., J.B., S.L.S., F.K., H.L.M., J.J.S.), l’institut du thorax; CHU Nantes (V.P., H.L.M., J.J.S.), l’institut du thorax, Service de cardiologie, Nantes, France; Department of Cardiology (A.A.M.W., P.G.M., H.L.T.), Academic Medical Center, University of Amsterdam, The Netherlands; Service de rythmologie (F.S.), Hôpital cardiologique du Haut Leveque, Bordeaux, France; Service de cardiologie B (D.B.), Hôpital Trousseau, Tours, France; Departement de cardiologie (P.M.), Hôpital Pontchaillou, Rennes, France; Service de cardiologie (J.M.), centre hospitalo-universitaire de Brest, Brest, France; Service de Génétique Médicale (F.K., C.L.C., J.A.), Institut de Biologie, CHU de Nantes, France; INSERM (P.G., L.G.), U582, Institut de Myologie, Paris, France; and AP-HP (P.G., L.G.), Groupe Hospitalier Pitié-Salpêtrière, Paris, France. Correspondence to Vincent Probst, MD, PhD, Service de cardiologie du CHU de Nantes, CHU de Nantes, Hôpital Nord, Bd Jacques Monod, 44093 Nantes Cedex, France. E-mail vincent.probst{at}chu-nantes.fr Received January 22, 2009; accepted July 14, 2009. Background— Mutations in SCN5A are identified in 20% to 30% of probands affected by Brugada syndrome (BrS). However, in familial studies, the relationship between SCN5A mutations and BrS remains poorly understood. The aim of this study was to investigate the association of SCN5A mutations and BrS in a group of large genotyped families. Methods and Results— Families were included if at least 5 family members were carriers of the SCN5A mutation, which was identified in the proband. Thirteen large families composed of 115 mutation carriers were studied. The signature type I ECG was present in 54 mutation carriers (BrS-ECG+; 47%). In 5 families, we found 8 individuals affected by BrS but with a negative genotype (mutation-negative BrS-ECG+). Among these 8 mutation-negative BrS-ECG+ individuals, 3, belonging to 3 different families, had a spontaneous type I ECG, whereas 5 had a type I ECG only after the administration of sodium channel blockers. One of these 8 individuals had also experienced syncope. Mutation carriers had, on average, longer PR and QRS intervals than noncarriers, demonstrating that these mutations exerted functional effects. Conclusions— Our results suggest that SCN5A mutations are not directly causal to the occurrence of a BrS-ECG+ and that genetic background may play a powerful role in the pathophysiology of BrS. These findings add further complexity to concepts regarding the causes of BrS, and are consistent with the emerging notion that the pathophysiology of BrS includes various elements beyond mutant sodium channels. Key Words: death, sudden (if surviving, use heart arrest) • Brugada syndrome • SCN5A • genetics • tachyarrhythmias • arrhythmia   CLINICAL PERSPECTIVE Drs Probst and Wilde contributed equally to this work. Related Article Nature’s Genetic Gradients and the Clinical Phenotype Ali J. Marian Circ Cardiovasc Genet 2009 2: 537-539. [Extract] [Full Text] [PDF]