Substrate-based catheter ablation in previously undiagnosed arrhythmogenic right ventricular dysplasia by means of an electroanatomic mapping system using cutaneous patches (original) (raw)
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Cardiac Electrophysiology Clinics, 2011
Catheter ablation for scar-related ventricular tachycardia (VT) in the postinfarction setting has become an established and effective therapy. The fact that the pathologic and electrophysiologic substrate for VT is uniquely subendocardial in this setting and the development of surgical subendocardial resection as a treatment that could be emulated percutaneously contributed to the modern evolution of VT ablation in ischemic cardiomyopathy. 2 In other contexts, including nonischemic dilated cardiomyopathy and arrhythmogenic cardiomyopathy (AC), the substrate for VT has been more difficult to locate, define, and ablate. In AC, the only available surgical therapy, right ventricular (RV) disconnection, could not provide definitive information regarding the mechanism of VT in these patients, and the current understanding of this has been derived largely from studies in the electrophysiology laboratory.
Europace, 2005
Background Ventricular tachycardia (VT) in arrhythmogenic right ventricular cardiomyopathy/dysplasia (ARVD) has been previously explored using entrainment mapping techniques but little is know about VT mechanisms and the characteristics of their circuits using an electroanatomical mapping system. Methods and results Three-dimensional electroanatomical mapping was performed in 11 patients with well tolerated sustained VT and ARVD. Sinus rhythm mapping of the right ventricle was performed in eight patients showing areas of low bipolar electrogram voltage (!1.2 mV). In total 12 tachycardias (mean cycle length 382 G 62 ms) were induced and mapped. Complete maps demonstrated a reentry mechanism in eight VTs and a focal activation pattern in four VTs. The reentrant circuits were localized around the tricuspid annulus (five VTs), around the right ventricular outflow tract (one VT) and on the RV free lateral wall (two VTs). The critical isthmus of each peritricuspid circuit was bounded by the tricuspid annulus with a low voltage area close to it. The isthmus of tachycardia originating from the right ventricular outflow tract (RVOT) was delineated by the tricuspid annulus with a low voltage area localized on the posterior wall of the RVOT. Each right ventricular free wall circuit showed an isthmus delineated by two parallel lines of block. Focal tachycardias originated on the right ventricular free wall. Linear radiofrequency ablation performed across the critical isthmus was successful in seven of eight reentrant tachycardias. The focal VTs were successfully ablated in
Cor et Vasa, 2013
Aims: This study analyzed the arrhythmogenic substrates and mechanisms of ventricular tachycardia (VT), and long-term outcomes of catheter ablation in patients with arrhythmogenic right ventricular cardiomyopathy/dysplasia (ARVC/D). Methods: Nine patients (1 female, 40717 years) with ARVC/D and sustained monomorphic VT (SMVT) exhibiting left bundle branch block morphology of the QRS complex were studied. The diagnosis of ARVC/D was confirmed by means of echocardiography, magnetic resonance imaging, and electroanatomic mapping in all patients. Results: The patients underwent 10 ablation procedures. At the initial ablation, the mean VT rate was 196721 (170-240) bpm. In total, 17 VT types were observed. One VT type with left axis (þI, aVL), or right axis (þII,III,aVF) of the QRS complex was present in 3 and 1 patient, respectively. Two VT types of left and intermediate (þI, II, aVL) axis or of left and right axis of the QRS complex were observed in 3 and 2 patients, respectively. Multiple VT types with left axis QRS complex recurred in 1 patient. One VT displayed characteristics of focal arrhythmia, the mechanism of remaining VTs was clearly macroreentrant. The critical slow-conducting isthmus of the reentry circuit was located at the infero-lateral aspect of tricuspid annulus and was bounded by the annulus and baso-lateral wall scar in 7 VTs; the isthmus was located within the scars in the remaining VTs. During 52731 (12-93) month follow-up since the last ablation, 8 (89%) patients remained free from any VT recurrence without antiarhythmic drug. Conclusions: Patients with ARVC/D frequently presented Z1 SMVT type. The critical isthmus of reentry circuit was dominantly located close to the tricuspid annulus. Longterm outcome of extensive endocardial ablation was favorable with isolated VT recurrences in one patient.
Journal of the American College of Cardiology, 2007
This study sought to evaluate the outcomes of radiofrequency catheter ablation (RFA) of ventricular tachycardia (VT) in arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C) patients. Particular focus was placed on defining the single-procedure efficacy over long-term follow-up. Background ARVD/C is an inherited cardiomyopathy characterized by VT and right ventricular dysfunction. Prior single-center studies have reported conflicting results concerning the efficacy of RFA of VT in ARVD/C patients. Methods The study population comprised 24 patients (age 36 Ϯ 9 years, 11 male), enrolled in the Johns Hopkins ARVD registry, who underwent 1 or more RFA procedures for treatment of VT. Patients were followed up for 32 Ϯ 36 months (range 1 day to 12 years). Recurrence was defined as the documentation of VT subsequent to the procedure. Results A total of 48 RFA procedures were performed using 3-dimensional electroanatomical (n ϭ 10) or conventional (n ϭ 38) mapping. Of these procedures, 22 (46%), 15 (31%), and 11 (23%) resulted in elimination of all inducible VTs, clinical VT but not all, and none of the inducible VTs, respectively. Forty (85%) procedures were followed by recurrence. The cumulative VT recurrence-free survival was 75%, 50%, and 25% after 1.5, 5, and 14 months, respectively. The cumulative VT recurrence-free survival did not differ by procedural success, mapping technique, or repetition of procedures. There was 1 procedure-related death. Conclusions Our study shows a high rate of recurrence in ARVD/C patients undergoing RFA of VT. This likely reflects the fact that ARVD/C is a diffuse cardiomyopathy with progressively evolving electrical substrate. Further studies are needed to define the precise role of RFA of VT in ARVD/C.
Ablation of Ventricular Arrhythmias in Arrhythmogenic Right Ventricular Dysplasia
Journal of Cardiovascular Electrophysiology, 2010
is a genetically determined myocardial disease characterized by fibrofatty replacement of the right ventricular wall. Ventricular tachyarrhythmias can be seen in the early stages of the disease, which is one of the most important causes of sudden death in young healthy individuals. Radiofrequency (RF) catheter ablation is an option for the treatment of medically refractory ventricular arrhythmias and it has shown to successfully abolish recurrent ventricular tachycardias (VT) as well as reduce the frequency in defibrillator therapies. However, variable acute and long-term success rates have been reported. The current mapping and ablation techniques include activation and entrainment mapping during tolerated VT and substrate ablation using 3-dimensional electroanatomic mapping systems. This article aims at providing a comprehensive review of RF catheter ablation of ventricular arrhythmias in the context of ARVD. (J Cardiovasc Electrophysiol, Vol. 21, pp. 473-486, April 2010) arrhythmogenic right ventricular dysplasia, right ventricular cardiomyopathy, ventricular tachycardia, catheter ablation
Heart Rhythm, 2011
BACKGROUND Most idiopathic right ventricular (RV) ventricular tachycardias (VTs) originate from the outflow tract. Data on VT from the lower body of the RV are limited. OBJECTIVE The purpose of this study was to describe a large experience with idiopathic VT detailing the prevalence and characteristics of VT arising from the body of the RV. METHODS The distribution of mapping confirmed VTs within the RV body, ECG characteristics, and results of radiofrequency (RF) ablation were analyzed. RESULTS Among 278 patients who underwent ablation for idiopathic VT or ventricular premature depolarizations (VPDs) arising from the RV, 29 (10%) had VT/VPDs from the lower RV body. Fourteen (48%) patients had VT/VPDs within 2 cm of the tricuspid valve annulus (TVA), 8 (28%) from the basal and 7 (24%) from the apical RV segments. Among the VT/VPDs from the TVA, 8 (57%) originated from the free wall and 6 (43%) from the septum. All but one RV basal or apical VT/VPDs originated from the free wall. All VT/VPDs had a left bundle branch block pattern. VT/VPDs from the free wall had longer QRS duration (P ϭ .0032) and deeper S wave in lead V 2 (P ϭ .042) and V 3 (P ϭ .046) than those from the septum. Apical VT/VPDs more often had precordial R wave transition ՆV 6 (P ϭ .0001) and smaller R wave in lead II (P ϭ .024) and S wave in lead aVR (P ϭ .001) compared to VT/VPDs from basal RV or TVA. RF catheter ablation eliminated VT/VPDs in 96% of patients. No complications were observed. During median follow-up of 27 months (range 4-131 months), 81% of patients had elimination of all symptomatic VT/VPDs. Nineteen percent had rare symptoms (8% without medications, 11% on beta-blocker). CONCLUSION Idiopathic VT/VPDs from the body of RV comprise an important subgroup of idiopathic RV VTs. Although most VTs originate from the RV free wall and nearly 50% from the TVA region, septal and more apical VTs are common. ECG characteristics distinguish free-wall versus septal and more apical origin of VTs, and RF catheter ablation provides good long-term arrhythmia control. KEYWORDS Catheter ablation; Idiopathic ventricular arrhythmia; Right ventricle; Ventricular premature depolarization; Ventricular tachycardia ABBREVIATIONS ARVC/D ϭ arrhythmogenic right ventricular cardiomyopathy/dysplasia; ECG ϭ electrocardiographic; EP ϭ electrophysiology; ICD ϭ implantable cardioverter-defibrillator; ICE ϭ intracardiac echocardiography; LBBB ϭ left bundle branch block; RBBB ϭ right bundle branch block; RF ϭ radiofrequency; RV ϭ right ventricle; RVOT ϭ right ventricular outflow tract; TVA ϭ tricuspid valve annulus; VPD ϭ ventricular premature depolarization; VT ϭ ventricular tachycardia