Background —The purpose of the present study was to determine the role of a novel, noncontact mapping system for assessing a variety of atrial reentrant tachycardias (ART) in patients after the surgical correction of congenital heart disease. Methods and Results —In 14 patients, an electrophysiological study using the Ensite 3000 system was performed to assess ARTs resistant to medical treatment. Sixteen different forms of ART were inducible in the 14 patients studied. The reentrant circuit of all ARTs could be characterized and localized with respect to anatomic landmarks such as atriotomy scars, intraatrial patches/baffles, and cardiac structures. In 15 of the 16 ARTs (in 13 of the 14 patients), a target area of the reentrant circuit for radiofrequency current application (ie, an area of conduction between 2 anatomical obstacles such as surgical barriers and cardiac structures of electrical isolation) could be localized within the systemic venous atrium. Nine patients exhibited macroreentry, and 4 showed microreentry. In 12 patients, ART could be terminated by creating linear radiofrequency current lesions (75°C, 180 to 390 s). Completeness of linear lesions after radiofrequency current delivery was proven by analyzing color-coded isopotential maps of atrial activation while applying atrial pacing techniques. The mean duration of the procedures was 286 minutes (range, 130 to 435 minutes); fluoroscopy time ranged from 7 to 33.8 minutes (mean, 17.4 minutes). Conclusions —In patients with ART after the surgical correction of congenital heart disease, the use of the noncontact mapping system allows for characterization of the tachycardia and guidance for effective radiofrequency current delivery.

Background Left cardiac sympathetic denervation (LCSD) may be a therapeutic adjunct for young patients with catecholaminergic polymorphic ventricular tachycardia (CPVT) and long QT syndrome (LQTS) who are not fully protected by beta-blockade. Objective The objective of this analysis was to report our institutional experience with LSCD in young patients for the management of life-threatening ventricular arrhythmias in CPVT and LQTS. Methods Ten young patients with CPVT and LQTS underwent transaxillary LSCD at our institution. Mean age at surgery was 14.0 (range 3.9–42) years, mean body weight was 45.7 (range 15.5–90) kg. Five patients had the clinical diagnosis of CPVT, three were genotype positive for a mutation in the ryanodine-receptor-2-gene. Four of five LQTS patients were genotype positive. Indications for LCSD were recurrent syncope, symptomatic episodes of ventricular tachycardias and/or internal cardioverter–defibrillator (ICD) discharges, and aborted cardiac arrest despite high doses of beta-blockers. Results LCSD was performed via the transaxillary approach. No significant complications were observed. Two patients already had an ICD, 6 patients received an ICD at the same operation or shortly thereafter. Median length of follow-up after LCSD was 2.3 (range 0.6–3.9) years. After LCSD a marked reduction in arrhythmia burden and cardiac events was observed in all patients while medication was continued. None of the patients had any further ICD discharge for sustained VT. Conclusions After LCSD, arrhythmia burden could significantly be reduced in all our young patients with CPVT and LQTS.

Background— We sought to evaluate tissue reactions within and at the surface of devices for interventional therapy of septal defects and to identify antigen characteristics of neotissues. Methods and Results— Atrial or ventricular septal defect–occlusion devices (Amplatzer, n=7; Cardioseal/Starflex, n=3) were processed using a uniform protocol after surgical removal from humans (implantation time, 5 days to 4 years). Devices were fixed in formalin and embedded in methylmethacrylate. Serial sections were obtained by sectioning with a diamond cutter and grinding, thus saving the metal/tissue interface for histologic evaluation. Immunohistochemical staining was performed using conventional protocols. Superficial endothelial cells stained positive for von Willebrand factor. Within the newly formed tissues, fibroblast-like cells were identified with a time-dependent expression of smooth muscle cell maturation markers (smooth muscle actin, smooth muscle myosin, h-caldesmon, and desmin) beside extracellular matrix components. Neovascularization of the newly formed tissues was demonstrated with the typical immunohistochemical pattern of capillaries and small vessels. Inflammatory cells could be identified as macrophages (CD68+) and both T-type and B-type lymphocytes (CD3+, CD79+). Conclusions— This is the first presentation of results from serial immunohistochemical staining of a collection of explanted human septal-occlusion devices. A time-dependent maturation pattern of the fibroblast-like cells in the neotissues around the implants could be described. Neoendothelialization was seen in all specimens with implantation times of 10 weeks or more. The time course of neoendothelialization, as seen in our study, further supports the clinical practice of anticoagulant or antiplatelet therapy for 6 months after implantation. This time interval should be sufficient to prevent thromboembolic events due to thrombus formation at the foreign surface of cardiovascular implants.