An Approach to Catheter Ablation of Cavotricuspid Isthmus Dependent Atrial Flutter

Much of our understanding of the mechanisms of macro re-entrant atrial tachycardia comes from study of cavotricuspid isthmus (CTI) dependent atrial flutter. In the majority of cases, the diagnosis can be made from simple analysis of the surface ECG. Endocardial mapping during tachycardia allows confirmation of the macro re-entrant circuit within the right atrium while, at the same time, permitting curative catheter ablation targeting the critical isthmus of tissue located between the tricuspid annulus and the inferior vena cava. The procedure is short, safe and by demonstration of an electrophysiological endpoint - bidirectional conduction block across the CTI - is associated with an excellent outcome following ablation. It is now fair to say that catheter ablation should be considered as a first line therapy for patients with documented CTI-dependent atrial flutter

Shortening of Fibrillatory Cycle Length in the Pulmonary Vein During Vagal Excitation

ObjectivesThe goal of the present prospective study is to evaluate the impact of vagal excitation on ongoing atrial fibrillation (AF) during pulmonary vein (PV) isolation.BackgroundThe role of vagal tone in maintenance of AF is controversial in humans.MethodsTwenty-five patients (18 with paroxysmal AF, 7 with chronic AF) were selected by occurrence of vagal excitation during AF (atrioventricular [AV] block: R-R interval >3 s) produced by PV isolation. Fibrillatory cycle length (CL) in the targeted PV and coronary sinus (CS) were determined before, during, and after vagal excitation. The CL was available at PV ostium during vagal excitation in 11 patients.ResultsForty-eight episodes of vagal excitation were observed. During vagal excitation, CL abruptly decreased both in CS and PV (CS, 164 ± 20 ms to 155 ± 23 ms, p < 0.0001; PV, 160 ± 22 ms to 143 ± 28 ms, p < 0.0001), and both returned to the baseline value with resumption of AV conduction. The decrease in PVCL occurred earlier (2.5 ± 1.5 s vs. 4.0 ± 2.6 s, p < 0.01) and was of greater magnitude than that in CSCL (16 ± 16 ms vs. 8 ± 9 ms, p < 0.01). A sequential gradient of CL was observed from PV to PV ostium and CS during vagal excitation (138 ± 29 ms, 149 ± 24 ms, and 159 ± 26 ms, respectively). The decrease in CL was significantly greater in paroxysmal than in chronic AF (CS, 11 ± 9 ms vs. 5 ± 7 ms, p < 0.05; PV, 23 ± 25 ms vs. 8 ± 14 ms, p < 0.05).ConclusionsVagal excitation is associated with shortening of fibrillatory CL. This occurs earlier in PV with a sequential gradient to PV ostium and CS, suggesting that vagal excitation enhances a driving role of PV

Genome-wide association analyses identify new Brugada syndrome risk loci and highlight a new mechanism of sodium channel regulation in disease susceptibility.

Brugada syndrome (BrS) is a cardiac arrhythmia disorder associated with sudden death in young adults. With the exception of SCN5A, encoding the cardiac sodium channel Na1.5, susceptibility genes remain largely unknown. Here we performed a genome-wide association meta-analysis comprising 2,820 unrelated cases with BrS and 10,001 controls, and identified 21 association signals at 12 loci (10 new). Single nucleotide polymorphism (SNP)-heritability estimates indicate a strong polygenic influence. Polygenic risk score analyses based on the 21 susceptibility variants demonstrate varying cumulative contribution of common risk alleles among different patient subgroups, as well as genetic associations with cardiac electrical traits and disorders in the general population. The predominance of cardiac transcription factor loci indicates that transcriptional regulation is a key feature of BrS pathogenesis. Furthermore, functional studies conducted on MAPRE2, encoding the microtubule plus-end binding protein EB2, point to microtubule-related trafficking effects on Na1.5 expression as a new underlying molecular mechanism. Taken together, these findings broaden our understanding of the genetic architecture of BrS and provide new insights into its molecular underpinnings

Predictive value of electrophysiologic studies during treatment of ventricular tachycardia with the beta-blocking agent nadolol

AbstractSixty patients with recurrent inducible sustained ventricular tachycardia were prospectively treated with nadotol (40 or 80 mg/day). Old myocardial infarction was present in 43 patients and dilated cardiomyopathy in 12. In group I (n = 36), nadolol was given alone, whereas in group II (n = 24), previously ineffective treatment with amiodarone was continued in combination with nadolol. Left ventricular ejection fraction was higher in patients in group I (0.40 ± 0.12) than in group II (0.30 ± 0.10, p < 0.01) patients. Electro-physiologic study was repeated after short-term treatment with nadolol, which was continued regardless of the results of this test, according to the scheme of the parallel approach.Recurrence of spontaneous tachycardia or sudden death occurred in 21 patients after 10 ± 9.2 months; sustained tachycardia was inducible in 19 on nadolol therapy. The remaining 39 patients (of whom 21 had inducible tachycardie while taking the drug) have had no recurrence of tachycardia after 27.8 ± 9.3 months of follow-up study. Sensitivity, specificity and predictive value of a positive and negative test were 90.5%, 46%, 47.5% and 90%, respectively. The results diner between group I and group II patients, the latter having a high percent of false positive responses. This difference is even more obvious with respect to left ventricular ejection fraction: the predictive value of a positive test was 86% when ejection fraction was >0.40 and 39% when it was < 0.40. A long (>400 ms) cycle length of the induced ventricular tachycardia seems more predictive of recurrence or sudden death (11 of 14 compared with 9 of 26 faster tachycardias, p < 0.01).Electrophysiologic studies are suitable for evaluation of the antiarrhythmic effect of a beta-blocker on the ventricular tachycardia substrate, with the same restrictions as for other drugs in patients with low left ventricular ejection fraction. A beta-blocker should be included in serial drug testing in patients with sustained ventricular tachycardia

Autocalibration algorithm in minute ventilation rate adaptive pacing

Chap. 21info:eu-repo/semantics/publishe

Techniques for curative treatment of atrial fibrillation

The definitive version is available at www.blackwell-synergy.comMélèze Hocini, Prashanthan Sanders, Pierre Jaîs, Li-Fern Hsu, Yoshihide Takahashi, Martin Rotter, Jacques Clémenty, Michel Haîssaguerr