Confirmation of novel noninvasive high-density electrocardiographic mapping with electrophysiology study: implications for therapy.

BACKGROUND: Twelve lead ECGs have limited value in precisely identifying atrial and ventricular activation during arrhythmias, including accessory atrioventricular conduction activation. The aim of this study was to report a single center's clinical experience validating a novel, noninvasive, whole heart, beat-by-beat, 3-dimensional mapping technology with invasive electrophysiological studies, including ablation, where applicable. METHODS AND RESULTS: Using an electrocardiographic mapping (ECM) system in 27 patients, 3-dimensional epicardial activation maps were generated from >250 body surface ECGs using heart-torso geometry obtained from computed tomographic images. ECM activation maps were compared with clinical diagnoses, and confirmed with standard invasive electrophysiological studies mapping. (1) In 6 cases of Wolff-Parkinson-White syndrome, ECM accurately identified the ventricular insertion site of an accessory atrioventricular connection. (2) In 10 patients with premature ventricular complexes, ECM accurately identified their ventricular site of origin in 8 patients. In 2 of 10 patients transient premature ventricular complex suppression was observed during ablation at the site predicted by ECM as the earliest. (3) In 10 cases of atrial tachycardia/atrial flutter, ECM accurately identified the chamber of origin in all 10, and distinguished isthmus from nonisthmus dependent atrial flutter. (4) In 1 patient with sustained exercise induced ventricular tachycardia, ECM accurately identified the focal origin in the left ventricular outflow tract. CONCLUSIONS: ECM successfully provided valid activation sequence maps obtained noninvasively in a variety of rhythm disorders that correlated well with invasive electrophysiological studies.

Azd7009: a new antiarrhythmic drug with predominant effects on the atria effectively terminates and prevents reinduction of atrial fibrillation and flutter in the sterile pericarditis model.

INTRODUCTION: We tested the hypothesis that AZD7009 terminates induced atrial fibrillation (AF) and flutter (AFL) and prevents their reinduction, and that effects on refractoriness, conduction, and excitability are predominantly on the atria. METHODS AND RESULTS: Thirty-eight electrophysiologic studies were performed during AZD7009 infusion in 11 dogs with sterile pericarditis. The effects of AZD7009 on refractoriness, conduction, and capture threshold were studied and its antiarrhythmic efficacy tested. Simultaneous multisite biatrial mapping was performed in 7 dogs to assess arrhythmia termination. AZD7009 prolonged arrhythmia cycle length (CL) from 121 +/- 7.8 to 157 +/- 9.7 msec (P < 0.001) before terminating 23 of 23 AF/AFL episodes. Mapping demonstrated that AF/AFL CL prolonged and then terminated in area(s) of slow conduction in a reentrant circuit. Arrhythmia reinduction failed in 19 of 20 attempts. At 400-msec CL, atrial and ventricular refractoriness and QT interval increased 33%, 17% (P < 0.001 vs atrial refractoriness), and 9%, respectively. Atrial capture threshold increased in a CL-dependent manner: 1.8 +/- 0.3 to 2.2 +/- 0.3 mA (CL 400 msec); 2.1 +/- 0.3 to 2.8 +/- 0.5 mA (CL 300 msec), and 2.2 +/- 0.3 to 5.3 +/- 0.8 mA (CL 200 msec). Only minor nonsignificant changes occurred in the ventricles: 0.95 +/- 0.05 to 0.98 +/- 0.06 mA (CL 400 msec), and 1.14 +/- 0.12 to 1.16 +/- 0.13 mA (CL 333 msec). Atrial conduction time increased 8 +/- 1.4 msec (CL 400 msec), 8.3 +/- 1.5 msec (CL 300 msec), and 13.2 +/- 1.6 msec (CL 200 msec, all P < 0.001), but ventricular conduction time was unchanged. CONCLUSION: AZD7009 is highly efficacious in terminating AF/AFL and preventing reinduction in this model. It exhibits marked effects on atrial electrophysiology but has only modest effects on the ventricle.