To avoid atrioventricular node-His bundle ablation, catheter ablation of the atrial myocardium was attempted in eight patients with drug refractory type I atrial flutter. In seven of eight patients, a zone of prolongation and fragmentation of the endocardial electrogram was found in the low posterior part of the right atrium. Entrainment of the atrial flutter by high right atrial pacing was accompanied by local recording of second-degree regional block in several atrial sectors but never in the low septal area. We, therefore, hypothesized that the latter represented the critical slow conduction zone of the reentrant flutter circuit. One or two cathodal DC shocks were locally delivered without immediate or late complications. One single ablation attempt was performed in five patients, whereas three patients underwent a second attempt because of early flutter recurrence. Patients were initially discharged without (and after a second session with) antiarrhythmic drugs. After a mean follow-up of 15.5 months (range, 10-23 months), five patients are free of arrhythmias without antiarrhythmic drug therapy. Two patients did not experience atrial arrhythmias while on a drug regimen that was previously found to be ineffective, and a third patient had flutter recurrences. This study suggests that patients with type I atrial flutter referred for atrioventricular node-His bundle ablation may be successfully managed by delivering the ablative shock directly on the atrial arrhythmia substrate. (Circulation 1990;81:762-771) T he goals of therapy in human atrial flutter are to restore sinus rhythm and prevent tachycardia recurrences. While the former is usually achieved, the latter is often difficult to obtain despite numerous antiarrhythmic drug trials, pacing therapy, and recently, direct atrial surgery.' This is the reason See p 1142 why recurrent atrial flutter, along with atrial fibrillation, accounts for as much as 60% of the indications for His bundle ablation.2 The chief drawback of this procedure is the development of pacemaker dependency, which may be undesirable in young and otherwise healthy patients. After the early work of Puech in the late 1950s,3 recent studies have confirmed that type I atrial flutter is a reentrant arrhythmia that is confined to the right atrium.4-6 In almost all patients, endocardial mapping during tachycardia allows recording of low voltage prolonged and fragmented potentials in the area of the low posterior right atrial septum, which is suspected as being the critical slow conduction area of the reentrant From the Hopital cardiovasculaire et pneumologique Louis,

SUMMARY Electrophysiologic studies were performed in three patients suffering from attacks of paroxysmal tachycardia with wide QRS complexes. Two patients had atrioventricular dissociation. The arrhythmia could be initiated and terminated by premature ventricular stimulation in all three patients. One patient developed the arrhythmia after rapid atrial stimulation. In each subject, the QRS complexes during tachycardia were identical to recorded supraventricular beats (left bundle branch block pattern in two cases and right bundle branch block pattern in one). A His bundle potential was noted before the QRS complex; the HV interval was equal to or longer than that of the sinus beats. The following observations suggested the presence of a bundle branch reentry mechanism: (1) the relationship between bundle branch block development and tachycardia initiation; (2) the occurrence of tachycardia after electrically induced His-Purkinje reentry; (3) the ability of premature ventricular stimulation during tachycardia to advance the timing of the His deflection and QRS complex, with an unchanged or slightly increased HV interval; and (4) the termination of arrhythmia by premature ventricular depolarization blocked within the bundle branch system. Our results support the idea that bundle branch reentry can play a role in the genesis of ventricular tachycardia.MOST paroxysmal tachycardias, both supraventricular and ventricular, are considered reentrant arrhythmias because they can be reproducibly initiated and terminated by programmed stimulation. Although the site of reentry has been established for most cases of paroxysmal supraventricular tachycardia,' 8 the site of reentry in ventricular tachycardia is not well defined. In patients with coronary artery disease, some ventricular tachycardias have been ascribed to reentry within the ischemic zone.9-'2 Only infrequent reports have suggested the involvement of the His bundle and its branches'0 13-16 in the reentrant circuit of ventricular tachycardia, but these cases have not eliminated doubts about the obligatory incorporation of the proximal His-Purkinje system in the tachycardias. We report three patients with ventricular tachycardia in whom electrophysiologic data strongly support a bundle branch reentry mechanism. made on an eight-channel, direct-writing, ink-jet recorder (Elema, Mingograph 81) at a paper speed of 100-200 mm/sec. Standard techniques of programmed atrial and ventricular stimulation (Janssen) were used.'8 All data were stored on magnetic tape (Hewlett-Packard). Informed consent was obtained from each patient before the studies. Case Reports Case 1A 53-year-old man with aortic valve disease was admitted in October 1977 for recurrent episodes of tachycardia accompanied by faintness and chest pain. Digoxin and verapamil had been prescribed without any effect. The tachycardia was regular, with wide QRS complexes (0.15 second) showing a complete right bundle branch block pattern and left-axis deviation (QRS of -85°) ( fig. 1). Atrial activity was not clearly ...

A 66 year old man presented with multiple episodes of tachycardia. Some had QRS complexes with a right bundle branch block configuration identical to those of sinus beats. The onset of the tachycardia was preceded by premature His bundle depolarizations. There was a His potential before each QRS complex of the tachycardia. Atrial activity was dissociated. Occasionally the appearance of sinus beats with a left bundle branch block pattern announced a tachycardia with an identical configuration and atrioventricular dissociation. His bundle activity occurred before the QRS complex and was followed by a right bundle branch deflection. A reentrant mechanism within the bundle branch system was invoked. One 200 J shock was delivered through an electrode catheter to the site of the right bundle branch. The postprocedure course was uneventful (follow-up 10 months).

No abstract

The effects of amiodarone on the sinuatrial node were studied in 24 patients after an intravenous injection of the drug (5 mg/kg). Sinuatrial function was assessed by rapid atrial pacing and premature atrial stimulation. Sinus cycle length did not change significantly, but the corrected sinus node recovery time was prolonged. While there was no significant change in sinuatrial conduction time, prolongation of the non-reset zone in 14 cases, as well as the abolition of the platesu in 2/24 patients, suggested that conduction of the atrial responses to the sinus node might have been depressed.