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Background and Objective: Electrical defibrillation is very effective in interrupting atrial fibrillation (AF). However, its mechanism is not completely understood. We report our observations in patients subjected to external electriocardioversion (ECV) of atrial fibrillation and contrast them with recent theories about defibrillation mechanism. Methods: In 13 consecutive patients transthoracic electrical cardioversion for AF was performed during an electrophysiological study (11 monophasic -200–360 J- and 9 biphasic shocks -50–150 J-). About 10–16 electrograms were obtained with multipolar catheters recording right atrium, coronary sinus, and right pulmonary artery. AF was defined by interelectrogram intervals and changing sequences among recordings, indicating complete lack of organization. We evaluated the presence of propagated activations immediately (<300 ms) after successful shocks (≥1 discrete electrogram in all recordings). In unsuccessful shocks we evaluated changes in electrogram morphology (discrete/fragmented) and interelectrogram intervals before and after defibrillation. Results: About 16/20 shocks terminated AF. In 6/16 one or two cycles of atrial activation were recorded just after the shock and before AF ended. In 10/16 AF was interrupted immediately after the shock. 4/20 shocks did not interrupt the arrhythmia. After these shocks, transient organization of recorded activity with longer interelectrogram cycle length and disappearance of fragmented activity were transiently observed. Conclusion: Our clinical findings in atrial defibrillation in vivo reproduce experimental data that show myocardial activations early after successful direct current shocks. These observations suggest that successful defibrillation depends not only on the immediate effects of the shock, but also on transient effects on electrophysiological properties of the myocardium, capable of interrupting persistent or reinitiated activations. [ABSTRACT FROM AUTHOR]

Introduction: The high posterolateral right atrium (RA) is considered the "sinus node area," but we tack information on endocardial atrial activation in sinus rhythm. We studied RA and left atrial (LA) endocardial activation in the etectrophysiology laboratory. Methods and Results: Thirty-five patients (21 men) aged 47 ± 16.4 years (mean ± SD) underwent RA mapping (22.2 ± 3.8 points). In 21 patients, LA activation was mapped (11.1 ± 3.9 points) through the coronary sinus (CS), right pulmonary artery, and/or a patent oval foramen. Fourteen patients had atrial arrhythmias, and 3 an ECG pattern of Bachmann's bundle block. Endocardial ILk activation preceded P wave in 5 (-14 ± 4.2 ms), coincided in 11, and followed P onset in 18 (16.7 ± 6.6 ms). Location of the zero point varied from the superior vena cava to the tow RA and from lateral to paraseptal ILk. In 19 patients, activation started simultaneously in 2 to 5 points located > 1 cm apart. RA activation was descending in most, but in 3 with low onset there was collision in the anterior and septal walls. In 15 of 21 patients, descending LA activation dominated, ending in the mid CS in 12, proximal CS in 1, and simultaneously throughout the CS in 2. In 3 with Bachmann's bundle block, CS activation was ascending and in 2 double potentials were recorded from the LA roof. Conclusion: During stable sinus rhythm, LA activation can start in different areas or simultaneously over large areas resulting in different activation patterns, both in the LA and the LA. LA activation is predominantly descending, but in Bachmann's bundle block it becomes ascending, and double potentials suggest a location of block in the LA roof. [ABSTRACT FROM AUTHOR]

COSÍO, F.G., et al.: Atypical Flutter: A Review. Understanding of typical flutter circuits led the way to the study of other forms of macroreentrant tachycardias of the atria, and to their treatment by catheter ablation. It has become evident that the ECG classification of atrial flutter and atrial tachycardia by a rate cutoff and the presence or absence of isoelectric baselines between atrial deflections is not a valid indicator of tachycardia mechanism. Macroreentrant circuits where activation rotates around large obstacles are the most common arrhythmias found in patients with atypical forms of flutter or atrial tachycardia, especially after surgery for congenital heart disease, however, focal mechanisms can also be found. Large areas of low voltage electrograms, suggestive of severe myocardial damage (fibrosis or infiltration) can be found in many atypical macroreentrant tachycardias at the center of the circuit. Many of these circuits can be mapped precisely, critical isthmuses can be defined, and effective catheter ablation can be performed. The need to match activation maps with anatomy precisely, makes computer assisted, anatomically precise mapping a useful tool. Entrainment techniques have to be used sparingly to avoid tachycardia interruption. In complex cases, ablation can be done in sinus rhythm, after definition of conducting channels between low voltage areas and scars or anatomic obstacles. Long-term prognosis is uncertain and depends on the underlying pathology. (PACE 2003; 26:2157–2169) [ABSTRACT FROM AUTHOR]

A case of severe mitral regurgitation with refractory heart failure, after atrioventricular junction ablation and pacemaker implant, was solved with left ventricular pacing. Mitral regurgitation was related to a change in segmental left ventricular motion during right ventricular pacing. [ABSTRACT FROM AUTHOR]

Loop Diagrams of Reentry. Cardiac clinical electrophysiology is difficult to teach because it requires mental integration of complex information on cardiac activation, which includes tridimensional spatial orientation of the cardiac structures involved and variables such as refractory period, conduction velocity, and cycle length. Commonly used representations of cardiac arrhythmias include snapshot sequences or ladder diagrams. The former lack time dimension, and the latter lack spatial dimension. We propose a schematic tridimensional representation of reentry as a helicoidal shape that is the result of adding a time dimension to a circular representation. This presentation, which also can be called a ‘loop diagram,’ allows better integration of spatial phenomena with recorded electrogram sequences and can help the teaching of basic clinical electrophysiology. [ABSTRACT FROM AUTHOR]

Anatomic Nomenclature of the AV Junctions. Current nomenclature for the AV junctions derives from a surgically distorted view, placing the valvar rings and the triangle of Koch in a single plane with anteroposterior and right-left lateral coordinates. Within this convention, the aorta is considered to occupy an anterior position, whereas the mouth of the coronary sinus is shown as being posterior Although this nomenclature has served its purpose for the description and treatment of arrhythmias dependent on accessory pathways and AV nodal reentry, it is less than satisfactory for the description of atrial and ventricular mapping. To correct these deficiencies, a consensus document has been prepared by experts from the Working Group of Arrhythmias of the European Society of Cardiology and from the North American Society of Pacing and Electrophysiology. It proposes a new, anatomically sound, nomenclature that will be applicable to all chambers of the heart. In this report, we discuss its value for description of the AV junctions and establish the principles of this new nomenclature. [ABSTRACT FROM AUTHOR]

Introduction: Typical flutter is due to reentry around caval veins and terminal crest. In patients with typical flutter, reversed (clockwise) reentry can be induced. We studied mechanisms of typical and reversed flutter induction. Methods and Results: Thirteen patients (11 men) underwent 16 radiofrequency (RF) ablation procedures for typical (12) or reversed flutter (1), High right atrium (RA) stimulation included 1 to 3 extrastimuli over cycle lengths 600 to 250 msec, and burst. We recorded simultaneously from three levels of septal and anterior RA. RF was delivered to the inferior vena cava-tricuspid isthmus (CTI). Of 25 inductions, 4 were a result of single, 9 double, and 11 triple extrastimuli, and 1 burst. Clinical basal flutter was induced (7 typical, 1 reversed). After RF, typical flutter was reinduced in 9 cases and reversed flutter in 7, with only typical flutter seen clinically. All flutters were interrupted by ablation or catheter pressure on the CTI. Typical flutter began by low RA septal activation block, preceded by repetitive responses in 12 instances, atypical flutter in 1, and directly from stimuli in 4. Reversed flutter started in 8 instances by low RA block of a stimulated front descending the anterior wall and in 1 by repetitive responses. Conclusion: Septal activation block was the usual mechanism of typical flutter induction by RA extrastimuli. Facilitation of reversed flutter after RF application is probably due to a new area of block in the CTI. Flutter induction without intermediate rhythms confirms the presence of block at the terminal crest at baseline. [ABSTRACT FROM AUTHOR]

The substrate of the permanent form of junctional reciprocating tachycardia is an accessory pathway with no spontaneous anterograde conduction, usually located in the posteroseptal area. We report a case of this type of tachycardia with overt anterograde ventricular preexcitation. Electrophysiologic study confirmed that tachycardia was due to an accessory pathway with long retrograde conduction time; electrophysiologic findings suggested longitudinal dissociation of the accessory pathway. Radiofrequency application at the coronary sinus os resulted in disappearance of preexcitation and cure of the tachycardia. [ABSTRACT FROM AUTHOR]

Atrial flutter (AF) mapping has shown circular activation in the right atrium (RA), with a ''counterclockwise" rotation in a frontal view. The myocardial isthmus between the inferior vena cava and the tricuspid valve (IVC-T) closes the activation circuit in its caudal end. The reproducibility of this activation pattern, and the fact that some "rare" AF with a "clockwise" rotation of activation use the same circuit, suggests that reentry is greatly facilitated by the anatomical arrangement of the caudal end of the RA. This suggested that ablation of the IVC-T isthmus may interrupt AF and prevent its recurrence. We have applied radiofrequency (RF) current to the IVC-T isthmus in nine patients, producing sudden interruption of activation at this point in five (all those treated with large surface electrode catheters). In three others, RF produced acceleration or disorganization, leading to interruption. Preliminary follow-up data suggest a favorable effect on AF recurrence, either by preventing it, or by making antiarrhythmic drugs effective. [ABSTRACT FROM AUTHOR]

We have studied the electrophysiological correlates of atrial repetitive responses, induced by single extrastimuli, in a group of 25 patients undergoing electrophysiologic studies for a variety of supraventricular and ventricular arrhythmias. The incidence of repetitive responses was not related to a previous history of atrial tachyarrhythmias. Repetitive responses were observed only when the extrastimulus elicited a significant intra-atrial conduction delay, as measured from the extrastimulus artifact, to two or three points in the atria. This condition was fulfilled only when the basic atrial rhythm was paced, and it was also facilitated by increasing atrial rate, which shortened the atrial effective refractory period. Atrial pacing thus seemed to facilitate the production of atrial repetitive responses by both promoting intra-atrial conduction delays during extrastimulation, and by shortening the atrial refractory period. Atrial repetitive responses are probably a nonspecific phenomenon, unrelated to a tendency towards atrial tachyarrhythmias; their mechanism is probably local re-entry, related to slow conduction of impulses during incomplete repolarization, and under favorable conditions they may precipitate atrial flutter or fibrillation in predisposed patients. [ABSTRACT FROM AUTHOR]

The author reflects on an article concerning the use of staged catheter ablation in the treatment of cardiac arrhythmias. He mentions transitions between atrial flutter and atrial fibrillation patterns are observable both during electrophysiologic studies and on electrocardiograms. He talks about the computer model that was used to support the multiple wavelet hypothesis and how activation was organized into a single figure-of-eight reentrant circuit when large, linear obstacles were introduced.

The article describes the case of a 48-year-old man who underwent aortic and mitral valve replacement in 1986 for rheumatic valve disease and examines the mechanism of the narrow QRS complex tachycardia with unusual atrial activation experienced by the patient. The characteristics of the tachycardia which confirm the intranodal reentry include very short ventriculararial interval and interruption with Wenckebach atrioventricular block. Radiofrequency applications were delivered to interrupt the tachycardia and make it non-inducible.

Typical ECG of that described for Brugada syndrome was elicited in a patient diagnosed with labyrinthopathy during Infusion of dimenhydrinate, a first-generation antihistamine usually used to treat motion sickness. Although the patient had no history of syncope or palpitations, and there was no family history of cardiac disease or sudden death, the ECG abnormality was reproduced later with intravenous flecainide, and an asymptomatic Brugada syndrome was diagnosed. [ABSTRACT FROM AUTHOR]

The author discusses the research "Clinical characteristics, management and prognosis of elderly patients with Brugada syndrome" by G Conte and others published in this issue. The topics discussed include Brugada Syndrome (BS) involving ventricular arrhythmias with an electrocardiographic (ECG) pattern of ST segment elevation, the treatment of patients with BS ECG and arrhythmias, and mechanism underlying ventricular arrhythmias.

Presents letters to the editor about the changes in atrial electrophysiologic parameters and effectiveness of antiarrhythmic drug therapy in patients with paroxysmal atrial fibrillation. Correlation of atrial effective refractory period prolongation with clinical efficacy; Role of extrastimuli in producing marked intraatrial conduction delay in patients with atrial arrhythmias; Differences in atrial electrophysiology in response to the atrial programmed stimulation between patients with and without paroxysmal atrial fibrillation; Role of ajmaline in prolonging atrial effective refractory period.