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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 (

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.

NUNEZ, A., et al.: Severe Mitral Regurgitation with Right Ventricular Pacing, Successfully Treated with Left Ventricular Pacing. 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.

Common atrial flutter is due to a macroreentry circuit in the right atrium, but the cranial path of the circuit has not been defined. The objectives of this article are to determine the cranial turning point of flutter activation in relation to a hypothetic obstacle, the superior vena cava opening, by examining the changes in activation sequence produced by entrainment from different points. In 13 cases of common atrial flutter with typical counter-clockwise right atrial circuits confirmed by endocardial mapping the atrium was paced from the high posterior and mid-septal walls. Entrainment was confirmed by simultaneous recordings of 6-7 right atrial electrograms. Changes in sequence of electrograms from high septum and high anterolateral walls was sought. Electrogram sequence and morphology did not change with entrainment at the posterior wall with respect to the basal flutter or mid-septal wall entrainment. Pacing "below" the superior vena cava did not advance the anterior wall electrogram in relation to the septal electrogram. These findings support the concept that common flutter activation turned around (cranial and anterior to) the superior vena cava opening, and not around the free end of a line of block below the superior vena cava in the posterior wall. Common atrial flutter activation rotates cranial (and anterior) to the superior vena cava opening, through the "right atrial roof." The line of functional block should span from inferior to superior vena cava openings.

Endocardial mapping has led to a detailed knowledge of reentry mechanisms in atrial flutter. Multipolar and deflecting tip catheters allow recording local electrograms from multiple areas of the right atrium, and from the coronary sinus. In common flutter, with the typical "sawtooth" pattern, there is circular activation of the right atrium in a "counterclockwise" direction, descending in the anterior and lateral walls, and ascending in the septum and posterior wall. Superior and inferior vena cava, linked by a "line" of functional block in the posterolateral wall, make the central obstacle for circular activation. The cranial and caudal turning points are the atrial "roof," and the isthmus between the inferior vena cava and the tricuspid valve. Complex conduction patterns, probably including slow conduction are detectable in the low septal area, around the coronary sinus. Atypical flutter, without the sharp negative deflections of common flutter, sometimes shows circular activation in the right atrium, rotating in the opposite direction of common flutter (clockwise). Other atypical flutters show no circular right atrial activation, and only partial data from coronary sinus activation, combined with the response to atrial stimulation (entrainment) allow the diagnosis of left atrial reentry, without a precise delimitation of the circuits. In patients having undergone cardiac surgery, atypical flutter may be based on reentry around surgical scars. To our knowledge, the mechanism of type II flutter has not been disclosed in humans.