INTRODUCTION: It has been suggested that some atrial regions may play a role in the maintenance of atrial fibrillation (AF), whereas little is known about the presence of critical areas for the initiation of AF. It is conceivable that the identification of such critical areas may lead to more localized and selective strategies of ablative therapy. METHODS AND RESULTS: A patient suffering from paroxysmal AF was extensively mapped in both the atria with a multielectrode basket catheter in right atrium and two decapolar catheters placed in the coronary sinus and along the left septum. During the mapping, seven identical patterns of initiation of AF were recorded. AF was initiated by an atrial premature beat (APB) arising from the superior right septum, followed by a reentrant beat originating from the same area that slowly propagated through the atria and resulted in late activation of the right lateral wall. During sinus rhythm, the majority of the electrograms were single potentials, whereas during the APB, and particularly during the first atrial reentrant beat, a high percentage of fragmented complexes was present, mainly located in the right superior septum. These fragmented complexes were present in the same sites in each initiating episode and remarkably, they showed an almost identical morphology. CONCLUSION: This case suggests that in some patients the initiation of AF could be caused by reentrant circuits localized in specific atrial regions and the reentrant circuits could be identical in the different episodes of AF. This highlights the importance of increasing our understanding of the mechanisms of the initiation of AF so that we can identify any critical area involved in the genesis of AF where selective RF lesions may be effective in curing this arrhythmia.
Reproducibility of spontaneous initiations of atrial fibrillation.
GAITA, Fiorenzo
1999-01-01
Abstract
INTRODUCTION: It has been suggested that some atrial regions may play a role in the maintenance of atrial fibrillation (AF), whereas little is known about the presence of critical areas for the initiation of AF. It is conceivable that the identification of such critical areas may lead to more localized and selective strategies of ablative therapy. METHODS AND RESULTS: A patient suffering from paroxysmal AF was extensively mapped in both the atria with a multielectrode basket catheter in right atrium and two decapolar catheters placed in the coronary sinus and along the left septum. During the mapping, seven identical patterns of initiation of AF were recorded. AF was initiated by an atrial premature beat (APB) arising from the superior right septum, followed by a reentrant beat originating from the same area that slowly propagated through the atria and resulted in late activation of the right lateral wall. During sinus rhythm, the majority of the electrograms were single potentials, whereas during the APB, and particularly during the first atrial reentrant beat, a high percentage of fragmented complexes was present, mainly located in the right superior septum. These fragmented complexes were present in the same sites in each initiating episode and remarkably, they showed an almost identical morphology. CONCLUSION: This case suggests that in some patients the initiation of AF could be caused by reentrant circuits localized in specific atrial regions and the reentrant circuits could be identical in the different episodes of AF. This highlights the importance of increasing our understanding of the mechanisms of the initiation of AF so that we can identify any critical area involved in the genesis of AF where selective RF lesions may be effective in curing this arrhythmia.
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