Lessons learned from computerized mapping of the atrium: Surgery for atrial fibrillation and atrial flutter

The supraventricular arrhythmias of atrial fibrillation (AF), both chronic and paroxysmal, and atrial flutter (AFL) have been more difficult to study than most other clinical arrhythmias. Initial epicardial mapping studies at Washington University in canine models and in patients undergoing surgical ablation of other supraventricular arrhythmias demonstrated that AFL resulted from a macroreentrant circuit that was thought to occur only on the right side of the atrium with passive depolarization of the left atrial tissue. Atrial fibrillation was initially demonstrated to be considerably more complex with multiple circuits present. Furthermore, these circuits occurred simultaneously on both the right and left atria. Inability to map the atrial septum and the orifices of the pulmonary veins, however, led to the development of second-generation form-fitting experimental endocardial templates for the canine studies and an endocardial right atrial template for the patient studies. These second-generation experimental maps demonstrated that AFL circuits could involve the fixed anatomic obstacles of the right and left atria and adjacent areas of conduction block, frequently involving the septal and pulmonary vein tissue, with passive depolarization of the contralateral atrium. In contrast to this single-circuit mechanism. AF was confirmed to result from varying degrees of multiple reentrant circuits, occurring transiently in time and migrating over the surface of both atria. Furthermore, the single clinical arrhythmia of AF could result from a spectrum of endocardially or epicardially mapped arrhythmias, ranging from rapid AFL with variable atrioventricular block on one end to very fine multiple-circuit AF on the other end. It was clear that the development of a surgical procedure to ablate AF would need to isolate the atrial tissue in such a way that the transient reentrant circuits responsible for AF could not form because they were extinguished by a fixed or surgically created (eg, a suture line) anatomic obstacle. Normal activation of the sinoatrial pacemaker complex, maintenance of atrioventricular synchrony with intact atrioventricular conduction, and reestablishment of atrial transport function were requirements for a successful procedure for AF. These requirements have been met with the maze procedure. Further elucidation of the electrophysiologic aspects of AF and AFL are in progress, including mapping of the spontaneous onset and termination of these arrhythmias. These data will certainly yield further insights into the mechanisms of clinical AF and AFL.