Catheter Ablation for AF: Past, Present, and Future

Abstract

Atrial fibrillation (AF) is a common tachyarrhythmia. There are over 2 million patients in the US with AF currently, 1 and as the median age of the population increases, the prevalence of AF likely will as well. Strategies for treating AF are diverse, and include options ranging from simple observation to pharmacotherapy to catheter-based and surgical interventions. Therapeutic approaches to AF historically have been divided into rate-control and rhythm-control categories, the former focusing on simply reducing ventricular response rates and the latter on restoration of sinus rhythm.Over the last 15 years, there has been an explosion of rhythmcontrol therapies, particularly in the field of catheter-based ablation. The proliferation of these ablative approaches has led to new insights into AF, both in terms of the mechanism(s) of the disease itself, and in the potential harm that patients can suffer during attempts at restoration of sinus rhythm. This review focuses on the complications, both the familiar and the newly appreciated, that may occur during catheter ablation of AF. Definition of Pericardial FatIn the late 1950s, Gordon Moe hypothesized that AF was the consequence of multiple, wandering reentrant waves coursing through atrial tissue.2,3 His hypothesis was confirmed by the work of Allessie and colleagues thirty years later, 4-6 when they demonstrated that sustained AF depended on functional reentry of multiple wavefronts through a critical mass of atrial tissue. At approximately the same time, Haisseguerre and colleagues demonstrated that initiation of AF was triggered by spontaneous ectopy originating from foci in the pulmonary veins(PV).7 Thus, the mechanisms of AF -functional reentry dependent on a critical mass of atrial tissue, triggered by ectopic beats within the PVs -were partially understood. Those mechanisms (triggers and substrate) constitute the primary targets for modern AF ablation. Other aspects of AF induction and perpetuation, including the role of ganglionic plexi and stable rotors, have also been proposed as important physiological modifiers of AF and as ablation targets. 8As the mechanisms underlying AF were determined, strategies to treat AF with catheter ablation evolved accordingly. Early ablative procedures focused on disrupting the critical mass of atrial tissue thought to be critical for perpetuation of AF. Linear lesion sets in the right atrium, left atrium, or both were delivered with the goal of interrupting reentrant circuits.9-12 These stra gies, though, were of limited efficacy at eliminating AF.