Abstract
It is a source of much frustration to clinicians and patients alike that outcomes of catheter ablation for persistent atrial fibrillation (AF) remain stubbornly suboptimal.1,2 It is clearly understood that paroxysmal AF is driven in the great majority of cases by electric triggers located in myocardial sleeves extending into the pulmonary veins (PVs)3 and, built on this, a large body of evidence has been generated to demonstrate that durable PV isolation can provide effective treatment for paroxysmal AF.4 Equivalent outcomes from catheter ablation of persistent AF have been hampered by ongoing uncertainty about the basic electrophysiological mechanisms by which this arrhythmia is sustained. Article see p 554 Early data from animal and computer models suggested the presence of multiple electric wavefronts meandering through the atrial wall, after the principles of Brownian motion.5 Subsequent data have highlighted the role of atrial myocardial structural remodeling in constraining the propagation of such wavelets,6 and the importance of the 3-dimensional nature of the wall has been highlighted,7 with dissociation between endocardial and epicardial layers and wavefront breakthroughs between these layers facilitating arrhythmia maintenance. Set against this is clear evidence from high-resolution optical mapping in animal models of spiral wave re-entry sustaining fibrillation of both the ventricles8 and the atria.9,10 Multiple groups have attempted to demonstrate such spiral waves and rotors by high-density epicardial mapping in human AF but, although transient rotational activity centered on a core of high-frequency activity consistent with the electrophysiology expected of rotors has been described,11,12 there are no reports of sustained spiral wave re-entry in human persistent AF demonstrated through such methods. Exciting developments in recent years have resulted from the application of innovative mapping techniques. Multielectrode vests have been used to record body surface …
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