480 Catheter Ablation for Atrial Fibrillation: Have We Come the Full Circle? HARIS M. HAQQANI, M.B.B.S., * ,† JONATHAN M. KALMAN, M.B.B.S., PH.D., F.A.C.C., * ,† and PETER M. KISTLER, M.B.B.S., PH.D.‡,§ * From the Department of Cardiology, Royal Melbourne Hospital, Australia; †The Department of Medicine, University of Melbourne Parkville, Victoria, Australia; ‡The Baker Heart Research Institute, Melbourne, Australia; and §The Heart Centre, The Alfred Hospital, Melbourne, Australia Editorial Comment That the apparent chaos of a fibrillating atrium could be successfully targeted by a mechanical therapy is indeed a trib- ute to the remarkable progress of modern medical science. This is testimony to an increased understanding of some of the mechanisms underpinning atrial fibrillation (AF). The multiple wavelet hypothesis proposed by Moe 1 found some support in the apparent success of the “cut and sew” sur- gical maze operation. 2 Attempts at replicating these results with a catheter-based procedure failed and were complicated by a significant incidence of thromboembolic and other ad- verse events. 3 In contrast, the ectopic focal theory proposed by Scherf in the 1940s postulated arrhythmia initiation by rapidly firing triggers and maintenance by fibrillatory con- duction. 4 These theories were validated by the seminal work of Haissaguerre et al. demonstrating triggers arising from the pulmonary veins (PV) as responsible for the majority of AF paroxysms. 5 Both triggered activity 6 and local reentry 7 have been postulated to be the electrophysiological mechanisms responsible for these rapidly firing regions that are located within the sleeves of atrial myocardium that extend a vari- able distance into the pulmonary veins. 8 In the decade that has elapsed since, the evolution of catheter ablation for AF has occurred at a staggering pace. The focal approach involved a sometimes laborious process of AF induction to attempt to reliably identify the responsi- ble site often deep within the pulmonary veins. This strat- egy was limited by difficulties in reproducibly initiating and mapping AF triggers coupled with a significant incidence of pulmonary vein stenosis 9 associated with radiofrequency applications deep within the veins. In addition, it became ap- parent that recurrent AF was often due to new triggers located in different regions of previously ablated veins. 10 J Cardiovasc Electrophysiol, Vol. 19, pp. 480-482, May 2008. Dr. Haqqani is the recipient of a Medical Postgraduate Scholarship from the National Health and Medical Research Council of Australia, and a Car- diovascular Lipid Research Grant. Dr. Kistler is the recipient of the Neil Hamilton Fairley Fellowship from the National Health and Medical Re- search Council and National Heart Foundation. Professor Kalman has received research funding support from St. Jude Med- ical and Medtronic. Address for correspondence: Peter M. Kistler, M.B.B.S., Ph.D., The Heart Centre, The Alfred Hospital, Commercial Road, Melbourne 3004, Australia. Fax: 61-3-9076-2461; E-mail: peter.kistler@baker.edu.au doi: 10.1111/j.1540-8167.2008.01142.x These observations prompted the development of an ostial approach to electrically isolate an arrhythmogenic pulmonary vein from the surrounding atrium guided by a circular mul- tipolar catheter. Theoretically, a durable electrical isolation of an arrhythmogenic vein should render it impotent to the reinitiation of AF. Marchlinski et al. demonstrated a sig- nificant improvement in outcomes both immediately after the procedure and at 12-month follow-up (80% freedom from AF in the isolation group vs 45% in the focal ablation group). 11 Despite this approach, recurrent AF remained problem- atic and in general frequently arose from previously “nonar- rhythmogenic” veins. This prompted a frame shift to empiric isolation of an increasing number of veins. With the advent of three-dimensional mapping systems, Pappone et al. pio- neered an approach of substrate modification that involved ablation encircling the pulmonary veins with additional in- terconnecting linear ablation. 12 Kuck and coworkers were responsible for the marriage of the approaches of wide encir- clement of the PVs in pairs with the electrophysiologic end point of electrical isolation. 13 This approach recognizes the importance of proximal arrhythmia foci, rotors anchored to the PV-LA junction and parasympathetic ganglia that might be missed when ablating closer to the veno-atrial junction. The role of the atrial substrate in AF maintenance is cur- rently addressed by adjuvant linear left atrial ablation 14,15 and by targeting complex fractionated atrial electrograms, 16 although their place in the ablation armamentarium continues to be defined. Nonetheless, the cornerstone for AF ablation procedures is successful and durable electrical isolation of the pulmonary veins. 17 The study by Pak et al. 18 in this issue of the journal is im- portant in reintroducing electrophysiology into a procedure that has become increasingly anatomically based. In patients with paroxysmal AF, the authors compared empiric isola- tion of all pulmonary veins with selective isolation of the arrhythmogenic vein (or veins). A group of 260 patients un- dergoing catheter ablation for AF were screened to identify 86 (33%) with a reproducible pulmonary vein trigger demon- strated after cardioversion and isoprenaline challenge on at least three occasions. After exclusion of patients with non-PV or bilateral PV triggers, 77 (30%) patients were included in this analysis, with 42 undergoing selective isolation of only the arrhythmogenic PV, and 35 having empirical electrical isolation of all pulmonary veins. However, in the selective isolation group, if isolation of the target vein was difficult due to residual PV potentials at the intervenous ridge, the ipsilateral vein was also isolated. This study involved the use of a 5-mm nonirrigated ablation catheter that may explain