Cardiac Rhythm Management
Articles Articles 2013 February

Focal Impulse and Rotor Modulation for Paroxysmal Atrial Fibrillation

DOI: 10.19102/icrm.2013.040203


University of California and Veterans’ Affairs Medical Centers, San Diego, California

PDF Download PDF

ABSTRACT.  Therapy for atrial fibrillation (AF) remains suboptimal, largely because of uncertainty in its mechanisms. While the “triggers” versus “substrate” debate continues to rage, it is not clear that this is central. All supra- and ventricular arrhythmias are initiated from sinus rhythm by “triggers,” and successful therapy targets their sustaining mechanisms rather than triggers. Paroxysmal AF, moreover, often sustains for hours or days after it is triggered, longer than many presenting supraventricular tachycardias. Accordingly, refocusing therapy on sustaining mechanisms for paroxysmal AF may improve upon the results of recent multicenter trials, in which trigger elimination yields a single procedure success rate of less than 50–60%, compared with more than 80–90% for other supraventricular arrhythmias. Wide-area (panoramic) contact mapping now shows that paroxysmal AF, and persistent AF, is maintained by a small number of stable rotors or focal sources that lie widely in both atria often remote from pulmonary veins. Mechanistically, targeted ablation at sources alone (focal impulse and rotor modulation, FIRM) has proven able to acutely terminate AF and render it non-inducible, often with very brief energy delivery (<5–10 min). Clinically, abolition of rotors and focal sources substantially improves the results from conventional pulmonary vein ablation alone. This review focuses on the evidence that stable rotors and focal sources drive clinical paroxysmal AF, and discusses their role as ablation targets either with trigger elimination or as solitary therapy.

KEYWORDS. ablation, atrial fibrillation, focal source, human, paroxysmal, spiral wave therapy, rotor.

Dr. Narayan reports being co-inventor on intellectual property owned by the University of California and licensed to Topera Medical, Inc. Dr. Narayan holds equity in Topera. Topera has not sponsored any research, including that presented here. Dr. Narayan also reports having received honoraria from Medtronic, St. Jude Medical and Biotronik Corporations and grant support from Biosense-Webster. Drs. Kawata, Schricker, Lalani, Baykaner and Krummen report no conflicts of interest.
Manuscript received November 11, 2012, final version accepted December 21, 2012.

Address correspondence to: Sanjiv M. Narayan, MD, PhD, MSc, Professor of Medicine, University of California, San Diego, Cardiology/111A, 3350 La Jolla Village Drive San Diego, CA 92161. E-mail:

Atrial fibrillation (AF) is the most prevalent arrhythmia in the Western world, and a leading cause of symptoms, hospitalization, and death.1 Individuals with paroxysmal AF are often very symptomatic, likely due to their symptomatic transitions from sinus rhythm, and often referred for ablation.2 Although ablation may reduce paroxysmal AF symptoms in many patients, several recent multicenter studies show a 1-year AF elimination of 50–60%35 that is lower than the 80–90% or more achieved for other supraventricular arrhythmias.69 Improvements in ablation therapy for paroxysmal AF may require a different ablation approach based upon the fundamental mechanisms of the arrhythmia.

Seminal observations by Haïssaguerre in 1998 10 revealed that ectopic beats from the pulmonary veins (PVs) can trigger AF.2 PV isolation effectively reduces AF symptoms,2,4,11,12 yet actually eliminates paroxysmal AF (silent and symptomatic AF) with 50–60% success after one35 and <70% after several2,4,5 procedures. Several factors may limit PV isolation, including difficulties in achieving durable isolation,2,13 frequent triggers outside the PVs2,4,11,12 and the fact that, unlike all other arrhythmias, AF-sustaining mechanisms are not defined.14,15 The multiwavelet hypothesis proposed that spatially meandering waves actually sustain AF,16,17 but cannot explain how AF may terminate by localized ablation.2,18 The alternative localized source hypothesis19 is supported by elegant experiments in which activation from localized spiral waves (rotors)15,20 or focal sources21 sustains AF, so that disorganization is an epiphenomenon. Until recently, however, there had been little22,23 or no16 evidence to support stable sources for human AF.

Recent studies from our group24 and independent25 laboratories show that paroxysmal and persistent AF is sustained by a small number of rotors or focal sources. Using wide-area contact mapping techniques, but not non-contact methods,22,26 sources are remarkably stable over time, enabling targeted source ablation (focal impulse and rotor modulation, FIRM) to rapidly terminate and render AF non-inducible, and greatly improve AF elimination on long-term follow-up24 in the CONFIRM (Conventional Ablation with or without FIRM) trial. Initial reports of stable human AF rotors24 have now been validated by at least eight independent groups worldwide.25,2729

This review summarizes the evidence for stable electrical rotors and focal sources for human paroxysmal AF, and their role as targets for ablation to achieve long-term maintenance of sinus rhythm.24

Contact panoramic mapping: approach

We recently mapped human AF sources using contact electrodes in a wide field of view (Focal Impulse and Rotor Mapping, FIRM)30 at clinical electrophysiology study (Figure 1). A commercially available basket catheter (Constellation, Boston Scientific, Boston, MA) is advanced first into the right atrium for mapping and ablation; then this process is repeated in the left atrium as shown in Figure 2. In the right atrium, signals are recorded from 64 poles and exported for analysis to a computational system (RhythmViewTM, Topera Medical, San Diego, CA). Analyses use physiologically adaptive algorithms to analyze AF in terms of biatrial action potential duration restitution and oscillations3134 and conduction velocity restitution.33,35 These analyses are concordant with the facts that paroxysmal AF and even lone AF patients exhibit the “substrates” of conduction slowing,35,36 repolarization abnormalities,33,34 and scar on delayed enhancement magnetic resonance imaging.37 In early studies, we attempted to use virtual (reconstructed) electrograms from the inverse solution, but found that their modest correlation with real (contact) AF electrograms38 prevented the detection of stable rotors amidst transient fibrillatory conduction (e.g., one to two spins)26,38 and abandoned that approach.


Figure 1: Method for contact FIRM mapping. Fluoroscopy of multipolar basket catheter (a) in the right atrium (25° left anterior oblique projection) and (b) in the left atrium across a transseptal puncture (30° right anterior oblique projection). An ablation catheter is positioned to ablate at rotor sites C3 in the high posterolateral right atrium, and F4 in the high posterior left atrium (see corresponding rotor maps in Figure 3a,b). Coronary sinus, esophageal temperature probe and intracardiac ultrasound catheters are also shown.


Figure 2: Flowchart for Focal Impulse and Rotor Mapping and Modulation (FIRM) for atrial fibrillation (AF) sources. Reported FIRM termination/slowing time is the time to achieve the endpoint at that source (i.e., “primary source”). Total FIRM time includes ablation to cover all source areas, including ablation performed after AF termination/non-inducibility (possibly in sinus rhythm). See text for details.

Animated movies (isopotentials) are created30 and used to identify AF mechanisms in any individual. Ablation (FIRM) is targeted at sources as described below, then the process is repeated in the left atrium. Anticoagulation is maintained with heparin for standard target activated clotting time (ACT), and, to date, there have been no complications during contact panoramic mapping.24,25 In the work flow illustrated in Figure 2, FIRM mapping and ablation time is ≈1 h after gaining intravenous and left atrial access. In published studies,16,17 PV isolation is then performed, although in our preliminary studies the procedure concludes after FIRM ablation alone.

Figure 3 shows illustrative FIRM maps. The three-dimensional atria are projected onto grids, with the right atrium opened vertically through the tricuspid valve and lateral and medial halves opened. The left atrium is opened horizontally through the mitral valve, and its superior and inferior halves folded upwards and downwards.


Figure 3: Atrial fibrillation (AF) termination by focal impulse and rotor modulation (FIRM) ablation at right atrial and left atrial rotors. (a) Counterclockwise rotor in high lateral right atrium, indicated by early-to-late (red-to-blue) activation with collision (white double lines) beyond organized spiral arm (single cycle snapshot of thousands of successive rotors45). Rotor core is in high posterolateral right atrium (see ablation catheter position in Figure 1a). (b) FIRM at right atrial rotor terminates AF to sinus rhythm in <1 min. (c) Counterclockwise rotor in posterior left atrium, also showing collision (white double lines) beyond organized spiral arm.45Rotor core is at high mid-left atrium (see ablation catheter position in Figure 1b). (d) FIRM at left atrial rotor terminates AF to sinus rhythm. ABL: ablation electrogram; CS: coronary sinus.

AF rotors were identified as rotational activity around a center. Focal impulses were identified as centrifugal activation from a point of origin. Rotors and focal sources are diagnosed if consistent for hundreds to thousands of cycles over multiple epochs spanning 10–20 min. This excludes transient or unstable activation22,23 that likely represents passive “fibrillatory conduction.”

Contact panoramic mapping: results

Figure 3a illustrates a right atrial AF rotor (same patient as the fluoroscopy in Figure 1a), showing head-to-tail (red-to-blue) activation in its organized domain with fibrillatory conduction causing disorganization and/or collision. Figure 3b illustrates a left atrial AF rotor (same patient as the fluoroscopy in Figure 1b). Each rotor activates sequentially (arrowed), precessing in an area ≈1–2 cm2 to lie over slightly varying electrodes from cycle to cycle.39 Notably, on detailed analysis39 we have found no relationship between AF rotors/focal sources and complex fractionated electrograms or low electrogram amplitude in patients with paroxysmal AF or persistent AF.

Stable sources were observed in all patients during paroxysmal AF and nearly all with persistent AF (98% in CONFIRM,24 100% in recent external validation25). AF sources were stable for thousands of cycles24 and, in a subset of subjects who failed conventional ablation then remapped for FIRM-guided ablation, for months.40 Fewer sources were observed in patients with paroxysmal than persistent AF (1.7±0.9 vs 2.2±1.0; p=0.03). Sources lay in both atria, surprisingly with 24% in right atrium. The ratio of rotors to focal sources is approximately 4:1.24,25

Focal impulse and rotor modulation ablation: approach

Stable rotors or focal sources are targeted directly for ablation (FIRM). Any clinical energy source can be used, and CONFIRM24 and external studies25 used irrigated and non-irrigated radiofrequency catheters and cryoablation. As recently described,24,25 the catheter is maneuvered to electrode(s) subtending each source on fluoroscopy (Figures 1 and 3); then energy is applied. The acute endpoint is “hyperacute” AF termination or 5–10 min ablation during FIRM ablation, whichever comes first. If AF terminates, then vigorous attempts are made to reinduce AF (using burst pacing). If AF is non-inducible, then the event is classified as “AF termination/non-inducible” (Figure 4). The composite acute endpoint is AF termination (with non-inducibility), or AF slowing >10% that indicates elimination of a secondary AF source in our studies (and computer simulations with a less stringent 3–4% cutpoint).41,42 Since 2.1±1.0 sources were observed per patient in the CONFIRM trial, typical total FIRM ablation time is 15–20 min. In CONFIRM, FIRM-guided patients then went on to conventional ablation. FIRM-blinded patients received only conventional ablation.


Figure 4: Focal impulse and rotor modulation (FIRM) terminates paroxysmal atrial fibrillation (AF) to sinus rhythm and renders it non-inducible.(a) Left atrial rotor in low mid-left atrium, outside pulmonary vein (PV) antra, with slight spatial precession. Rotor shows clockwise activation (red to blue) in AF. B. FIRM ablation at left atrial rotor terminated AF to sinus rhythm without PV (or other) ablation. (c) Non-inducible AF after FIRM. Although vigorous pacing (cycle length 170 ms) and isoproterenol triggered AF, the atrium could no longer sustain AF (AF <2.9 s) once pacing stopped. This patient received only FIRM ablation (no PV isolation) on protocol, and remains free of AF off-drugs at 10 months. V1, V6 electrocardiogram leads; Abl-D, Abl-P: ablation electrodes; CS-P, CS-M, CS-D: coronary sinus electrograms. Atrial orientation labeled same as Figure 3.

FIRM only ablation: acutely terminates and renders AF non-inducible

Figure 3 shows AF termination by FIRM ablation at (a) a right atrial AF rotor, (b) a left atrial rotor, prior to any other ablation. Figure 4 shows AF termination by FIRM alone, prior to any other ablation. In each case, multiple and vigorous attempts at reinitiation showed that burst pacing was able to trigger AF but that the atria were no longer capable of sustaining AF after burst pacing stopped (<2.9 s in Figure 4c). This strict endpoint of termination/non-inducibility predicts freedom from AF for conventional43 and FIRM24 ablation.

In a recently presented multicenter FIRM experience44 (n = 201 patients with CPM, n = 136 with FIRM-guided ablation), termination and non-inducibility was achieved in 92% of n = 38 patients with paroxysmal AF after a median of 6 min (interquartile range (IQR) 2–10 min) of FIRM ablation at the primary source, or 11 min (IQR 8–22 min) total FIRM ablation (Figure 2). By comparison, Jais et al43 reported that PV isolation terminated and rendered paroxysmal AF non-inducible in 57% of patients using 36±13 min of ablation. Additional linear lesions (20±8 min ablation) at the left atrial roof and/or mitral isthmus increased the rate of AF termination and non-inducibility.43

In persistent as well as paroxysmal AF patients, FIRM ablation caused AF termination and non-reinducibility in 56%24 and 67%25 of patients before PV isolation. The composite acute endpoint (termination/non-inducibility and slowing) was achieved by FIRM alone in 86% (31/36) of patients in the FIRM-guided limb of the CONFIRM trial24 and 100% (12/12) of mapped patients in an external series.25 Notably, AF termination by FIRM was predominantly to sinus rhythm(23/28 terminations in both pooled studies, 82%24,25) unlike prior studies in which conventional (non-FIRM guided) ablation terminates non-paroxysmal AF typically to atrial tachycardia.42

A videotaped case of FIRM-guided ablation demonstrating acute AF termination to sinus rhythm with non-inducibility is available as an online video report.45

Long-term outcome after firm-guided ablation at AF sources: the CONFIRM trial

We hypothesized that abolition of patient-specific AF sources by FIRM would portend long-term maintenance of sinus rhythm. The CONFIRM trial (CONventional ablation with or without Focal Impulse and Rotor Modulation) was a prospective case cohort study24 that enrolled 92 patients at 107 consecutive AF ablation procedures, of whom 31 had paroxysmal AF.

In patients with paroxysmal AF, freedom from AF (or atrial tachycardia) after a single procedure was 83.3% in those receiving FIRM-guided ablation compared with 59.1% in those receiving conventional ablation alone (FIRM-blinded) after a median of 470 days of follow-up. Although FIRM ablation is being performed in larger cohorts, these indicate that a single FIRM-guided procedure provides a higher elimination of paroxysmal AF on rigorous follow-up than PV isolation alone.35 For comparison, FIRM-blinded paroxysmal AF patients (PV isolation) had similar success to the 60% single procedure freedom from paroxysmal AF reported by Jais et al43 after AF termination with non-inducibility.

For all patients (2/3 persistent AF, 1/3 paroxysmal AF), single-procedure AF elimination in CONFIRM was higher for FIRM-guided than conventional FIRM-blinded cases (82.4% vs 44.9%, p<0.001) after 273 days (median; IQR 132–681). Figure 5 illustrates a Kaplan–Meier curve showing benefit for FIRM-guided versus FIRM-blinded cases for patients off antiarrhythmic medications (p<0.001). CONFIRM is among the largest AF trials to compare a novel ablation strategy to state-of-the-art conventional ablation46,47 rather than to failed antiarrhythmic medications.4,48,49


Figure 5: Cumulative freedom from atrial fibrillation in the CONFIRM trial off antiarrhythmic medications, for all cases (solid lines) and those undergoing first ablation (dashed lines). Intention-to-treat analysis, and p-values reflect the complete follow-up period. (Adapted from Narayan et al24with permission).

The main limitation of CONFIRM is that it was non-randomized, although subjects were enrolled consecutively and treated prospectively for prespecified endpoints, and FIRM-guided subjects had more comorbidities and more rigorous follow-up (implanted electrocardiogram monitors in 88.2% vs 26.1%; p<0.001) than FIRM-blinded patients. Although CONFIRM included patients with prior ablation, FIRM-guided ablation maintained its benefit over FIRM-blinded therapy in patients at first ablation, and in all prespecified subgroups.


Paroxysmal atrial fibrillation, like other supraventricular tachycardias, is sustained by patient-specific mechanisms after it has been initiated from diverse triggers. Independent laboratories now show that localized stable rotors and focal sources sustain AF across a wide-range of clinical presentations. In paroxysmal AF, FIRM mapping shows stable rotors and focal sources in patient-specific locations in both atria. Abolition of all patient-specific sources (FIRM-guided ablation) can terminate AF and render it non-inducible prior to any other ablation, and increase single-procedure freedom from conventional ablation by >70% in patients with paroxysmal AF. Ongoing studies will determine the efficacy of FIRM ablation alone (to eliminate sustaining mechanisms rather than other eliminating triggers) in patients with paroxysmal AF.


  1. Miyasaka Y, Barnes ME, Gersh BJ, et al. Secular trends in incidence of atrial fibrillation in Olmsted County, Minnesota, 1980 to 2000, and implications on the projections for future prevalence. Circulation 2006; 114:119–125. [CrossRef] [PubMed]
  2. Calkins CH. 2012 HRS/EHRA/ECAS expert consensus statement on catheter and surgical ablation of atrial fibrillation: recommendations for patient selection, procedural techniques, patient management and follow-up, definitions, endpoints, and research trial design. Heart Rhythm 2012; 9:632–696.e21. [CrossRef] [PubMed]
  3. Morillo C, Verma A, Natale A. Radiofrequency ablation vs antiarrhythmic drugs as first-line therapy of atrial fibrillation (RAAFT 2) trial (Abstract). Heart Rhythm 2012:Abstract. [CrossRef]
  4. Wilber DJ, Pappone C, Neuzil P, et al. Comparison of antiarrhythmic drug therapy and radiofrequency catheter ablation in patients with paroxysmal atrial fibrillation: A randomized controlled trial. JAMA 2010; 303:333–340. [CrossRef] [PubMed]
  5. Nielsen JC, Johannessen A, Raatikainen P, et al. Radiofrequency ablation as initial therapy in paroxysmal atrial fibrillation. N Engl J Med 2012; 367:1587–1595. [CrossRef] [PubMed]
  6. Feld GK, Fleck RP, Chen PS, et al. Radiofrequency catheter ablation for the treatment of human type 1 atrial flutter: identification of a critical zone in the re-entrant circuit by endocardial mapping techniques. Circulation 1992 Oct;86(4):1233-40. [CrossRef] [PubMed]
  7. Jackman WM, Wang XZ, Friday KJ, et al. Catheter ablation of accessory atrioventricular pathways (Wolff-Parkinson-White syndrome) by radiofrequency current. N Engl J Med 1991; 324:1605–1611. [CrossRef] [PubMed]
  8. Jackman WM, Beckman KJ, McClelland JH, et al. Treatment of supraventricular tachycardia due to atrioventricular nodal reentry by radiofrequency catheter ablation of slow-pathway conduction. N Engl J Med 1992; 327:313–318. [CrossRef] [PubMed]
  9. Saoudi N, Nair M, Abdelazziz A, et al. Electrocardiographic patterns and results of radiofrequency catheter ablation of clockwise type i atrial flutter. J Cardiovasc Electrophysiol 1996; 7:931–942. [CrossRef] [PubMed]
  10. Haïssaguerre M, Jais P, Shah DC, et al. Spontaneous initiation of atrial fibrillation by ectopic beats originating in the pulmonary veins. N Engl J Med 1998; 339:659–666. [CrossRef] [PubMed]
  11. Oral H, Chugh A, Good E, et al. Randomized comparison of encircling and nonencircling left atrial ablation for chronic atrial fibrillation. Heart Rhythm 2005; 2:1165–1172. [CrossRef] [PubMed]
  12. Elayi CS, Di Biase L, Barrett C, et al. Atrial fibrillation termination as a procedural endpoint during ablation in long-standing persistent atrial fibrillation. Heart Rhythm 2010; 7:1216–1223. [CrossRef] [PubMed]
  13. Reddy VY, Shah D, Kautzner J, et al. The relationship between contact force and clinical outcome during radiofrequency catheter ablation of atrial fibrillation in the toccata study. Heart Rhythm 2012; 9:1789–1795. [CrossRef] [PubMed]
  14. Nattel S. New ideas about atrial fibrillation 50 years on. Nature 2002; 415:219–226. [CrossRef] [PubMed]
  15. Vaquero M, Calvo D, Jalife J. Cardiac fibrillation: from ion channels to rotors in the human heart. Heart Rhythm 2008; 5:872–879. [CrossRef] [PubMed]
  16. Allessie MA, de Groot NM, Houben RP, et al. The electropathological substrate of longstanding persistent atrial fibrillation in patients with structural heart disease: Longitudinal dissociation. Circ Arrhythm Electrophysiol 2010; 3: 606-615. [CrossRef] [PubMed]
  17. Moe GK, Rheinboldt W, Abildskov J. A computer model of atrial fibrillation. Am Heart J 1964; 67:200–220. [PubMed]
  18. Haissaguerre M, Sanders P, Hocini M, et al. Catheter ablation of long-lasting persistent atrial fibrillation: Critical structures for termination. J Cardiovasc Electrophysiol 2005; 16:1125–1137. [CrossRef] [PubMed]
  19. Lewis T. Observations upon flutter and fibrillation as it occurs in patients. Heart 1921; 8:193–227.
  20. Skanes AC, Mandapati R, Berenfeld O, Davidenko JM, Jalife J. Spatiotemporal periodicity during atrial fibrillation in the isolated sheep heart. Circulation 1998; 98:1236–1248. [CrossRef] [PubMed]
  21. Sahadevan J, Ryu K, Peltz L, et al. Epicardial mapping of chronic atrial fibrillation in patients: preliminary observations. Circulation. 2004; 110:3293–3299. [CrossRef] [PubMed]
  22. Cuculich PS, Wang Y, Lindsay BD, et al. Noninvasive characterization of epicardial activation in humans with diverse atrial fibrillation patterns. Circulation 2010; 122:1364–1372. [CrossRef] [PubMed]
  23. Zhao J, Huang W, Yao Y, et al. Electropathological substrate detection of persistent atrial fibrillation—a novel method to analyze unipolar electrograms of noncontact mapping. Conf Proc IEEE Eng Med Biol Soc 2011; 2011:1471–1474. [CrossRef] [PubMed]
  24. Narayan SM, Krummen DE, Shivkumar K, Clopton P, Rappel W-J, Miller J. Treatment of atrial fibrillation by the ablation of localized sources: the conventional ablation for atrial fibrillation with or without focal impulse and rotor modulation: Confirm trial. J Am Coll Cardiol 2012; 60:628–636. [CrossRef] [PubMed]
  25. Shivkumar K, Ellenbogen, Kenneth A, et al. Acute termination of human atrial fibrillation by identification and catheter ablation of localized rotors and sources: first multicenter experience of focal impulse and rotor modulation (firm) ablation. J Cardiovasc Electrophysiol 2012. [CrossRef] [PubMed]
  26. Schilling RJ, Kadish AH, Peters NS, Goldberger J, Davies DW. Endocardial mapping of atrial fibrillation in the human right atrium using a non-contact catheter. Eu Heart J 2000; 21:550–564. [CrossRef] [PubMed]
  27. Ganesan AN, Kuklik P, Lau DH, et al. Bipolar electrogram shannon entropy at sites of rotational activation: Implications for ablation of atrial fibrillation (abstract). Heart Rhythm 2012; suppl. [CrossRef] [PubMed]
  28. Lee G, Kumar S, Teh A, et al. Epicardial wave mapping in human long-lasting persistent af. Rotors, complex wavefronts and disorganized activity (abstract). Heart Rhythm 2012; suppl [CrossRef] [PubMed]
  29. Lin Y-J, Lo M-T, Lin C, et al. The role of rotors in maintaining non-paroxysmal atrial fibrillation: Insight from the mapping and catheter ablation, substrate characteristics, and prevalence (abstract). 2012
  30. Narayan SM, Krummen DE, Rappel W-J. Clinical mapping approach to identify rotors and focal beats in human atrial fibrillation. J Cardiov Electrophysiol 2012; 23:447–454. [CrossRef] [PubMed]
  31. Narayan SM, Bode F, Karasik PL, Franz MR. Alternans of atrial action potentials as a precursor of atrial fibrillation. Circulation 2002; 106:1968–1973. [CrossRef] [PubMed]
  32. Narayan SM, Franz MR. Quantifying fractionation and rate in human atrial fibrillation using monophasic action potentials: Implications for substrate mapping. Europace 2007e9:vi89–vi95. [CrossRef] [PubMed]
  33. Narayan SM, Kazi D, Krummen DE, Rappel W-J. Repolarization and activation restitution near human pulmonary veins and atrial fibrillation initiation: A mechanism for the initiation of atrial fibrillation by premature beats. J Am Coll Cardiol 2008; 52:1222–1230. [CrossRef] [PubMed]
  34. Narayan SM, Franz MR, Clopton P, Pruvot EJ, Krummen DE. Repolarization alternans reveals vulnerability to human atrial fibrillation. Circulation 2011; 123:2922–2930. [CrossRef] [PubMed]
  35. Lalani G, Schricker A, Gibson M, Rostamanian A, Krummen DE, Narayan SM. Atrial conduction slows immediately before the onset of human atrial fibrillation: A bi-atrial contact mapping study of transitions to atrial fibrillation. J Am Coll Cardiol 2012; 59:595–606. [CrossRef] [PubMed]
  36. Teh AW, Kistler PM, Lee G, et al. Electroanatomic remodeling of the left atrium in paroxysmal and persistent atrial fibrillation patients without structural heart disease. J Cardiovasc Electrophys 2012; 23:232–238. [CrossRef] [PubMed]
  37. Mahnkopf C, Badger TJ, Burgon NS, et al. Evaluation of the left atrial substrate in patients with lone atrial fibrillation using delayed-enhanced mri: Implications for disease progression and response to catheter ablation. Heart Rhythm 2010; 7:1475–1481. [CrossRef] [PubMed]
  38. Earley M, Abrams D, Sporton S, Schilling R. Validation of the non-contact mapping system in the left atrium during permanent atrial fibrillation and sinus rhythm. J Am Coll Cardiol 2006; 48:485–491. [CrossRef] [PubMed]
  39. Narayan SM, Shivkumar K, Krummen DE, Miller JM, Rappel W-J. Panoramic electrophysiological mapping but not individual electrogram morphology identifies sustaining sites for human atrial fibrillation (AF rotors and focal sources relate poorly to fractionated electrograms). Circ Arrhythm Electrophysiol 2013 Feb;6(1):58-67. [CrossRef] [PubMed]
  40. Narayan SM, Krummen DE, Enyeart MW, Rappel W. Computational mapping approach identifies stable and long-lived electrical rotors and focal sources in human atrial fibrillation. PLos One 2012; 7:e46034. [CrossRef] [PubMed]
  41. Haissaguerre M, Lim KT, Jacquemet V, et al. Atrial fibrillatory cycle length: Computer simulation and potential clinical importance. Europace. 2007; 9(Suppl 6):vi64–70. [CrossRef] [PubMed]
  42. Takahashi Y, O’Neill MD, Hocini M, et al. Characterization of electrograms associated with termination of chronic atrial fibrillation by catheter ablation. J Am Coll Cardiol 2008; 51:1003–1010. [CrossRef] [PubMed]
  43. Jais P, Hocini M, Sanders P, et al. Long-term evaluation of atrial fibrillation ablation guided by noninducibility. Heart Rhythm 2006; 3:140–145. [CrossRef] [PubMed]
  44. Narayan SM, Day J, Ellenbogen K, et al. Elimination of sources for human atrial fibrillation (focal impulse and rotor modulation, firm) organizes and acutely terminates af prior to pulmonary vein isolation: a multicenter experience (abstract). Circulation 2012.
  45. Narayan SM, Patel J, Mulpuru SK, Krummen DE. Focal impulse and rotor modulation (firm) of sustaining rotors abruptly terminates persistent atrial fibrillation to sinus rhythm with elimination on follow-up. Heart Rhythm 2012; 9:1436–14369. [CrossRef] [PubMed]
  46. Oral H, Chugh A, Good E, et al. Radiofrequency catheter ablation of chronic atrial fibrillation guided by complex electrograms. Circulation 2007; 115:2606–2612. [CrossRef] [PubMed]
  47. Oral H, Chugh A, Yoshida K, et al. A randomized assessment of the incremental role of ablation of complex fractionated atrial electrograms after antral pulmonary vein isolation for long-lasting persistent atrial fibrillation. J Am Coll Cardiol 2009; 53:782–789. [CrossRef] [PubMed]
  48. Oral H, Pappone C, Chugh A, et al. Circumferential pulmonary-vein ablation for chronic atrial fibrillation. N Engl J Med 2006; 354:934–941. [CrossRef] [PubMed]
  49. Wazni OM, Marrouche NF, Martin DO, et al. Radiofrequency ablation vs antiarrhythmic drugs as first-line treatment of symptomatic atrial fibrillation: A randomized trial. JAMA 2005; 293:2634–2640. [CrossRef] [PubMed]



BAO Extension 2019 Advertisement