Europace Advance Access originally published online on July 14, 2008
Europace 2008 10(11):1336-1339; doi:10.1093/europace/eun189
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SHORT COMMUNICATIONS
Is atrial fibrillation with very short cycle length suitable for ablation? A case report
1 Institute of Cardiology, University of Bologna, Azienda Ospedaliera S.Orsola-Malpighi, Bologna, Italy; 2 Department of Cardiac Electrophysiology, The Heart Hospital, UCLH Foundation Trust, 16–18 Westmoreland Street, London W1G 8PH, UK
Manuscript submitted 5 May 2008. Accepted after revision 25 June 2008.
* Corresponding authors. Tel: +39 0516363498 (I.D.); +44 2075738888; fax: +44 2075838847 (A.W.C.C.) E-mail address: igor.diemberger{at}gmail.com (I.D.) or anthony.chow{at}uclh.nhs.uk (A.W.C.C.)
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Abstract |
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We present a case of a 36-year-old woman with highly symptomatic persistent atrial fibrillation (AF) refractory to sotalol, flecainide, and external direct current (DC) cardioversion. The patient underwent biatrial mapping and ablation procedure for AF. Both atria were characterized by refractory properties which were much shorter than reported previously. Global fibrillatory activity was present with a median cycle length of 120 ms (range: 62–143). Extensive map-guided ablation sets had to be delivered to both left and right sides before effective DC cardioversion enabled sinus rhythm (SR) restoration. The patient remained in SR at 9 months of follow-up.
Key Words: Atrial fibrillation, Ablation, Mapping, Remodelling, Persistent
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Introduction |
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Most strategies currently used to ablate persistent atrial fibrillation (AF) are aimed at eradicating discrete high-frequency regions of activity to increase atrial wavelength and prevent AF. Specific patients may require different extent of atrial ablation to achieve success.1
However, there are no current reports of marked global changes in atria refractoriness, leading to a widespread short cycle length (CL) AF. We present the case of a young woman with both atria globally fibrillating with very short CL. Strategies used to perform ablation are also presented. |
Case report |
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A 36-year-old woman was referred for AF lasting
10 years, despite previous treatment with sotalol and later flecainide plus diltiazem. She presented hypertensive cardiomyopathy and complained of exertional chest pain, although angiography excluded coronary artery disease. She also presented sickle cell trait. She had undergone at least three previous electrical direct current (DC) cardioversions for persistent AF; the last one in 2003 which led to the maintenance of sinus rhythm (SR) until 2006. In this occasion, although previously effective, electrical cardioversion (combined with pre-treatment with flecainide plus diltiazem) failed to restore SR. In view of her age, symptoms, and deterioration of the LV function with AF, a decision was made to proceed with AF ablation. After obtaining informed consent, an electrophysiological cardiac mapping study was performed. Multipolar catheters were placed in the right atrium, His-bundle, right ventricular apex, and coronary sinus (CS). A 4 mm irrigated tipped ablation catheter and a circumferential 20-pole mapping catheter were advanced into the left atrium (LA) through trans-septal catheterization. The three-dimensional LA geometry was reconstructed using the Ensite NavX system (St Jude Medical, Endocardial Solutions, St Paul, MN, USA). The average CL of the fibrillatory waves recorded at the pulmonary veins ostia and almost the entire LA was unusually short (median 120 ms, range 62–143; Figures 1 and 2). As shown by the dominant frequency map (Figure 2), the majority of the LA had an activation frequency within 7 and 16 Hz. The strategy used for radiofrequency (RF) ablation initially consisted of wide area circumferential ablation and ostial isolation until all pulmonary veins were electrically disconnected, followed by a roof line and a line encircling the LA appendage, which had particularly short AF CLs activation (Figure 1B). The patient remained in AF despite initial regularization of activation in the LA (Figure 3). The ablation was then extended to the CS, until complex fractionate signals were eradicated. However, further mapping of the right atrium confirmed that most of the myocardium had very short CL similar to the LA before the ablation (Figure 4). Accordingly, the right atrium was then targeted for AF ablation, with lesions delivered at the superior vena cava junction, isthmus, and lateral wall. Despite regularization and an initial increase in the CL to 230 ms (without any noticeable fluctuations in AF CL), restoration of SR was achievable only through electrical DC cardioversion (200 J biphasic single shock). The patient has been taken off all anti-arrhythmic drugs and warfarin after 6 months from the ablation and is still maintaining SR at 9 months from the procedure.
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Discussion |
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Studies of human atrial electrophysiology suggest that normally atrial refractoriness is
180–250 ms, but can be shorter in focal driver areas often associated with complex fractionated electrograms.1 This case evidences advanced atrial remodelling with profound global electrophysiological changes in refractoriness, involving both atria to an extent (almost global) that exceeds previously reported values both in humans2 and in animal3 studies. It is now recognized that persistent AF can progressively shorten atrial effective refractory periods,1 but rarely below 180 ms. This is the first report of AF intervals averaging 120 ms on both atria, with areas presenting intervals that reach 50–60 ms. Such short AF intervals pose further difficulties in forming global strategies for RF ablation in patients with persistent AF.
In these patients, the ablation procedure is a sequential-tailored approach focusing on different targets such as complex fractionated atrial electrograms, areas of short CL activity, and sites of dominant frequency.1 During ablation, AF CL usually prolongs until the atrium can no longer sustain the fibrillatory process and AF terminates (converting directly to SR or to atrial tachycardia, which can then be ablated). However, in this patient, despite achieving a broad regularization of local activity after extensive ablation of selected areas, the global atrial activity appeared to be almost unchanged. The persistence of AF with areas of short CL activity after pulmonary vein isolation (Figure 3) supports the concept that (at least in chronic AF), despite their importance in AF triggering, their role of AF maintenance appears to be less definite. These results and our data highlight the extent of human substrate remodelling, which occurs in chronic AF. This phenomenon can also explain the absence of a left-to-right gradient in atrial frequency in patients with AF lasting >1 month but present in patients with paroxysmal AF.4
Additional factors affecting atrial refractoriness include autonomic impairment, scars, and changes in the cellular membrane function. Intriguingly, sickle cell trait is associated with a shift in the autonomic nervous system activity,5 which can explain some of the peculiarities of this case. Of note, we required electrical cardioversion to restore SR, despite the extensive ablation of the high-frequency nests on both left and right sides. This appears to be in contrast with previous findings by Nademanee,6 showing a high incidence of AF conversion during ablation. However, Oral et al.7 provided different results while adopting a similar approach to AF ablation (i.e. guided by complex atrial electrograms), and they also underlined the absence of a relationship between acute AF termination (during ablation) and long-term freedom from recurrent arrhythmia. A plausible explanation of our results can be that in such cases a complete elimination of the substrate may be unattainable, but the modification of arrhythmic triggers and probably of the autonomic influences8 might had been enough to avoid AF re-induction. This finding suggests that AF ablation can still be effective to achieve SR in patients with persistent patients, but may require extensive substrate modification.
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Limitations of the study |
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We performed a electrophysiological study according to the routine protocol adopted in our Institution for AF ablation: this includes the use of bipolar recordings. To avoid the possible bias of ‘double-counting’ atrial fibrillatory signals9
, we used only sharp discrete atrial electrograms with a minimum sampling time of 10 s per site to confirm consistency of the reported average AF CLs and of the dominant frequency map. Despite the limited duration of the follow-up (9 months from the procedure and 3 months from anti-arrhythmic drugs discontinuation), we think that the persistence of SR in this particular case might have been unlikely without extensive modification of arrhythmic triggers (and probably of autonomic influences). |
Funding |
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J.M. has a research grant supported by St Jude Medical. A.W.C.C. also holds a research grant from Boston Scientific.
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References |
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[1] Fuster V, Rydén LE, Cannom DS, Crijns HJ, Curtis AB, Ellenbogen KA, et al. ACC/AHA/ESC 2006 guidelines for the management of patients with atrial fibrillation-executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines (writing committee to revise the 2001 guidelines for the management of patients with atrial fibrillation). Circulation (2006) 114:700–52.
[2] Lin Y-J, Tai C-T, Kao T, Tso H-W, Higa S, Tsao H-M, et al. Frequency analysis in different types of paroxysmal atrial fibrillation. J Am Coll Cardiol (2006) 47:1401–7.
[3] Niwano S, Kojima J, Fukaya H, Sato D, Moriguchi M, Niwano H, et al. Arrhythmogenic difference between the left and right atria during rapid atrial activation in a canine model of atrial fibrillation. Circ J (2007) 71:1629–35.[CrossRef][Web of Science][Medline]
[4] Lazar S, Dixit S, Marchlinski FE, Callans DJ, Edward P. Presence of left-to-right atrial frequency gradient in paroxysmal but not persistent atrial fibrillation in humans. Circulation (2004) 110:3181–6.
[5] Connes P, Martin C, Barthelemy JC, Monchanin G, Atchou G, Forsuh A, et al. Nocturnal autonomic nervous system activity impairment in sickle cell trait carriers. Clin Physiol Funct Imaging (2006) 26:87–91.[CrossRef][Web of Science][Medline]
[6] Nademanee K. Trials and travails of electrogram-guided ablation of chronic atrial fibrillation. Circulation (2007) 115:2592–4.
[7] Oral H, Chugh A, Good E, Wimmer A, Dey S, Gadeela N, et al. Radiofrequency catheter ablation of chronic atrial fibrillation guided by complex electrograms. Circulation (2007) 115:2606–12.
[8] Oral H, Morady F. Autonomic innervation, atrial electrogram morphology, and atrial fibrillation. J Am Coll Cardiol (2007) 50:1332.
[9] Narayan SM, Krummen DE, Kahn AM, Karasik PL, Franz MR. Evaluating fluctuations in human atrial fibrillatory cycle length using monophasic action potentials. Pacing Clin Electrophysiol (2006) 29:1209–18.[CrossRef][Medline]
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