(Circulation. 2000;101:1409.)
© 2000 American Heart Association, Inc.
Clinical Investigation and Reports |
Electrophysiological End Point for Catheter Ablation of Atrial Fibrillation Initiated From Multiple Pulmonary Venous Foci
Presented in part at the 20th Annual NASPE Meeting, Toronto, Canada, May 12 to 15, 1999.
From the Hôpital Cardiologique du Haut-Lévêque, Bordeaux-Pessac, France.
Correspondence to Professeur Michel Haïssaguerre, Hôpital Cardiologique du Haut-Lévêque, Ave de Magellan, 33604 Bordeaux-Pessac, France.
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Abstract |
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 Top Abstract IntroductionMethodsResultsDiscussionReferences |
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Background—The end point for catheter ablation of pulmonary vein (PV) foci initiating atrial fibrillation (AF) has not been determined.
Methods and Results—Ninety patients underwent mapping during
spontaneous or induced ectopy and/or AF initiation. Ostial PV ablation
was performed by use of angiograms to precisely define targeted sites.
Success defined by elimination of AF without drugs was correlated with
the procedural end point of the abolition of distal PV potentials. A
total of 197 arrhythmogenic PV foci (97%)—single in 31% and multiple
in 69%—and 6 atrial foci were identified. A discrete radiofrequency
(RF) application eliminated the PV potentials in 9 PV foci, whereas 2
foci from the same PV required RF applications at separate sites in 19
cases. In others, a wider region was targeted with progressive
elimination of ectopy. In 49 patients, multiple sessions were necessary
owing to recurrent or new ectopy. The clinical success rates were 93%,
73%, and 55% in patients with 1, 2, and 
3 arrhythmogenic PV foci.
Recovery of local PV potential and the inability to abolish it were
significantly associated with AF recurrences (90% success rate
with versus 55% without PV potential abolition). PV stenosis
was noted acutely in 5 of 6 cases, remained unchanged at restudy, and
was associated with RF power >45 W.
Conclusions—Multiple PV foci are involved in initiation of AF, and elimination of PV muscle conduction is associated with clinical success.
Key Words: atrial fibrillation • catheter ablation • electrophysiology
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Introduction |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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The pulmonary veins (PVs) have been shown to trigger paroxysms of atrial fibrillation (AF), and radiofrequency (RF) ablation of these foci can eliminate AF.1 2 3 4 5 However, the efficacy of ablation is limited by a high percentage of recurrences and the unknown frequency of venous stenosis, and the end point of successful ablation, particularly in patients with scant ectopy, has not been defined. The present study was prospectively performed to assess these issues.
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Methods |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Patient Characteristics
The study population consisted of 90 consecutive patients (Table 1
). Thirty-seven had >700
ectopies per day (Figure 1).
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Electrophysiological Study
The study was performed as described previously with the use of
2 or 3 electrode catheters and after confirmation of the absence of
intracardiac thrombi by transesophageal
echocardiography.5 The left atrium
(LA) and PVs were explored through either a patent foramen ovale (19
patients) or a transseptal catheterization. Selective
PV angiography was performed by hand injection of 5 to 10 mL of
contrast with an NIH catheter and displayed during the procedure.
Heparin was titrated to maintain a partial thromboplastin time of 60 to
90 seconds (control, 30 seconds).
In patients with few ectopies or sustained AF necessitating cardioversion, 2 steerable ablation catheters (with different curves) were used to map the PVs simultaneously. When few ectopies were observed, the following provocative maneuvers were performed: vagal maneuvers, including carotid sinus massage, deep breathing, and Valsalva; slow-rate atrial pacing (bursts of 3 to 10 stimuli at 100 to 200 bpm for postpause ectopy); isoproterenol infusion (2 to 4 µg/min); high-rate pacing; and their combinations. If long-lasting AF was induced, internal (n=6) or external electrical cardioversions were performed, sometimes followed by AF reinitiation. ATP injection (20 to 80 mg) or saline infusion (500 mL in 15 minutes) was tried in 4 patients each. A swallowing maneuver was a reproducible mode of induction in 1 patient.
Mapping was performed in 2 sites in the superior PV(s) either
sequentially or simultaneously and thereafter in the
inferior veins (Figures 2 and 3). If the earliest activity could not be
traced from any PV, both atria were mapped.
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Definition of an Arrhythmogenic PV
An arrhythmogenic PV4 5 was defined on the basis of
documented ectopy—single or multiple and with or without conduction to
the LA. During sinus rhythm, double or multiple potentials were
recorded in a progressively later temporal sequence, synchronous
with the first (right PVs) or second (left PVs) half of the P wave
(Figure 3
). The first low-frequency potential reflected
activation of the adjacent atrium. The latest high-frequency potentials
indicated PV muscle potentials (PVPs). The ostial PVPs were sometimes
not obvious in the left PVs because of the superimposed LA potential
during sinus rhythm; however, pacing of the distal coronary
sinus (or LA appendage) allowed their separation and thus easy
recognition of PVP (Figure 4).
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During ectopy from an arrhythmogenic PV, there was a reversal in
activation sequence, from the distal PV trunk (source) to the ostium
and LA (exit), with the PVP preceding the LA potential. Ectopic
discharges with the shortest coupling interval were not conducted to
the LA producing isolated PVP confined within the PV (Figures 2 and 3). They were recognized as a PVP coincident with or just
after the ventricular electrogram and could be
distinguished from a potential of ventricular origin by
their spontaneous disappearance (intermittent PVP) or suppression
during atrial pacing.
Conversely, if the explored PV was not the origin of ectopy, it was
"passively" activated as in sinus rhythm with a
proximal-to-distal sequence and a PVP after or fusing with the LA
potential. Multiple foci in the same PV were defined by the presence of
2 different sources and exits at opposite locations of the PV
perimeter (eg, roof and bottom) demonstrated by selective PV
angiography.
Ablation Procedure
RF ablation of atrial foci was performed at the site of earliest
activation. RF ablation of arrhythmogenic PV was performed within
15 mm of the PV ostium; the exact location depended on catheter
stability. This was thought to be safer (vis-à-vis the risk of PV
stenosis) than more distal applications in smaller veins. The
perimeter of the PV ostium was mapped to localize the ostial sector
showing the earliest activity during ectopy, and the highest and
sharpest PV potential was first targeted for ablation. Subsequent RF
applications were performed if needed at contiguous sites showing PVP.
The end point was elimination of ectopy, spontaneous or induced by
provocative maneuvers, and elimination of PV muscle
conduction (during sinus rhythm) distally to the ablation site(s) on
the basis of either abolition or dissociation of distal PVP. To assess
capture of the LA, local pacing was performed from these sites.
RF energy was delivered at the distal electrode of the thermocouple-equipped catheter (target, 50°C) with a power limit of 45 to 50 W in the first 35 patients. Because of the occurrence of several acute PV stenoses (see later), a maximal power limit of 25 to 30 W was subsequently set for the last 55 patients. If >1 PV was arrhythmogenic, the PV producing the most repetitive ectopy and/or initiating AF was first targeted; then, RF energy was delivered in a second PV after angiographic verification of the unchanged patency of the first one. PV angiography was performed at the end of ablation in all but 4 patients (technical problems). PV stenosis was defined as a diameter reduction of >50%. Repeated PV angiography was performed >1 month later in 58 patients.
Patients were discharged beyond the third day under oral anticoagulant. In the event of recurrent AF, all patients were advised to undergo a new study, and ablation was performed if there was no PV stenosis. The procedure was considered a success when the AF episodes were totally eliminated without antiarrhythmic drugs both clinically and on Holter recordings. Any suggestive but undocumented symptoms were attributed to AF recurrence. Anticoagulants were interrupted 3 months after successful elimination of AF unless there were other risk factors.
Statistical Analysis
Continuous variables are expressed as group mean±SD and
compared with the use of a Kruskal-Wallis or Student’s t
test. Noncontinuous variables were compared by use of the
2 or Fisher’s exact test. Statistical
significance was selected at P<0.05.
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Results |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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In 4 patients, initiation and maintenance of AF were due to a rapidly firing focus with a persistent distal-to-proximal PV activation sequence during AF (focal AF). The remaining patients had focally initiated AF with a short burst of focal discharges initiating typical intra-atrial fibrillation, which continued independently.
Mapping of Triggering Ectopic Beats
In 58 patients, provocative maneuvers were needed to
elicit ectopy (Table 2). Sustained AF
required electrical external or internal cardioversions in 38
patients.
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Ectopy originating from a single PV was found in 27 patients, 2 in 22,
3 in 29, and 4 in 11, for a total of 197 arrhythmogenic PVs in 89
patients, and from the atrial muscle in 6 patients (right atrium in 1,
atrial septum in 1, and posterior LA in 4). A single arrhythmogenic PV
was associated with female sex, younger age, less frequent and shorter
AF paroxysms, and smaller atrial dimensions (Table 3).
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RF Ablation of Foci Initiating AF
Atrial Foci
One patient (patient 11) had a single atrial focus and underwent 3
ablation sessions because of 2 recurrences after ablation. Five
patients had atrial foci in addition to arrhythmogenic PV; ablation was
successful in 3 and failed in 2 because of insufficient ectopy.
Frequently Discharging PV Foci
Mapping of ectopy from 9 PVs (4 left inferior PVs
[LIPVs], 3 right inferior PVs [RIPVs], 1 right superior
PV [RSPV], and 1 left superior PV [LSPV]) showed a discrete source
from the ostium of a venous branch and a discrete exit at the ostium of
the venous trunk reflected by a localized (which disappeared with small
catheter movements on either side) continuum of the PVP-LA potential.
Ectopy was abruptly eliminated by a discrete RF ablation, which
abolished the ostial and corresponding distal (site activated
later into the venous branch) PVP during sinus rhythm (Figure 5).
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In 19 PVs (9 LIPVs, 6 LSPVs, and 4 RSPVs), there were 2 sources of
ectopy from different PV branches associated with 2 distinct ostial
exits necessitating ablation at separate points of the ostium (Figure 6). This produced abrupt disappearance of
targeted ectopies and sequentially eliminated the ostial and distal
PVPs in each corresponding venous branch.
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In the remaining PVs, mapping of the ostium during ectopy showed
synchronous local activation in a large sector of the venous perimeter
(Figure 7). Correspondingly, during sinus
rhythm, PVPs were recorded in a large part of the ostium ranging
from one quarter to the full circumference. In 14, differing activation
times during ectopy suggested various ectopy sources or activation
courses. Sequential RF applications at the ostium produced a
progressive decrease in ectopies or an initial disappearance of
repetitive followed by that of isolated ectopy; the first applications
commonly produced exacerbation of ectopies. Ablation eliminated
progressively the local PVPs, usually requiring 2 or 3 series of RF
applications along the entire sector (Figure 8). A progressive prolongation of the
LA-PVP conduction time (both locally and distally) was observed during
sinus rhythm, and ablation at the remaining site(s) without atrial-PVP
delay (gap like continuum electrogram) resulted in abrupt disappearance
of local and distal PVPs, indicating disconnection. An abrupt
reappearance of local and distal PVPs was noted in 19 patients, and
reablation as described above was successfully performed.
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In 9 patients, after ablation, residual isolated ectopies were found to originate at the atrial edge of the PV ostium (instead of inside the PV), indicating a modification of the source of earliest activity as a result of RF delivery and necessitating additional RF applications.
Patients With Insufficient PV Ectopy
In 12 patients, only 1 to 5 ectopies were noted despite multiple
provocative maneuvers; however, this was sufficient to
identify the arrhythmogenic PV. RF applications were performed during
sinus rhythm or distal coronary sinus pacing at the sites
exhibiting PVPs, resulting in total elimination of the distal PVPs
(Figure 9).
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In 8 other patients, PV ectopy immediately produced sustained AF, which recurred after repeated cardioversions (5±2). In 5 patients, a circumferential PV ostial ablation was performed during AF, and progressive abolition of the PVP (sharpest potentials) could be seen distally inside the PV; after a new cardioversion, AF did not reappear, and additional RF applications abolished the residual PVP during sinus rhythm. In the last 3 patients, amiodarone (300 to 600 mg) was infused and ablation was performed after conversion in sinus rhythm.
Reablation and Final Mapping Results
A total of 155 ablation sessions were performed: 1 in 41 patients,
2 in 36, 3 in 10, and 4 in 3, for total procedure duration and
fluoroscopy times of 278±154 and 82±44 minutes, respectively (149±71
and 45±21 minutes per session).
At the end of the first session, ectopy was persistent in 9 patients,
and all had early recurrences of AF. Of the remaining 81, 40
(50%) had recurrent AF. These 49 patients underwent 1 to 3 (total, 65)
reablation sessions. During these sessions, mapping showed that the
ectopy was related to the persistence or recovery of a previously
targeted PVP in 24, originated from another part of a previously
targeted PV in 12, originated from a different PV in 21, and was
related to combinations of the above in 8. The recovered PVP was
delayed and thus obvious during sinus rhythm; it was present
(ostially and distally) at a discrete area in 9 patients and abolished
with a single RF application (Figure 10). In 4, it disappeared
intermittently by simple mechanical catheter pressure. Sequential RF
applications were needed in others to eliminate PVPs.
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After all ablation, mapping in 96 PVs showed preservation of the distal PVP. Local PV pacing from the area with PVP, even when it was very discrete, could capture the LA. All PVPs were eliminated in 86 PVs or dissociated in 15 (superior) PVs; pacing could not capture the LA.
Safety
Air embolism during catheter exchange was responsible for
transient ECG changes in 5 patients. A transient bradycardia occurred
in 3 patients during LSPV ablation. Patient 11 developed a
hemopericardium that was percutaneously drained during
the first ablation session. One patient had an episode of binocular
blurred vision for 2 minutes without thrombus visible at
transesophageal echocardiography.
One patient developed a reversible ischemic neurological
deficit 36 hours after ablation.
Angiograms performed just after ablation in 86 patients revealed a
narrowing of the ostium in 5 ablated PVs; in an additional patient who
received a single RF application at 30 W, the angiogram performed 5
minutes later showed stenosis of a 6-mm-diameter branch. PV
angiograms (n=115, including all those not angiographically studied
just after ablation) 1 month after ablation (mean, 5±4 months)
demonstrated a persistent similar stenosis in these PVs plus an
additional case that had not had an angiography just after ablation.
Thus, a total of 6 ablated PVs (3%) had stenosis of the PV
trunk: 1 patient had a double PV stenosis (RSPV and LIPV) and 4
had a single PV stenosis (3 LIPV and 1 LSPV). All
stenoses were located at the most distal ablation site in the
PV trunk. The mean gradient across the stenosis was 4±2
mm Hg (range, 2 to 7 mm Hg), but no patient had
pulmonary hypertension. However, 2 had symptoms: 1 described
dyspnea during strong effort, and 1 patient developed hemoptysis and
pleural effusion 1 week after interruption of warfarin (3 months after
ablation). PV thrombosis demonstrated by spiral CT scan subsided after
2 weeks of heparin; a repeated scan showed only PV stenosis.
Stress tests in 4 of 5 patients showed an unchanged performance
relative to their peak effort before ablation. Analysis showed
that the prevalence of PV trunk stenosis was the highest for
LIPV (7% of LIPV versus 1.5% of all other PVs, P<0.05)
and when the maximal delivered RF power reached 45 W (5 of 37 versus 1
of 160, P<0.01). No ostial PV stenosis was observed
with a RF power limit of 30 W, including after circumferential
ablation.
Final Outcome
With a mean follow-up of 8±5 months after discharge, AF was
completely eliminated in 64 patients (71%) without antiarrhythmic
drugs (success group), and anticoagulants were interrupted in 52. The
other 26 patients were prescribed a drug that was ineffective before
ablation, resulting in total elimination of AF in 12.
Table 4 compares the variables
according to outcome. The presence of a single arrhythmogenic PV and
successful elimination of PVPs were significant predictors of success.
The success rate was 90% (36 of 40) when PVPs were eliminated in all
arrhythmogenic PVs and 55% (27 of 49) when PVPs were still persistent
in 1 arrhythmogenic PVs.
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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This study describes the results of electrophysiologically directed curative treatment for paroxysmal AF targeting the initiating triggers. It demonstrates plurifocal sources within the PV, a significant extent of local arrhythmogenic tissue, and better clinical outcome with the interruption of all conduction from the PV.
Multiple Sources of Ectopy
The study population included consecutively referred patients with
drug-resistant paroxysmal AF without selection criteria, thus
covering a broad range of situations encountered clinically.
Spontaneous ectopy was absent in most patients, and the average AF
duration was variable, ranging from 0 to 24 h/d. Spontaneous or
provoked AF paroxysms were initiated similarly by sudden trains of
focal discharges, with some PV foci, notably from the LIPV, discharging
only in bursts and without isolated ectopy. The prevalence of multiple
arrhythmogenic PVs was high (69%), perhaps because of wide inclusion
criteria, greater mapping experience, the use of
provocative maneuvers with simultaneous
exploration of different PV, and repeated
electrophysiological studies in cases of
recurrence. Moreover, multiple sources of AF in the same PV or
even a focal source "wandering" to the atrial edge of the PV were
observed. Multiple arrhythmogenic PVs were associated with older age,
longer AF duration, and larger atrial dimensions.
Electrophysiologically Guided
Ablation
Ablation guided by mapping ectopy was limited by its
unpredictability, its inconsistent inducibility, and the risk
of inducing AF requiring cardioversion. In patients with few ectopies,
the arrhythmogenic PV could still be readily identified, and then all
PVPs were ablated in sinus rhythm at the ostium, possibly
eliminating multiple potential foci in the same trunk. LA or distal
coronary sinus pacing separated the LA and PVPs, facilitating
PVP identification notably in the left PV.
The results indicate that elimination of the PVPs correlated better with clinical success than the acute suppression of arrhythmias. However, it should be noted that a successful outcome could be observed without complete PVP elimination and that some "unsuccessfully" treated patients were remarkably improved with a previously ineffective drug. The PVP reflects activation of muscular LA bands extending into the PV with longitudinal, oblique, or complex courses and ending in a cul-de-sac or even looping back in the LA.1 2 3 The source, its course within the pulmonary vein, and its exit into the LA may all be considered appropriate individual targets for ablation. The PVP was recorded over a broader area proximally but with great variability. Therefore, a few seconds of energy application was sufficient at some proximal sites to eliminate downstream PV muscle activity, whereas wide or repeated RF applications were required in most others. PV disconnection was demonstrated by either dissociated or abolished distal PVP and confirmed by the inability to capture the LA by pacing from the PV. On the other hand, the inability to abolish the arrhythmogenic PVP or its recovery (even in a very discrete area and with a prolonged conduction time) was associated with recurrence of AF. This occurred obviously more frequently for multiple PVs, representing a challenge both in terms of efficacy and safety that may be overcome with the use of more appropriate mapping and ablation catheters.
PV stenosis occurred in 5 patients; however, all had no pulmonary hypertension, so no treatment was required. With the limitation of RF power to <30 W, acute and late PV stenosis was not observed at the ostium (although it occurred in a branch), but a longer follow-up is needed for confirmation. Given this uncertainty, a curative AF procedure based on PV ablation that uses current technologies should be reserved for patients with frequent drug-resistant paroxysmal AF who are exposed to the thromboembolic and hemodynamic risks of persistent arrhythmia and its inherent increased morbidity and mortality.
Received June 18, 1999; revision received October 1, 1999; accepted October 12, 1999.
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V. Fuster, L. E. Ryden, D. S. Cannom, H. J. Crijns, A. B. Curtis, K. A. Ellenbogen, J. L. Halperin, J.-Y. Le Heuzey, G. N. Kay, J. E. Lowe, 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) Developed in Collaboration With the European Heart Rhythm Association and the Heart Rhythm Society J. Am. Coll. Cardiol., August 15, 2006; 48(4): 854 - 906. [Full Text] [PDF]
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V. Fuster, L. E. Ryden, D. S. Cannom, H. J. Crijns, A. B. Curtis, K. A. Ellenbogen, J. L. Halperin, J.-Y. Le Heuzey, G. N. Kay, J. E. Lowe, et al. ACC/AHA/ESC 2006 Guidelines for the Management of Patients With Atrial Fibrillation: 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) Developed in Collaboration With the European Heart Rhythm Association and the Heart Rhythm Society J. Am. Coll. Cardiol., August 15, 2006; 48(4): e149 - e246. [Full Text] [PDF]
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V. Fuster, L. E. Ryden, D. S. Cannom, H. J. Crijns, A. B. Curtis, K. A. Ellenbogen, J. L. Halperin, J.-Y. Le Heuzey, G. N. Kay, J. E. Lowe, et al. ACC/AHA/ESC 2006 Guidelines for the Management of Patients With Atrial Fibrillation: 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): Developed in Collaboration With the European Heart Rhythm Association and the Heart Rhythm Society Circulation, August 15, 2006; 114(7): e257 - e354. [Full Text] [PDF]
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V. Fuster, L. E. Ryden, D. S. Cannom, H. J. Crijns, A. B. Curtis, K. A. Ellenbogen, J. L. Halperin, J.-Y. Le Heuzey, G. N. Kay, J. E. Lowe, 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): Developed in Collaboration With the European Heart Rhythm Association and the Heart Rhythm Society Circulation, August 15, 2006; 114(7): 700 - 752. [Full Text] [PDF]
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Authors/Task Force Members, V. Fuster, L. E. Ryden, D. S. Cannom, H. J. Crijns, A. B. Curtis, K. A. Ellenbogen, J. L. Halperin, J.-Y. Le Heuzey, G. N. Kay, 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) Developed in collaboration with the European Heart Rhythm Association and the Heart Rhythm Society Eur. Heart J., August 2, 2006; 27(16): 1979 - 2030. [Full Text] [PDF]
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M. Jahangiri, G. Weir, K. Mandal, I. Savelieva, and J. Camm Current strategies in the management of atrial fibrillation. A |