Hemodynamic Deterioration FollowingRadiofrequency Ablation of the AtrioventricularConduction System

MARC VANDERHEYDEN, MARC COETHALS, IGNASI ANCUERA,*PAUL NELLENS. ERIK ANDRIES, [OSEP BRUGADA,* and PEDRO BRUGADA

From the Cardiovascular Center, O.L.V, Ziekenhuis, Aaist Belgium;and the "Hospital Clinic, University of Barcelona, Barcelona, Spain

VANDERHEYDEN, M., ET AL.: Hemodynamic Deterioration Following Radiofrequency Ablation of theAtrioventricular Conduction System. Radiofrequeucy ablation of the atrioventricular conduction system(ACS) has become an estoblished theTapy for patients with drug refroctory atrial fihTiUation. We observedeight patients with hemodynamic deterioration ofteT radiofrequency oblotion of the otTioventTicular con-duction system. As we found hemodynamic deterioration related to worsening mitral regurgitation, wecompared the clinical history, eiectrophysiologicai, ond echocardiographic dato from the patients withhemodynamic deteriorotion and worsening mitral regurgitation (group 1) to those without hemodynamicdeterioration and stable mitral regurgitation after the procedure (group 2). Eight out of 108 patients (7.4%)undergoing ablation of the ACS deteriorated hemodynamically with acute pulmonary edema in three andcongestive heart failure in five patients occurring at a mean of 3 and 8 weeks, respectively, after the pro-cedure. Three of these patients were referred for mitral valve surgery. Two patients underwent ablationusing a left-sided approach. A right-sided approach was used in five patients. In one patient, a left- andright-sided approach was used. Compared to group 2 patients, group 1 patients had significantly higherleft ventricular end-diastolic diameters (64 ± 6 mm vs 56 ± 9 mm) at baseline despite similar fractionalshortening (32% ± Il%vs34% ± 13%), left ventricular end-systolic diameters (43 ± 9 mm vs 36 ± 7 mm)and degree of mitral regurgitation (1.4 ± 1.1 vs 1.4 ± 0.7) on echocardiographic analysis. Thus, hemody-namic deterioration together with progression of mitral regurgitation is a potential complication of abla-tion of the ACS (up to 7.4%). Patients with high left ventricular end-diastolic diameters ond moderate mi-tral regurgitation at baseline seem prone to this complication. (PACE 1997: 20[Pt. I]:2422-2428)

radiofrequency ablation, atrial fibrillation, heart failure, mitral regurgitalion

IntroductionRadiofrequency ablation of the atrioventricu-

lar (AV) conduction system has hecome a safe andeffective therapy^'^ for patients with drug resistantatrial fibrillation. Improved quality-of-life, relief ofthe proarrhythmic potential of lifelong drug ther-apy, and decreased need for hospitalization havebeen demonstrated after successhil ablation of theAV conduction system.^ Despite these salutary ef-fects, adverse effects of ablation include the need

Address for reprints: Dr. Marc Vandtirheyden, M.D., Cardin-vaKCuiar Center, O.L.V. Ziekenhuis, Moorselhaan 164, B9300Aalst, Belgium. Fax: 32-53-72-45-87.

Received September 12. 1995; revision February 7. 1996; ac-cepted lime 24. 1996.

for lifelong cardiac pacing and a possihle risk ofsudden death, the latter predominantly in thosewith underlying cardiac disease.' Since we re-cently have witnessed hemodynamic deteriorationin eight patients after radiofrequency ahlation ofthe AV conduction system, we retrospectively an-alyzed our data in order to define the characteris-tics of this group of patients with unfavorahle out-come. Finally we tried to nnderstand the reason forthe hemodynamic compromise after ablation.

Methods

Patients and Study Population

A consecutive series of 108 patients aged23-84 years (mean age B2) was studied. They werereferred to our department between May 1991 and

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HEMODYNAMIC DETERIORATION FOLLOWING RADIOFREQUENCY ABLATION

September 1993 for ablation of tbe AV conductionsystem followed by implantation of a permanentpacen:iaker. Of tbem, 76% underwent ablation be-cause of drug refractory atrial fibrillation and 9%for therapy resistant atrial flutter. Fifteen percentwere ablated for atrial arrhythmias. Tbere were 70males and 38 females.

Valvular heart disease was present in 23%, is-cbemic heart disease in 17%, and congestive car-diomyopathy in 23%. A diagnosis of lone atrialfibrillation was made in 30%. In 7% a diagnosis ofhypertensive heart disease was made.

As we found bemodynamic deterioration re-lated to mitral regurgitation, a group of 19 patients(18%) with mitral regurgitation before tbe proce-dure and in wbom serial echocardiograms wereavailable, was selected out of the consecutive se-ries of 108 patients. Finally these 19 patients weredivided into two separate groups, according to tbeoccurrence of bemodynamic deterioration afterthe procedure. Echocardiograpbic, clinical, andelectropbysiological data of these two groups werecompared retrospectively.

Electrophysiological Studyand Ablation Procedure

After informed consent, electrophysiologicalstudies were performed witb the patient in tbepostabsorptive nonsedated state. A 7 Fr Mansfield(Mansfield-Webster. Mansfield, MA, USA) or a 7Fr Cardiorhythm (Medtronic, Inc., Minneapolis,MN, USA) catheter was introduced tbrough therigbt femoral vein or artery as ablation catbeter.The radiofrequency device used was a MedtronicCardiorhytbm with temperature monitoring andautomatic switch off for temperature rise above70°C. A temporary pacemaker was introducedtbrough tbe rigbt femoral vein followed by im-plantation of a permanent pacemaker witbin 24hours after ablation, using tbe rigbt cephalic orsubclavian vein. In all patients a rate responsiveVVIR or DDDR pacemaker was implanted, usingQT interval, accelerometer, or minute ventilationas sensor. After tbe procedure, patients were mon-itored electrocardiograpbically for 48 bours. Allantiarrhytbmic drugs were discontinued after tbeablation procedure. No antiarrhytbmic drugs hadto be restored and the cardiac medication re-mained unchanged until follow-up.

Echocardiographic EoIIow-Up

A high quality two-dimensional guided M-mode and a color Doppler ecbocardiogram wereobtained hefore the ablation procedure and at tbetime of hemodynamic deterioration. All echocar-diograms were obtained by the same investigators.Measurements of left ventricular end-systolic, leftventricular end-diastolic, left atrial diameter, andfractional shortening were made on M-mode trac-ings according to recent recommendations by theAmerican Society of Echocardiograpby.^ Mitralregurgitation was defined by Doppler color flowmapping as mosaic color or multireversal colordisplay through tbe mitral valve into the leftatrium. Mitral regurgitation was graded accordingto a modified scale; minimal (1 + ) wben the maxi-mal regurgitant area was < 4 cm^, mild (2 + ) whenit was ^ 4 cm^ and < 14 cm^. and moderate (3 + )when it was > 14 cm^. If apart from a maximal re-gurgitant area of > 14 cm^ reversal of blood flowin the pulmonary veins was detectable, mitral re-gurgitation was graded severe (4 + )/' Tbe baselineecbocardiograms were reviewed blindly in orderto avoid bias and echocardiographic measure-ments were repeated with the investigator blindedto tbe fact wbetber tbe patient deteriorated or not.

Statistics

Data are expressed as mean ± standard devia-tion. Comparisons were performed by paired andunpaired Student's Ntest as appropriate. A P valueof < 0.05 was considered significant.

Results

Baseliue Characteristics

As we found bemodynamic deterioration as-sociated with worsening mitral regurgitation, wedepicted two groups of patients witb mitral regur-gitation at baseline in whom serial echocardio-grams were available; group 1 consisting of eigbtpatients witb symptoms of congestive heart failureand worsening mitral regurgitation at follow-upand group 2 consisting of 11 patients withoutsymptoms of congestive heart failure and with sta-ble mitral regurgitation after tbe procedure (Table

I).All except one patient were affected by

chronic atrial fibrillation or atrial flutter, witb a

PACE, Vol. 20 October 1997, Parti 2423

VANDERHEYDEN, ET AL.

Baseline

AgeMale/FemaleIndication

AfibrillationAflutterAtachycardia

EtiologyVHDHHDIHDCCMPLONE

ApproachRVLVRV + LV

N" Applications

Table 1.

Clinical and ElectrophysiologicalCharacteristics

Group 1(8 pts)

59 ± 95/3

620

21131

512

7 ± 7

Group 2(11 pts)

62 ± 95/6

821

42122

443

7 ± 6

Total

10/9

1441

63253

955

Afibrillation = atrial fibrillation; Aflutter = atrial flutter; Atachycar-dia = atrial tachycardia; CCMP = congestive cardiomyopathy;HHD = hypertensive heart disease; IHD = ischemic heart dis-ease; LONE = lone atrial fibrillation; VHD = valvular heart dis-ease; LV = left ventricular access; RV == right ventricular access.Valves are mean ± SD or number of subjects.

heart rate exceeding 90 beats/min on standardECG. Before ablation no single patient ever expe-rienced an episode of congestive heart failure andthe main complaints involved palpitations. Thedistribution between the two groups with regardto age, underlying heart disease, and indicationfor ablation is shown in Table 1. All patients hadbeen taking a variety of antiarrhythmic Class I, II,and III drugs including sotalol, amiodarone, fle-cainide, propafenone, /3-blockers, and combina-tion of these without any success. Class I, II, andIII antiarrhythmic drugs were discontinued beforethe study. The other cardioactive drugs were con-tinued and remained unchanged until follow-up.In group 1, 6 patients were receiving digoxine, 5diuretics, 4 angiotensin converting enzyme in-hibitors. Whereas in group 2, 7 patients were re-ceiving ACE inhibition, 5 digoxin, and 3 diuretics.After the procedure no antiarrhythmic drug had tobe restored.

There were no significant differences in anybaseline characteristic between the two groups.

Ablation Endpoint

Initial success was achieved in all 19 patients.Fourteen patients underwent radiofrequencyablation because of drug resistant atrial fibrilla-tion, and four for therapy resistant atrial flutter.One patient was ablated for incessant atrial tacby-cardia.

Of the 19 patients studied one patient ofgroup 2 had a preexisting right bundle branchbiock before the procedure. All other patients hadnormal ventricular activation on standard 12-leadECG.

Nine of these patients underwent ablationusing a right-sided approach (RV) with a meanof 11 radiofrequency applications; five patientsunderwent ablation using a left-sided approach(LV) with a mean of four radiofrequency appli-cations. Five patients underwent successfulablation by a mean of nine radiofrequency lesionsusing both a left- and right-sided approach(LV + RV). No statistically significant intergroupdifferences in approach or number of applications(7 ± 7 vs 7 ± 6 applications; P = 0.98) wereobserved.

Clinical FoUow-Up

Eight out of 108 patients (7.4%) deterioratedhemodynamically. This hemodynamic deteriora-tion consisted of congestive heart failure, appear-ing for the first time after the procedure. Five ofthem were male, three female, mean age 59 ± 9years. In all these patients no episodes of conges-tive heart failure were encountered before the pro-cedure. The hemodynamic deterioration in theseeight patients was related to worsening of the mi-tral regurgitation, resulting in acute pulmonaryedema in three and congestive heart failure in fiveoccurring at a mean of 3 weeks and 8 weeks, re-spectively, after the procedure. Three of themwere referred to surgery for mitral valve replace-ment. The otber patients could be stabilized onmedical therapy with vasodilators and diuretics.In contrast to group 1, group 2 patients remainedfree of symptoms after the ablation procedure. Par-ticularly no episodes of congestive heart failurewere observed at follow-up.

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HEMODYNAMIC DETERIORATION FOLLOWING RADIOFREQUENCY ABLATION

Echocardiographic Follow-Up

Serial echocardiograms were obtained amean of 100 days (range: 20-135 days) after abla-tion. Mitral regurgitation assessed by colorDoppler echocardiography increased signifi-cantly in group 1 (1.4 ± 1.1 VS2.5 ± 0.8: P < 0.01)(Fig. 1). No appreciable changes were seen ingroup 2 (1.4 ± 0.7 vs 1.3 ± 0.8: P - 0.34). Whereasno significant difference in mitral regurgitationwas seen at baseline between groups 1 and 2, itbecame significant after the procedure (P < 0.01)(Table II). Before ablation, group 1 was character-ized by a larger end-diastolic diameter comparedto group 2 (64 ± 6 mm vs 56 ± 9 mm; P < 0.05)(Table II). End-diastolic diameter increased ap-preciably in group 1 patients (Fig. 2) with symp-tomatic heart failure (64 ± 6 mm vs 72 ± 9 mm: P< 0.01) compared to group 2 patients with stablemitral regurgitation (56 ± 9 mm vs 56 ± 8 mm: P= 0.33). Intergroup differences in end-diastolicdiameter were significant at follow-up (56 ± 8mm vs 72 ± 9 mm; P < 0.01) (Table II). Althoughstatistically significant, intergroup differences inend-systolic diameter were only seen at follow-up(52 ± 13 mm vs 35 ± 6 mm; P < O.Ol), end-sys-tolic diameter appeared appreciably, althoughnot significantly, greater in group 1 compared togroup 2 at baseline (43 ± 9 mm vs 36 ± 7 mm: P= 0.06) (Table 11). Although there was no appre-ciable change in end-systolic diameter in either

GROUP 1: MR

Figure 1. Bar graph showing mitral regurgitation as-sessed by transthoracic echocardiography at baseline(MR) and at follow-up (MR 2) in patients with hemody-namic deterioration following ablation of the atrioven-tricuhir conduction system (GROUP 1). P < 0.01. Dataare expressed as mean ± SD.

Table il.

Echocardiographic Characteristics

LVEDD baselineLVESD baselineLA diam baselineMR baselineFS baselineLVEDD follow-upLVESD follow-upLA diam follow-upMR follow-upFS follow-up

Group 1(n = 8)

64 ± 643 ± 951 ± 31.4 ± 1.132 ± 1172 ± 9'52 ± 1352 ± 102.5 ± 0.8*29 ± 10

Group 2(n = 11)

56 ± 936 ± 748 ± 61.4 ± 0.734 + 1356 ± 835 ± 647 ± 101.3 ± 0.837 ± 10

P Va\ue

<0.050.06

NSNSNS

< 0.01< 0.01

NS<0.01

NS

FS = fractional shoriening {%): LA ^ left atrium (mm); LVEDD= left ventricular end-diastolic diameter (mm): LVESD = left ven-tricular end-systolic diameter (mm); MR = mitral regurgitation.NS = not significant. * P < 0.01 compared to baseline. Valuesare expressed as mean ± SD.

group at baseline and follow-up (group 1; 43 ± 9mm vs 52 ± 13 mm, P = 0.06: group 2: 36 ± 7 mmvs 35 ± 6 mm, P = 0.38) (Fig. 3), the increase inend-systolic diameter following the ablation pro-cedure was significantly greater in group 1 pa-tients compared to group 2 patients (A-LVESD: 8± 5 mm vs 1 ± 6 mm; P = 0.01).

Left atrium diameter did not change signifi-cantly in either group at baseline and at follow-up(group 1: 51 ± 3 mm vs 52 ± 10 mm, P - 0.73;group 2: 48 ± 6 mm vs 47 ± 10 mm, P = 0.94). Sig-nificant intergroup differences were not observed(Table II). Although we noticed a trend towardlower fractional shortening following radiofre-quency ablation in group 1 and higher fractionalshortening in group 2, it never appeared statisti-cally significant in either group {group 1: 32% ±11% vs 29% ± 10%; P - 0.48: group 2; 34% ±13% vs 37% ± 10%; P = 0.28). No significant in-tergroup differences were observed at baselineand during follow-up (Table II).

Discussion

Radiofrequency ablation has become the pro-cedure of choice for patients requiring AV junc-tion ablation. Suitable candidates for ablation in-

PACE. Vol. 20 October 1997, Part I 2425

VANDERHEYDEN, ET AL.

GROUP 1: LVEDD

Figure 2. Bar graph showing left ventricular end-dias-tolic diameter assessed by transthoracic echocardiogra-phy at baseline (LVEDD) and at follow-up (LVEDD 2) inpatients with hemodynamic deterioration following ab-lation of the atrioventricular conduction system(GROUP 1). P < 0.01. Data are expressed as mean ± SD.

elude patients with atrial fibrillation who proverefractory or intolerant to drug therapy. Althoughseveral studies indicate improvement in left ven-tricular function and cardiac performance after ab-lation of tbe AV conduction system for drug re-fractory atrial fibrillation," '̂̂ retrospective analysisof our data identified a group of patients witbhemodynamic deterioration at follow-up. Tbe ob-served hemodynamic deterioration resulted inclinical symptoms of congestive heart failure in 8out of 108 patients (7.4%).

The patients with ensuing congestive heartfailure after radiofrequency ablation of the AVconduction system were characterized by higherend-diastolic diameters and a trend toward higherend-systolic diameters compared to a controlgroup. Fractional sbortening and mitral regurgita-tion were similar in both groups at baseline. Atfollow-up tbere was a trend toward higher end-systolic diameters, a significant increase in end-diastolic diameters together witb significant wors-ening of the mitral regurgitation. Whether mitralregurgitation is cause or consequence of thishemodynamic deterioration remains speculative.

In contrast to previous studies, the expectedimprovement in left ventricular function,^" mea-sured by fractional shortening was not seen inboth groups. This lack of improvement of left ven-tricular function was also reported by Brignole etal." who showed a deterioration of left ventricularfunction in patients with fractional shortening >

30% 90 days after His-bundle ablation. However,in contrast to the data of Brignole et al/' the lack ofimprovement of fractional shortening in our group1 patients was related to a dramatic rise in left ven-tricular end-diastolic and end-systolic diameter.The bigb end-diastolic diameters witb normalend-systolic diameters and normal fractionalshortening at baseline may have been the reflec-tion of a compensated state of chronic mitral re-gurgitation. Tbe progressive increase in left ven-tricular end-diastolic and end-systolic diameter,despite similar fractional sbortening after tbe ab-lation procedure, can be interpreted as the finaltransition from a compensated to a decompen-sated situation.'" Similar fractional sbortening to-getber witb increased severity of mitral regurgita-tion may reflect left ventricular muscledysfunction due to chronic volume overload.

Although the exact mechanism why those pa-tients deteriorated from a compensated to a de-compensated situation remains unclear, severalphenomena could have contributed to this com-plication.

First of all, this complication could be relatedto the ablation procedure itself. During radiofre-quency catbeter ablation radiofrequency currentpasses tbrougb tbe tissue in close contact with theelectrode and thermal injury to the myocardiumoccurs. Histologic examination of these lesions re-veals coagulation necrosis witb destruction of the

fM l» -

701

60'

50 <

40'

301

?0

GROUP 1

^ ^ ^ ^

^ ^

LVESD

LVESD LVESD2

Figure 3. Bar graph showing left ventricular end-sys-tolic dianjeter assessed by transthoracic echocardiogra-phy at baseline (LVESD) and at follow-up (LVESD 2} inpatients with hemodynamic deterioration following ab-lation of the atrioventricular conduction system(GROUP l).P<0.01. Data are expressed as mean ± SD.

2426 October 1997, Part I PACE. Vol. 20

HEMODYNAMIC DETERIORATION FOLLOWINC RADIOFREQUENCY ABLATION

myofibril arcbitecture and contraction bandnecrosis.'^ Although we did not measure plasmaCK and its MB fraction extensive myocardial is-chemia or necrosis is not a plausible mechanismfor tbe observed deterioration as previous studiesbave demonstrated little or no increase in MB frac-tion following radiofrequency application.'^'"'

Theoretically the ablation migbt have in-duced injury to the valve itself. However, inspec-tion of tbe mitral valve in tbe three patients oper-ated, showed thickening and calcification of tbemitral leaflets and cbordae suggestive of degener-ative valvular disease. No ruptured chorda, valveperforation, nor vegetation was observed. Micro-scopical examination of the excised valves did notreveal radiofrequency generated lesions. More-over, a direct radiofrequency generated valvularinjury could be excluded as five of tbese patientswere ablated using a rigbt-sided approach, imped-ing direct contact between tbe mitral valve and theablation catheter.

Since all group 1 patients bad normal ventric-ular conduction on tbe standard 12-lead ECG be-fore the procedure, abnormal ventricular activa-tion due to rigbt ventricular apex pacing mighthave contributed to the increase in severity of tbemitral regurgitation and tbe occurrence of conges-tive beart failure. Right ventricular apex pacingmay affect the competence of the mitral valve dueto changes in timing of activation of the mitralvalve apparatus and/or due to altered tension gen-eration of tbe papillary muscles.

Tbe function of tbe mitral valve dependsupon tbe integrity of the leaflets, cbordaetondineae, mitral annulus, and papillary muscles.The closure of the valve results from a complexinteraction between tbe leaflet area needed to oc-clude tbe orifice and the leaflet area available.The size of tbe orifice determines the leaflet areaneeded to occlude. Since botb ventricular and an-nular dimensions vary during the cardiac cycle,the position of the papillary muscle and its com-plex interaction witb tbe mitral valve leaflet areaavailable will result in a varying regurgitant ori-fice area throughout the cardiac cycle. Aberrantactivation of the papillary muscle due to rightventricular pacing may impair leaflet tension de-velopment. Finally, this may result in loss ofcoaptation and an increased orifice area in sys-tole.'"

Moreover, tbe timing of papillary muscle con-traction may affect mitral valve closure. As differ-ent pacing sites result in altered timing of papil-lary muscle activation, tbis mechanism migbt alsohave contributed to worsening mitral valve clo-sure. Tberefore, mitral regurgitation may bavebeen present in our patients due to altered timingof activation of botb the papillary muscle and theadjacent myocardium. In tbis way, pacing fromdifferent sites may cause different amounts of mi-tral regurgitation.'"* In bunians the deleterious ef-fects of right ventricular pacing upon mitral regur-gitation have been described. In a subset of fourpatients, rigbt ventricular apex pacing resulted inprecipitation of congestive beart failure togetherwith worsening mitral regurgitation.'"'

Prospective studies, investigating tbe impactof rigbt ventricular apex pacing upon severity ofmitral regurgitation are needed to test this hy-pothesis.

Despite tbese immediate negative effects ofright ventricular apex pacing, altered asyn-chronous electrical activation of the left ventriclemay also have a late negative impact upon leftventricular function itself. Right ventricular apexpacing is associated witb progressive myocardialdysfunction and decreased survival compared toatrial pacing.'*' Tbe altered sequence of activation,associated with right ventricular apex pacing re-sults in altered mechanical stress vectors, hetero-geneity of regional coronary blood flow, and ele-vated tissue catecholamine levels. These changesmay induce remodeling of the global ventricularsbape'^ with progressive changes in left ventricu-lar performance. At the end, this left ventricularremodeling will lead to higher volumes and wors-ening of the mitral regurgitation due to dilatationof tbe mitral valve annulus. In some of our pa-tients witb worsening of tbe mitral regurgitationmontbs after tbe procedure, tbis mechanism couldhave played a major role,

Finally as patients with already slightly de-pressed left ventricular function are not able to in-crease tbeir stroke volume, any increase in cardiacoutput is dependent upon an increase in beartrate. After the ablation procedure tbis compen-satory mechanism is lost and these patients arenot able anymore to increase their cardiac outputresulting in clinical symptoms of congestive heartfailure.

PACE. Vol. 20 October 1997, Part I 2427

VANDERHEYDEN, ET AL.

Conclusion

Altbougb several publications bave demon-strated a bigb success rate and few serious proce-dure related complications witb radiofrequencyablation,^•^•'' one must remain cautious not tounderestimate the risks. We describe eight pa-tients witb hemodynamic deterioration and wors-ening mitral regurgitation after ablation of AVjunction. Retrospective analysis sbowed that pa-tients witb high left ventricular end-diastolic di-mensions and moderate mitral regurgitation areprone to tbis complication. In tbose operated on

no clear ablation related lesions could be detected.Immediate and chronic effects of aberrant ventric-ular activation due to rigbt ventricular apex pac-ing may bave contributed to this serious compli-cation. Permanent pacing by means of a screw-in electrode located near tbe His bundle may pre-vent tbe abnormal sequence of ventricular activa-tion, thereby preventing tbe abnormalities seenin tbese patients. Furtber prospective studies areneeded to explore tbese possibilities. Wbenevera patient is candidate to ablation of the AV junc-tion, one sbould not forget tbis possible seriouscomplication.

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8. Heinz C, Siostrzonek P, Kreiner G, et al. Improve-ment in left ventricular systolic function after suc-cessful ablation for drug refractory, chronic atrialfibrillation and recurrent atrial flutter, Am J Car-diol 1992; 69:489-492.

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