Early recurrence of accessory pathways after radiofrequency catheter ablation does not preclude long-term cure

mitral valve prolapse. .I Intern Med 1989;226:433436. 7. Davison G, Greenland P. Predictors of left atrial thrombus in mitral valve disease. J Gen Intern Med 1991:6:108-112. 8. Black IW, Hopkins AP, Lee LCL, Walsh WF. Left atrial spontaneous echo contrast: a clinical and echocardiograpbic analysis. JAm Coil Ca~diol1991;18:398%404. 9. Movsowitz C, Meyerowitz CB, Jacobs LE, Meyerwitz CB, Podolsky L, Ioli A, Kotler MN. Significant mitral regurgitation is protective against left atrial spontaneous echo contrast and tbrombus as assessed by tramesophageal echocardiography. J Am Sot Echocardiogr 1993;6: 107-l 14. 10. The Stroke Prevention in Atrial Fibrillation Investigators. Predictors of tbromboembolism in ahial fibrillation: I. Clinical features of patients at risk. Ann Intern Med 1992;116:1-5.

11. Coulshed N, Epstein EJ, McKendrick CS, Galloway RW, Walker E. Systemic embolism in mitral valve disease. Br Heap2 J 1970;32:2&34. 12. Hofmann T, Kasper W, Meinertz T, G&e1 A, Just H. Echocaxhograpbic eviluation of patients with clinically suspected art&xl emboli. Lancet 1990;336: 1421-1424. 13. Daniel WG. Nellessen U. Scbmder E. Nonnast-Daniel B. B&a&i P. Nikutta P, Lichtlen PR. Left atrial spontaneous echo contrast in mitral valve disease; an indicator for an increased tbromboembolic risk. J Am Coil Cardiol 1988;ll: 1204-1211. 14. Tsai LM, Cben JH, Fang CJ, Lin LJ, Kwan CM. Clinical implications of left ahial spontaneous echo contrast in nonrheumatic atrial fibrillation. Am J Cardiol 1992;70:327-331.

Early Recurrence of Accessory Pathways After Radiofrequency Catheter Ablation Does Not Preclude Long-Term Cure Alan B. Wagshal, MD, Luis A. Pires, MD, Robert S. Mittleman, MD, Carlos Cuello, MD, Gregory J. Bonavita, MD, and Shoei K. Stephen Huang, MD adiofrequency catheter ablation of accessory pathR ways is generally accepted as the procedure of choice for managing symptomatic patients with tachy-

same site with the same or slightly higher power: The patient was then monitored for 230 minutes and then reassessed for evidence of accessory pathway function car&as resulting from an accessory pathway.‘” Previous or inducible tachycardias both with and without isostudies have shown an approximate 10% incidence of proterenol infusion at 2 to 4 E.Lgimin. recurrence of accessory pathway function after initially After ablation, all patients were monitored for at successful ablation, which can occur anytime from with- least 24 to 48 hours using a retrievable telemetry sysin 12 hours after ablation until as long as several months tem (Hewlett-Packard Inc., model 7856OA, Palo Alto, later.4J In this report we describe a group of patients California) programmed to recognize any recurrence of having early recurrence of accessory pathway function preexcitation or episodes of atrioventricular reciprocat(within 24 hours after ablation), who at the time of ing tachycardia. A I2-lead electrocardiogram was obscheduled repeat ablation 1 week to 1 month later, were tained within 2 hours after ablation and every morning found to have no evidence of accessory pathway func- before discharge. All patients with recurrent accessory tion. pathway function remained hospitalized for at least I to Catheter ablation was pe$ormed using a 6 or 7Fr 2 extra days to document either continued presence or deflectable catheter with a 4 mm distal tip electrode and disappearance of accessory pathway function. In either a Radionics RFG3C radiofrequency lesion generator event, the patients underwent a follow-up electrophysio(Radionics Inc., Burlington, Massachusetts). Left-sided logic study between I and 4 weeks latep, and prepared accessory pathways were approached using the retro- to undergo repeat ablation at the same session if acgrade left ventricular approach by passing the ablation cessoty pathway function remained. All patients undercatheter through the aortic valve to the ventricular as- went long-term follow-up either at this institution or by pect of the mitral annulus. In 2 patients in whom this the referring electrophysiologists; presence or absence was unsuccessful, a transseptal approach was under- of symptoms was monitored with telephone calls to the taken at a separate session and the accessory pathway physicians and patients. In addition, all patients were was ablated from the atria1 aspect of the mitral annu- encouraged to have a routine follow-up electrophysiolus. Right-sided and posteroseptal accessory pathways logic study approximately I month after the ablation to were approached from the atria1 side of the tricuspid document persistent absence of accessory pathway annulus. Appropriate sites for ablation were determined function. based on discrete atria1 and ventricular electrograms Between July 1991 and December 1992,.X5 patients with a closely spaced atrioventricular interval during with a total of 57 accessory pathways underwent initial sinus rhythm with anterograde preexcitation or ven- attempted ablation of their accessory pathways at triculoatrial interval during orthodromic atrioventricuour institution. Ft@y-one of these patients (93%) had lar reciprocating tachycardia or during ventricular pac- successful ablation, 46 after 1 session and 5 after a ing in patients with concealed accessory pathways. second session. Of the 4 patients who did not achieve After identifying a suitable site, radiofrequency energy successful ablation, 1 with an existing permanent pacewas delivered for 30 to 40 seconds at a power typical- maker and an accessory pathway with weak anteroLy between 20 and 40 W while monitoring for loss of grade conduction was managed with complete atriovenaccessory pathway junction (during ventricular pacing tricular node ablation, I went to another institution for for concealed pathways) or abrupt increase in repeat ablation, and 2 were managed with medications impedance. If success occurred at a particular site 1 or after refusing a repeat ablation attempt. 2 “booster” applications were given immediately at the Eight patients (16%) had recurrent accessory pathway conduction, with 4 early recurrences (within 24 From the Section of Cardiac Electrophysiology and Pacing, Division of hours of the ablation), which are discussed later, and 4 Cardiovascular Medicine, Department of Medicine, University of Masoccurring after hospital discharge (between I week and sachusetts Medical Center, 55 Lake Avenue North, Worcester, Massa2 months later). Three of these latter 4 patients were chusetts 01602. Manuscript received March 16, 1993; revised manuscript received and accepted May 4, 1993. iden@ed by recurrent episodes of symptomatic tachyBRIEF REPORTS 843

TABLE I Recurrence of Accessory Pathway Function After Radiofrequency Ablation According to Accessory Pathway Location (n = 57 total accessory patients)

Catheter pathways

in 55

Early Accessory Pathway

Recurrence (within 24

Successful Ablation (no recurrence)

Location Left free wall

hours)

37* (14 concealed)

Posteroseptal

2

4

Late Recurrence (after hospital discharge)

Unsuccessful Ablation

Total

3 (1 concealed)

2 (1 concealed)

44

0

1

(1 concealed)* Right free wall

0

5

2*

8

(concealed)

4*

2

0

(1 concealed) Total

45

4

(15 concealed)

4

(1 concealed)

4

(2 concealed)

57

(1 concealed)

*Two patients each with 2 accessory pathways.

TABLE II Ablation

Early Recurrence

Patient Number

Age (yr) &Sex

1 2 3

22F 43M 55M

of Accessory

AP Location and Conduction

Ablation Electrogram AV or VA Interval Pathway

R free wall

Function

Function

1.8 7.5 2*

Catheter

Number of Time Until Ablation Recurrence Attempts (hours)

at Time of Follow-Up

20 35 35

Manifest L anterior Manifest L anterior

After Radiofrequency

Time to AP Disappearance bed

(ms)

No Evidence of Accessory Manifest

Pathway

Duration of Recurrence

(hours)

Study

44 3 24

12 4 6

54 12 24

(AP potential present) Complete Return of Accessory 32F

4

Pathway

Function

Concealed R free wall

and Inducible Tachycardia

30

2.5

46

Requiring

Repeat Ablation 5

-

*Catheter dislodged after approximately 2 seconds of radiofrequency energy delivery. AP = accessory pathway: AV = atrloventricular; L = left; R = right: VA = ventriculoatrial.

cardia and 1 patient was diagnosed during the routine l-month follow-up electrophysiologic study; all 4 underwent successfil repeat ablation. Long-term cure of the accessory pathways in the remaining 43 patients was conjrmed not only by normal electrocardiograms and lack of symptoms, but also by follow-up electrophysiologic study approximately I month after initial ablation in all but 1 patient. Table I shows the breakdown of these various patient groups by accessory pathway location. Patient ages, accessory pathway locations, characteristics of local electrograms, and time and manifestations of the recurrence are listed in Table II for all 4 patients exhibiting early recurrence of accessory pathway function. All 4 patients underwent repeat electrophysiologic study with a plan of possible repeat ablation at the same session between I and 4 weeks later. At that time, 3 patients were shown to have completely absent ticcessory pathway function and accordingly did not undergo repeat ablation; all 3 have remained symptomfree with no evidence of recurrence after 9 to 15 months of follow-up. In all 3 patients the initial recurrence was within the fi?st 12 hours and was intermittent for at least part of the time. Preexcitation persisted for 24 hours and as long as 54 hours in 1 patient (Figure I). The remaining patient (no. 4 in Table II) underwent suc844

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cessful repeat ablation without further recurrence after 10 months of follow-up. Our study demonstrated that 3 of 4 patients presenting with early (within 24 hours after ablation) recurrence of accessory pathway function after seemingly successful initial radiofrequency catheter ablation were shown on subsequent follow-up electrophysiologic study 1 to 4 weeks later as well as long-term follow-up to have no residual accessory pathway function. We were able to identify factors in these 4 patients that may have predisposed to a suboptimal ablation temperature and thus perhaps to a greater tendency for transient recurrent accessory pathway function. Three of the cases were dticult requiring >20 ablation attempts, suggesting the pathways were in an area where good tissue contact was diflicult to maintain. Patients witb right-sided or posteroseptal accessory pathways have been shown to be at a higher risk of recurrence4,5 and 2 of our patients with early recurrence had right-sided pathways (1 of whom was a delayed cure). Correspondingly, right-sided and posteroseptal ablation sites have been shown to have a high incidence of suboptimal ablation temperatures (49 f 7°C compared with 60 + 16°C for left-sided ablations)6 and of transiently effective pulse~,~ suggesting that transiently effective pulses and the early recurrences described in our patients may be all related phenomena

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resulting from suboptimal ablation temperature. In one study$ the mean time to reach steady-state temperature during ablation was 2.2 seconds, with some lesions requiring 5 seconds; thus, our patient 3 (see Table II)

who had dislodgment of the ablation catheter after only 2 seconds of radiofrequency energy may also have achieved only a suboptimal local tissue temperature. Finally, our patient 2 required 7.5 seconds of radiofre-

FlGURE 1. A, intracardiac electrograms taken during ablation of patient 1, demonstrating a short atrioventkular interval in the ablation electro@am (20 ms). B, After application of radiofrequency energy there was prompt disappearance of preexcitation (1.8 second). Bespite this, preexcitation recurred 12 hours later and persisted for a total of 94 hours, as shown in C. C, 124ead electrocardiogram recorded from this same patient 49 hours after ablation showing continued presence of praexcitation identical to the preablation electrocardiogram at a heart rate of 97 beats/min, which subsequently disappeared later that same day and dii not recur. Followup electrophysiologic study several weeks later revealed no anterograda or retrograde evidence of accasr~y pathway function. A q atdal electrogram; BP q blood pressure; CS q coronary sinus; RVA = ri@t ventricular apex; V q ventricular electrogram.

BRIEFREPORTS 845

quency energy until accessory pathway loss, suggesting that this accessory pathway may have been slightly removed from the ablation catheter, thus resulting in a suboptimal ablation temperature. Although one might suspect our patients with an early recurrence and delayed cure would be at risk of subsequent recurrence of accessory pathway function, the absence of accessory pathway function on the follow-up electrophysiologic study as well as their complete lack of symptoms for 9 to 15 months of additional follow-up strongly suggests that they are cured of their accessory pathways. Our patients are therefore different from those of Leitch et aJ8 who reported a group of 4 patients undergoing seemingly unsuccessful ablation who had delayed loss of preexcitation 3 to 5 days after ablation, but subsequently regained accessory pathway function 3 to 5 months later. The explanation these investigators advanced was that their patients’ accessory pathways were located in the rim of tissue edema and intlammation surrounding the area of complete necrosis so that accessory pathway conduction disappeared between the third to fifth days (when the local edema and inflammation would be expected to be at its peak) and then recurred as further healing took place during the next several weeks. The fact that .our patients did show immediate loss of accessory pathway function would suggest their pathways were closer to the center of the radiofrequency lesion than those of Leitch et al, and this may account for their eventually being completely cured.

Whatever the exact mechanism of our patients’ response, our observation implies that patients exhibiting early recurrence after apparently successful radiofrequency catheter ablation should be observed for at least several days to 1 week or more to rule out a potential delayed cure before proceeding with repeat ablationparticularly if the recurrence begins within the iirst 12 hours and the recurrent preexcitation is intermittent. 1. Calkins H, Sousa J, El-Atassi R, Rosenheck S, de Buitleir M, Kou WH, Kadish AH, Langberg JJ, Morady F. Diagnosis and cure of the Wolff-Parkinson-W syndrome or paroxysmal supraventricular tachycxdias during a single electrophysiologic test. N Engl J Med 1991;324:1612-1618. 2. Jackman WM, Xtiang W, Friday KJ, Roman CA, Moulton KP, Beckman KJ, McClelland JH, Twidale N, Ha&t Z, Prior MI, Margolis PD, &lame JD, Overholt ED, Lazzara R. Catheter ablation of accessory ahioventricula pathways (Wolff-Parkinson-W syndrome) by radiofrequency current. N Engl .l Med 1991;324:1605-1611, 3. Scheimnan MM, for the NASPE Ad Hoc Committee on Catheter Ablation. Catheter ablation for cardiac arrhythmias, personnel, and facilities. PACE 1992;15:711-721. 4. Langbag JJ, Calkins H, Kim Y, Sousa J, El-Atassi R, Leon A, Borganelli M, Kalbfleisch SJ, Morady F. Recurrence of conduction in accessory atrioventricular connections after initially successful radiofrequency catheter ablation. J Am CoN Cardid 1992;69:1588-1592. 5. Twiddle N, Wang X, Beckman KJ, McClelland JH, Moulton KP, Prior MI, Ha&t HA, Lazzara R, Jackman WM. Factors associated with recurrence of accessory pathway conduction after radiofrequency catheter ablation. PACE 1991; 142042%2048. 6. Langberg JJ, Calkim H, El-Atassi R, Borganelli M, Leon A, Kalbfleisch SJ, Morady F. Temperature monitoring during radiofrequency catheter ablation of accessoty pathways. Circulation 1992;86:146%1474. 7. Chen X, Borggrefe M, Hiidricks G, Haverkamp W, Karbenn LJ, Shenasa M, Breithardt G. Radiofrequency ablation of accessory pathways: characteristics of transiently and permanently effective pulses. PACE 199&15:1122-l 130. 8. Leitch JW, Klein GJ, Yee R, Leather RA, Kim YH. Does delayed loss of preexcitation after unsuccessful radiofrequency catheter ablation of accessory pathways result in permanent cure? Am J Cardiol 1992;70:83&832.

Prognosis of Congestive Heart Failure in Patients Aged 262 Years with Unoperated Severe Valvular Aortic Stenosis Wilbert S. Aronow, MD, Chul Ahn, PhD, ltzhak Kronzon, MD, and Michael Nanna, MD oss and Braunwaldl reported that the average surR vival rate after the onset of congestive heart failure (CL-IF) in patients with severe aortic stenosis (AS) was

vascular congestion present on the chest roentgenogram interpreted by both an experienced radiologist and the senior author. 1.5 to 2 years. We reported that left ventricular (LV) M-mode and 2-dimensional echocardiograms, and ejection fraction was the most important prognostic vari- continuous-wave Doppler recordings for determining able for mortality in elderly patients with CHF associ- LV ejection fraction and the severity of AS were obated with coronary artery disease.2 We report the results tained as previously described.2-4 The peak transvalvufrom a prospective study of elderly patients with CHF lar gradient was determined by using the simpl@ed associated with unoperated severe valvular AS, correlat- Bernoulli equation: AP = 4V2 (where AP = peak presing normal and abnormal LV ejection fraction with car- sure gradient in mm Hg; and V = peak transvalvular diac and total mortality. flow velocity in mls). The peak pressure gradient across In a prospective study, CHF was diagnosed in 48 el- the aortic valve was 30 mm Hg if the peak aortic flow derly patients with severe valvular AS who refused aor- velocity was 23.6 mls. Aortic valve area was calculattic valve replacement or balloon aortic valvuloplasty. ed, when feasible, by the continuity equation using CHF was diagnosed if the following 2 criteria werefulpulsed Doppler echocardiography to evaluate LV outfilled: (I) pulmonary basilar vales heard by 2 physi- flow tract flow velocity, continuous-wave Doppler echocarcians, including the senior author; and (2) pulmonary diography to evaluate transvalvular flow velocity, and the 2-dimensional parasternal long-axis view to measure LV outflow tract area.5 Severe AS was diagnosed From the Hebrew Hospital Home, 801 Co-op City Boulevard, Bronx, New York 10475; the Department of Geriatrics and Adult Developtf the aortic valve area was ~0.7 cm2, or in the absence ment, Mount Sinai School of Medicine, New York, New York, the of a measured aortic valve area, tf the peak pressure Department of Biostatistics, City of Hope National Medical Center, gradient across the aortic valve was 250 mm Hg. Duarte, California; and the Department of Medicine, New York UniLV volumes at end-diastole and end-systole were versity School of Medicine, New York, New York. Manuscript received March 8,1993; revised manuscript received and accepted May 20,1993. calculated by planimetry from the digitized 2-dimen846

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