Related : Response to Control of the

BURT I. BROMBERG, M.D., MACDONALD DICK 11, M.D., A. REBECCA SNIDER, M.D., WILLIAM A. SCOTT, M.D., GERALD A. SERWER, M.D., EDWARD L. BOVE, M.D., and KATHLEEN P. HEIDELBERGER, M.D.

From the Division of Pediatric , C. S. Mott Children S Hospital, and the Departments of Pediatrics, Surgery, and Pathology, University of Michigan, Ann Arbor, Michigan

To evaluate the clinical response of five children ingfraction (20% pre vs 34% post; P = 0.006), with automatic atrial tachycardia (AA T) and as- mean ejection fraction (36% pre vs 50% post; P sociated cardiomyopathy to arrhythmia control, < 0.01), mean velocity of’ circumferential fiber we compared pretreatment and posttreatment 24- shortening (0.62 pre vs 1.20 post; P = 0.003). hour ECG rates, cardiothoracic ratio by Mean E-point septa1 separation corrected for end- chest radiograph, and echocardiographic mea- diastolic dimension also showed a trend toward sures of ventricular ,function. Two children were improvement (0.25 pre vs 0.16 post; P = 0.11). treated with amiodarone, two with surgical exci- Right ventricular endocardial biopsies in four were sion and cryoablation of the ectopicfocus, and one nonspecific; an atrial biopsy from surgery showed with alone. Signijicantly slower mean a Purkinje fiber-like tissue in one patient, but was heart rates were achieved, along with a dominant nonspecijic in another. We conclude that cardio- sinus rhythm and improvement in symptoms. myopathy can be causally linked to automatic Control of the AAT resulted in improved mean atrial tachycardia and that aggressive medical cardiothoracic ratio (0.53 pre vs 0.49 post; P and/or surgical management is warranted in those = 0.021, as well as improvement in a number of patients with of impaired ven- echocardiographic measurements: mean shorten- tricular function. (J Interven Cardiol 1989:2:4)

Introduction matic atrial tachycardia (AAT), accounts for < 10% of SVT in children’,’ is usually slower than the more common reentrant forms of SVT, and Supraventricular tachycardia (SVT) from an ec- may be virtually incessant. At one time considered topic automatic atrial focus, herein called auto- AAT, in the absence of structural heart disease, has recently been associated with cardio- myopathy (CM). Although AAT is often refractory Presented, in part, at the 37th Annual Scientific Sessions, to conventional medical therapy, several reports American College of Cardiology, Atlanta, 1988. suggest that control of the arrhythmia improves Drs. Brombergand Scott were supported, in part, by fellowships cardiac perf~rmance.~~’In recent years, new phar- from the American Heart Association of Michigan. macologic agents8-’’ as well as surgical exci- Address for reprints: Macdonald Dick 11, MD, C.S. Mott Chil- sion 12-1 9 and catheter electrical ablation20-22have dren’s Hospital, Room FI 126, Box 0204, University of Michi- led to successful control of intractable AAT. To gan Medical Center, 1500 East Medical Center Drive, Ann Arbor, MI 48 109-0204. further examine the proposition that control of persistent AAT favorably alters cardiac function in Submitted for publication December 26, 1989; accepted with revisions January 30, 1990; revisions received February 7, some patients with cardiomyopathy, we compared 1990. the clinical course and noninvasive measures of

Vol. 2, No. 4, 1989 Journal of Interventional Cardiology 21 1 BROMBERG, ET AL.

ventricular function before and after therapy in sive shortening of the tachycardia cycle length five children with AAT. In addition, the findings after the initial several beats (“warm up”), atrial of two right atrial and three right ventricular biop- depolarization during the tachycardia that reset sies obtained from these patients are summarized. the atrial cycle, and failure of a single or a train of Recommendations for treatment based on this ex- atrial premature depolarizations to initiate or in- perience are outlined. terrupt the tachycardia]. In one patient the diag- nosis was made by the surface ECG and Holter tracings alone (initiating P wave of the tachycardia Methods as the same morphology of the subsequent beats, “warm-up” period, and atrioventricular dissocia- Five patients referred to the Pediatric Arrhyth- tion during SVT). Persistentjunctional reciprocat- mia Clinic at C.S. Mott Children’s Hospital, Uni- ing tachycardia was excluded by either the absence versity of Michigan, exhibited poorly controlled, of 1: 1 atrioventricular conduction during the virtually incessant SVT (Fig. 1) and had developed tachycardia or the absence of ventriculoatrial con- fatigue, exercise intolerance, increased heart size duction during ventricular pacing as well. The se- on chest radiograph, and echocardiographic find- lection of medical or surgical treatment was based ings of decreased ventricular function, suggestive upon the duration of the patient’s symptoms, their of cardiomyopdthy. Four patients underwent elec- anticipated compliance with a medical regimen, trophysiologic study (EPS) using programmed ex- and, in two patients, their decision against chronic trastimulation (PES), overdrive pacing, and map- antiarrhythmic medication. ping of atrial activation during the tachycardia. Response to therapy was evaluated by pre- and Four patients had hemodynamic study and two posttreatment 24-hour ambulatory electrocardio- right ventricular endom yocardial biopsy; one had graphic tracings (CardioData Corp., Northboro, a right ventricular biopsy and two atrial biopsies at MA, USA), chest radiographs, and two-dimen- surgery. The diagnosis of automatic atrial tachy- sional and M-mode echocardiograms (Advanced cardia (AAT) was based upon the criteria of Gol- Technology Laborotones, Seattle, WA, USA and/ et al. and [initiation of the or Acuson Computer Sonography, Mountain tachycardia by spontaneous atrial depolarizations View, CA, USA). All five patients were free of val- identical to successive atrial depolarizations dur- vular, congenital, ischemic or other structural ing the tachycardia, independence of the tachycar- heart disease by two-dimensional echocardiogram, dia cycle length on AV node conduction, succes- Doppler analysis, and cineangiography (four pa-

. .a ...... , .., .. , . .. . . ’ . ... 1 ‘.I I ! ; : 1 ..,. I: ;I :.I

Figure 1. Representative EUG tracings from leads I1 and 111 from patient #4 before and after final treatment. Note the pretreatment heart rate of 125 bpm and the inverted P waves in both leads (left hand tracings). Following trealment the rate is 75 bpm and the P waves are upright in both leads (right hand tracings).

212 Journal of Interventional Cardiology Vol. 2, No. 4, 1989 TREATMENT OF AAT tients). Cardiac rhythm and mean 24-hour heart ity, two noted dizziness, and one had exercise in- rates were determined by computer generated tolerance. Electrophysiological study in four pa- analysis and confirmed by full disclosure tracings. tients localized the origin of the AAT at the coro- The cardiothoracic ratio (CTR) was measured nary sinus 0s in two patients and the low septal from the chest radiograph in the posterior-anterior right in one. In the fourth patient, earliest projection during maximal inspiration. The left atrial activation during SVT occurred both at the ventricular shortening fraction (SF), mean veloc- mouth of the coronary sinus and the atrioventricu- ity of circumferential fiber shortening corrected lar node, suggesting that the abnormal impulse for heart rate (VCF,), E-point septal separation arose equidistant between these two points. He- normalized for end-diastolic demension (EPSS/ modynamic studies in the four patients undergo- EDD) were measured from the M-mode echocar- ing electrophysiologic study demonstrated a mean diogram; the left ventricular ejection fraction (EF) left ventricular end-diastolic pressure (LVEDP) determined from the apical four-chamber view of of 16 mmHg (range 10-26 mmHg), and a mean the two-dimensional echocardiogram was calcu- cardiac index of 2.8/min/m2 (range 1.6-3.2 lated using the Simpson's rule algorithm. All pre- L/min/m2). treatment studies were obtained within 1 week Treatment. An average of 2.3 drug trials were prior to initiation of therapy. The mean interval used in three patients before satisfactory control of between pre- and posttreatment examination was the AAT was achieved (Table I). Digoxin alone 1.5 years. Results are expressed as the mean * one provided adequate control in only one patient. standard deviation and are compared using a Beta blockade was ineffective in the two patients in paired t-test. Differences in the mean were consid- whom it was tried. Two patients, ages 9 and 11 ered significant when the P value was 10.05. years, received amiodarone therapy for control of the SVT. After initial success with amiodarone, occurred in one of these pa- Results tients. Amiodarone was withdrawn and flecainide initiated with a return of control of the tachycar- Symptoms. The clinical data are summarized in dia. The remaining two patients, ages 15 and 20 Table I. All patients complained of easy fatigabil- years, who had received digoxin and propranolol

Table I. Clinical, Therapeutic, Biopsy, and Follow-up Data

SVT Heart Duration of Duration of Current Duration Rate Early Conventional Subsequent Myocardial Subsequent Patient Age of SVT (bgm) Symptoms Treatment Therapy Treatment Biopsy Outcome Treatment

I 9.3 years 3.5 years 140 fatigue, digoxin 2 years amiodarone Not available NSR 1.5 years dizziness verapamil flecainide 2 9.8 years 0.6 years 135 fatigue digoxin 0.5 year amiodarone R Vent: 90% NSR 1.0 year flecainide flecainidc Normal I O'% SVT 0.5 year 3 11.3 years 0.1 year 175 fatigue, dyspnea digoxin - digoxin R Vent: NSR 1 .O year Normal 4 14.1 years 13.8 years 130 fatigue, digoxin 13 years cryodblation/ R Atrium: 60%NSR 3 years dizziness digoxin Normal 40%SVT 5 19.5 years 13.5 years 135 fatigue, exercise digoxin 8 years cryoahlation/ R Atrium: NSR 3 years intolerance nadolol excision Purkinje- RARE APB quinidine like Fibers propranolol RAA: Purkinje- like Fibers R Vent: Normal

APB = atrial premature beat; bpm = beats per minute; NSR = normal sinus rhythm; R = right: RAA = right atrial appendage; SVT = supraventricular tachycardia; Vent = ventricle.

Vol. 2, No. 4, 1989 Journal of Interventional Cardiology 213 BROMBERG, ET AL.

either alone or together for greater than 13 years, sinus rhythm, there was a significant reduction in elected surgery. The five patients have been fol- the CTR by chest x-ray (53% precontrol vs 49% lowed for an average of 1.5 years. postcontrol, P = 0.02). Heart Rate and Cardiothoracic Ratio. There was Echocardiographic Measures of Ventricular a significant (P I0.002) reduction in the mean Function. Figure 2 summarizes the improvement heart rate (128 f 24 vs 91 f 10 bpm) as deter- in cardiac function. Both the systolic and diastolic mined by 24-hour ambulatory electrocardiograms. dimensions significantly decreased yielding an im- The dominant mechanism of the post-treatment proved shortening fraction (mean 2 I % to mean cardiac rhythm was sinus (Fig. 1) in all five pa- 34%, P I 0.05). The two-dimensional echocardio- tients. Patients 1-3 were treated medically, and graphic ejection fraction, reflecting a more global each required adjustments of the medication, in- measurement, also increased from a mean 36% to cluding other antiarrhythmia trials, for satisfactory mean 50% following control of the tachycardia (P control (a few isolated atrial premature beats). Pa- I0.01). The mean heart rate corrected VCF in- tient 4 had marked reduction in the incidence and creased from a mean of 0.62 to a mean of 1.20 persistence of SVT but still had runs of tachycar- circs/sec (P = 0.003). The EPSS/EDD, a measure dia. Patient 5 is virtually free of arrhythmia with independent of preload, was abnormal (i.e., only a few isolated atrial premature beats and a greater than 0.2-the 95th percentile) in three of normal heart rate response to treadmill exercise the five patients prior to treatment. Although one (i.e., no ectopic tachycardia during exercise). of these three remained >95th percentile following Along with the above noted return to a slower arrhythmia control, all three were improved.

SHORTENING FRACTION

16- VCFC SF 14- 0s 12-

10- 02 08

06 01- 04 0.01 02 BEFORE AFTER :g

EJECTION FRACTION 0.7, ESPP/EDO 0.5 1 EF 0.6-

0.5 -

04-

03-

02-

0.1 I 0.0 J- BEFORE AFTER BEFORE AFTER

Figure 2. Echocardiographic measures of left ventricular function before and after final treatment in the five patients. SF = shortening fraction; VCF, = velocity of circumferential fiber shortening corrected for heart rate; EF = ejection fraction: EPSS/EDD = E-point septa1 separalion/end-diastolicdimension.

214 Journal of lnterventional Cardiology Vol. 2, No. 4, 1989 TREATMENT OF AAT

Patient 2 is of particular interest (Fig. 3). Amio- echocardiographic measured cardiac function was darone successfully restored sinus rhythm but was observed. discontinued because of hyperactivity possibly re- Myocardial Biopsies. Light microscopic exami- lated to hyperthyroxinemia. Although flecainide nation of the biopsies from the right ventricle replaced the amiodarone, the AAT resumed. After showed no evidence for or storage thyroid function was determined to be normal, disease in any patient. Nonspecific myofibril hy- amiodarone was restarted with return to sinus pertrophy and focal fibrosis that were within the rhythm. Thus, during two separate treatment pe- range of normal were present in two patients nods over a 6-month period, a direct relationship (Table I). The atrial biopsy from patient 4 dis- between the control of the tachycardia and normal closed normal atrial tissue. In contrast, the atrial

EPSS/EDD VCVF

EPSS/EDD 0.18 - - 1.4 0.16 - - 1.3 0.14- - 1.2 Q EPSS/EDD 0.12 - - 1.1 + VCFc 0.10 - - 1.0 0.08 - - 0.9 0.06 0.8 3NORXI RXI NOW RX2

SHORTENING FRACl'ION/EJECTION FRACTION

- 0.7 SF EF - 0.6

- 0.5

- 0.4 4 SF *EF - 0.3

- 0.2

0.0 10.1 NORX1 RXI NORX2 RX2

Figure 3. Echocardiographic measures of left ventricular function in patient #I during two trials of amiodarone. The interval between NORX 1 and RX 1 is 7 months; between RX 1 and NORXZ, 14 months: and between NORXZ and RX2,4 months. EPSS/EDD = E-point septa1 separation/end-diastolic dimension; VCF, = velocity of circumferencial fiber shorten- ing corrected for heart rate: SF = shortening fraction; EF = ejection fraction.

Vol. 2, No. 4, 1989 Journal of Intervenlional Cardiology 215 BROMBERG, ET AL. tissue excised from patient 5 during surgery dem- rates produces congestive in 2-3 onstrated Purkinje fiber-like tissue in specimens weeks. Although no direct evidence for a similar from the coronary sinus, the mapped origin of his effect of chronic atrial pacing has been reported, tachycardia, as well as from the right atrial ap- the association of sustained supraventricular pendage (Table I). tachycardia and congestive heart failure in in- Complications. No significant complications fant~~~,~'as well as in older individuals4 has been were encountered. Patient 2 required evaluation of recognized for several decades. The progression to his thyroid function because of the suspicion dat a myopathy is less clear. Nonetheless, a number of he might be thyrotoxic. However, further thyroid repo~s6.7,13,16-18,26that indicate resolution ofa di- studies excluded this possibility and amiodarone lated heart after control of supraventricular tachy- was resumed. Patient 4 experienced 2: 1 heart cardia, along with our experience, support these block postoperatively, but permanent normal 1: 1 experimental data. Patient 3 represents a fortui- conduction resumed within 5 days. tous clinical experiment supporting those observa- Follow-up. All patients except patient 4 are tions. This patient demonstrated over a 6-month asymptomatic and virtually free of their tachyar- period a direct relationship between control of the rhythmia at mean 1.5 years following treatment. tachycardia and improvement in ventricular func- Following control of the tachycardia, three pa- tion. Further, the observation from our two oper- tients resumed full activity, and the other two have ated patients that the return of cardiac function had a marked but not complete return to previous was not instantaneous suggests that the observed activity level. Patient 4 was recently hospitalized change in the echocardiographic measures of ven- following a suicide attempt. Non-invasive evalua- tricular function are not simply a function of heart tion at that time disclosed normal left ventricular rate but reflect genuine improvement in ventricu- function by echocardiogram, normal cardiac size lar performance. on chest radiograph, normal exercise treadmill Previous report^'^,^^,^^ have suggested Purkinje- test, normal sinus rhythm during 12 of the 24 like or mesenchymal type tumors causing auto- hours on Holter , and much matic tachycardia as well as other complex ar- less tachycardia that during the pretreatment pe- rhythmias; on the other hand atrial biopsies in 10 riod. Because of a complex social situation, further other patien& with sustained AAT63'2715.'7*19were cardiac and arrhythmia evaluation was deferred. nonspecific. Patient 5 had Purkinje-like fibers ex- cised from the area of tachycardia focus. Interest- ingly, similar cells were found in his incidentally Discussion discarded right atrial appendage taken for cannu- lation. These abnormal mesenchymal cells/Pur- Our data are in accord with the observations of kinje fibers argue against a abnor- others that indicate that sustained automatic atrial mality as the cause of the AAT and lead to the tachycardia at only moderately elevated rates possibility of multiple subclinical abnormal cells above normal ( 120- 1 70 bpm) may produce signif- in patients with automatic atrial tachycardia, giv- icant impairment of cardiac function. Further- ing rise to the possibility of late recurrence. In more, our experience demonstrates that this im- contrast, the atrial tissue excised from Patient 4 pairment is associated with the appearance of failed to disclose unusual cells, perhaps suggesting symptoms. Finally, our experience confirms not an incomplete ablation of her ectopic focus and, only improved control of the tachycardia follow- thus, explaining, in part, her less successful result. ing pharmacological and/or surgical intervention, The nonspecific right ventricular biopsy material but also, as a result, significant recovery of cardiac from our three patients, along with the five re- function.6.7.13,1426 ported by others,6 underscores the absence of a The exact causal relationship between chronic primary ventricular abnormality as the proximate atrial tachycardia and the development of a car- cause of the observed impairment in cardiac func- diomyopathic state has not been fully established. tion. Recent studie~~~-~~have demonstrated that ven- Conventional therapy is rarely effective. Di- tricular pacing of the canine heart at accelerated goxin alone failed to control the SVT in four of our

216 Journal of Interventional Cardiology Vol. 2, No. 4, 1989 TREATMENT OF AAT five patients; the addition of beta blockade in two References patients was also unsuccessful. Both patients who received amiodarone converted to sinus rhythm. I. Gillette K.The mechanism of supraventricular tachycar- dia in children. Circulation 1976; 54: 133- 139. Thus, similar to other report^,^^,^^ our experience 2. Campbell RM, Dick M, Rosenthal A. Cardiac arrhyth- suggests that no single therapeutic regimen mias in children. Am Rev Med 1984; 35:397-410. emerges as the clear treatment of choice. Because 3. Keane JF, Plauth WH, Nadas AS. Chronic ectopic tachy- cardia of infancy and childhood. Am Heart J 1972; of the infrequency of this disorder, its variable nat- 84:748-757. ural history, including documented spontaneous 4. Weiss HB, McGuire J. Ectopic tachycardia, auricular in remission of the tachy~ardia~~,~~and the nonran- origin, of unusual duration. Am Heart J 1936; 12585- 591. dom use of the different forms of therapy, a single 5. Hay JD, Keidan SE. Persistent ectopic auricular tachycar- optimal treatment for all patients will probably not dia in children. Br Heart J 1952; 14:345-349. be forthcoming. Thus, a step-wise approach may 6. Parker DL, Gust HB, Seth JW, et al. Tachycardia-in- duced cardiomyopathy: A reversible form of left ventricu- be prudent. In the absence of symptoms and with lar dysfunction. Am J Cardiol 1986; 57563-570. no evidence of impaired ventricular function, ther- 7. Kugler JE, Baisch SO, Cheatham JP, et al. Improvement apy may not be necessary. Because control of the of left ventricular dysfunction after control of persistent tachycardia. J Pediatr 1984; 105:543-548. tachycardia will restore ventricular function, with 8. Evans EL, Garson A Jr, Smith RT, et al. Ethmozine: A increasing improvement over time, noninvasive promising drug for automatic atrial ectopic tachycardia. evidence for decreased ventricular function war- Am J Cardiol 1987; 60:83F-86F. 9. Kunze KP, Kuck KH, Schluter M, et al. Effect of Encain- rants treatment. New antiarrhythmic medications, ide and Recainide on chronic atrial tachycardia. J Am including flecainide, encainide, ethmozine, and Coll Cardiol 1986; 7: 1 12 1 - 1 126. amiodarone,*-" along with the development of 10. Berns E, Rinkenberger RL, Jeang M, et al. Efficacy and safety of flecainide acetate for atrial tachycardia or fibrilla- electrophysiological-cryosurgical tion. Am J Cardiol 1987; 59:1337-1341. offer several avenues for management. However 11. Coumel P, Fidelle J. Amiodarone in the treatment of car- the recent experience with flecainide and encain- diac in children: One hundred thirty-five cases. Am Heart J 1980; 100: 1063- 1069. ide36underscores the need for a careful weighing of 12. Wyndham CRC, Arnsdorf MF, Levitsky S, et al. Success- the risks of treatment (as well as no treatment) ful surgical excision of focal paroxysmal atrial tachycar- along with the benefits expected before initiating dia: Observations in vivo and vitro. Circulation 1980; 62: 1365-1372. unexplored pharmacological therapy. 13. Olson SB, Blomstrom P, Sabel KG, et al. Incessant ec- topic atrial tachycardia: Successful surgical treatment with regression of picture. Am J Car- diol 1984; 53:1465-1466. Conclusions 14. Josephson ME, Spear JF, Harken AH, et al. Surgical exci- sion of automatic atrial tachycardia: Anatomic and elec- trophysiologic correlates. Am Heart J 1982; 104: 1076- 1085. We conclude that AAT may be causally linked 15. Iwa T, Ichihashi T, Hashizume Y, et al. Successful surgical to the development of cardiomyopathy. Poorly treatment of left atrial tachycardia. Am Heart J 1985; controlled AAT may present clinically as conges- 109: 160-162. 16. Ott DA, Garson A, Cooley PA, et al. Definitive operation tive heart failure, or more subtly, with impairment for refractory cardiac tachydysrhythmias in children. J of ventricular function prior to the onset of overt Thorac Cardiovasc Surg 1985; 90:68 1-689. failure. In the experience reported herein, as well 17. Frank G, Baumgart D, Klein H, et al. Successful surgical treatment of focal atrial tachycardia-a case report and as those of others, aggressive management results review of the literature. J Thorac Cardiovasc Surg 1986; in resolution of the SVT, symptomatic improve- 34~398-402. ment, and normalization of ventricular function. 18. Gillette PC,Smith RT. Canon A Jr, et al. Chronic supra- , a curable cause of congestive car- Because AAT is a treatable arrhythmia, any child diomyopathy. J Am Med Assoc 1985; 253:391-392. presenting with symptoms, signs, and echocardio- 19. Giorgi LV, Hartzler GO, Hamaker WR. Incessant focal graphic evidence of cardiomyopathy should be atrial tachycardia: A surgically remediable cause of car- diomyopathy. J Thorac Cardiovasc Surg 1984; 87:466- carefully evaluated by ECG, 24-hour ambulatory 473. ECG, and, if necessary, electrophysiologic studies. 20. Gillette PC, Wamplec PL, Garson A Jr, et al. Treatment of Treatment should be instituted if either symptoms atrial automatic tachycardia by ablation procedures. J Am Coll Cardiol 1985; 6:405-409. or the noninvasive findings of decreased ventricu- 21. Davis J, Scheinman MM, Ruder MA, et al. Ablation of lar function are present. cardiac tissues by an electrode catheter technique for

Vol. 2, No. 4, 1989 Journal of Interventional Cardiology 217 BROMBERG, ET AL.

treatment of ectopic supraventricular-tachycardia in 29. Armstrong PW, Stopps TP, Ford SE, et al. Rapid ventricu- adults. Circulation 1986; 74: 1044-1053. lar pacing in the dog: Pathophysiologic studies of heart 22. Borggrefe M, Breithardt G. Ectopic atrial tachycardia after failure. Circulation 1986; 74: 1075-1084. transvenous catheter ablation of a posteroseptal accessory 30. Silverman JJ, Race OM. with a pathway. J Am Coll Cardiol 1986; 8:441-445. ventricular rate of 365 per minute. Am Heart J 1949; 23. Goldreyer BN, Gallagher JJ, Damato AN. The electro- 37: 1 139-1 143. physiologic demonstration of atrial ectopic tachycardia in 31. Nadas AS, Daeschner CW, Roth A. Paroxysmal tachycar- man. Am Heart J 1973; 85:205-215. dia in infants and children. Pediatrics 1952; 9 167- 18 1. 24. Scheinman MM, &bal B, Hollenberg M. Electrophysio- 32. James TN, Beeson CW,Sherman EB, et al. De Subitaneis logic studies in patients with persistent atrial tachycardia. Mortibus, XIII. Multifocal Purkinje cell tumors of the Circulation 1974; 50:266-273. heart. Circulation 1975; 52:333-344. 33. Rossi L, Piffer R, Turolla E, et al. Multifocal Purkinjslike 25. Gillette PC,Garson A Jr. Electrophysiologicand pharma- cologic characteristics of automatic ectopic atrial tachy- tumor of the heart: Occurrence with other anatomic ab- cardia. Circulation 1977; 5657 1-575. normalities in the atrioventricular junction of an infant with , LownGanong-Levine syn- 26. Gallagher JJ. Tachycardia and cardiomyopathy: The drome, and sudden death. Chest 1985; 87:340-345. chicken-egg dilemma revisited. J Am Coll Cardiol 1985; 34. Mehta AV, Sanchez GR, Sacks El, et al. Ectopic auto- 6:1172-1173. matic atrial tachycardia in children: Clinical characteris- 27. Coleman HN, Taylor RR, Pool PE, etal. Congestive heart tics, management, and follow-up. J Am Coll Cardiol failure following chronic tachycardia. Am Heart J 197 1; 1988; 11~379-385. 8~760-798. 35. Koike K, Hesslein PS, Finlay CD, et al. Atrial automatic 28. Wilson JR, Douglas P, Hickey WF, et al. Experimental focus tachycardia in children. Am J Cardiol 1988; congestive heart failure produced by rapid ventricular 61: 1 127-1 130. pacing in the dog: Cardiac effects. Circulation 1987; 36. CAST Investigators. The cardiac arrhythmia suppression 75:857-867. trial. N Engl J Med 1989; 321:406-412.

218 Journal of Interventional Cardiology Vol. 2, No. 4, 1989