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Electrical ablation of atrial muscle. I. Early and late anatomic observations in canine atria
Electrical ablation of atrial muscle. I. Early and late anatomic observations in canine atria Electrode catheter ablation (ECA) of atrial muscle may be a useful technique for the treatment of drug-refractory supraventrlcular tachycardlas originating in the rlght atrial free wall (RAFW). We performed this study in order to determine: (1) the safety of electrical shocks applled to the RAFW and (2) the early and late anatomic effects of ECA. Twelve beagle puppies, ranging in age from 2.0 to 7.5 months and weighing 2.3 to 8.0 kg, underwent electrical ablation of the RAFW, using energy doses of 100 to 400 J. At the highest energy doses tested (400 J), one puppy died of refractory ventricular fibrillation and one of low cardiac output. Atria1 perforation and cardiac tamponade occurred in two puppies, each of which received one shock of 200 J. The area of myocardlal damage following ECA shocks of 150 J was greater than for shocks of 100 J, 94 + 14 vs 56 + 11 mm’, respectively (p < 0.02). Acutely, ECA produced transmural hemorrhagic necrosis. Eleven weeks after electrical ablation, atrial fibrosis was apparent at the site of ablation. In conclusion, ECA may be used to fulgurate atrial tissue In the RAFW. We recommend 150 J as a safe upper limit in small subjects, although higher energy doses may not produce cardiac perforation or adverse hemodynamic effects in larger subjects. (AM HEART J 1987;113:139?.)
Jeffrey P. Moak, M.D., Richard A. Friedman, M.D., and Arthur Garson, Jr., M.D. Houston,
Tex.
Atrial ectopic tachycardia is a common mechanism of supraventricular tachycardia in the pediatric population.’ This arrhythmia has proved refractory to treatment with digitalis glycosides, local anesthetic, and slow channel blocking antiarrhythmic agents.2At our institution, we have used the intraoperative cryoablative technique to successfully manage this arrhythmia.3 Direct electrode catheter ablation of the ectopic atrial focus may have similar applicability without requiring cardiothoracic surgery and may avoid the pacemaker dependency inherent in His bundle ablation.4 To be clinically useful, electrode catheter ablation must be free from the complication of atrial perforation, yet effective in necrosing at least 80 mm2 of atrial tissue, the area comparable to a 1 cm diameter cryofreeze lesion. The purpose of this study was twofold: First, to test the safety of electrical shocks applied to the canine right atrial free wall. It is From the Lillie Frank Abercrombie Section of Cardiology, Department of Pediatrics, Baylor College of Medicine and Texas Children’s Hospital. Supported in part by Grant No. RR0542523 from the National Institutes of Health Biomedical Research Support Grant, by Grant No. HL07190 from the National Institutes of Health, United States Public Health Service, and by a grant from the J. S. Abercrombie Foundation. Received for publication Feb. 10, 1986; accepted Nov. 3, 1986. Reprint requests: Jeffrey P. Moak, M.D., Pediatric Cardiology, Texas Children’s Hospital, 6621 Fannin, Houston, TX 77030.
important to establish a range of applied energy to the right atrial free wall that does not result in atria1 perforation. Since puppies have a thinner atrial myocardial wall than humans, we reasoned that the range of applied energies found safe in the immature, thin canine atrium should prove safe for usage in children and adults. The second goal was to assess the early and late anatomic effects of electrical shocks applied to the right atrial free wall. METHODS
Twelve beagle puppies, ranging in age from 2.0 to 7.5 months (median = 2.5 months) and weighing between 2.3 and 8.0 kg (median = 3.0 kg) underwent electrical ablation of the right atrium. The electrode catheters were inserted by the percutaneoustechnique and were positioned under biplane fluroscopic guidance. The electrode catheter was connectedto a Statham defibrillator (model 1210B,Gould Inc. CardiovascularProducts, Oxnard, Calif.) via an isolation unit (R2 Corporation, Skokie, Ill.). The discharge wave form had a rise time of 1.8 msec.The isolation unit wasplaced on the dischargecircuit and allowed triggering
of the electrical defibrillator. The cathode electrode pad was replaced with a pin jack connector to allow the electrode catheter to becomethe cathode in the discharge circuit. No. 5 French or No. 6 French tripolar catheters (USC1 Division of C. R, Bard, Billerica, Mass.) with 1 cm spacing between the electrode poles and 2 mm electrode widths were used for electrical ablation. The catheters were not 1397
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Fig. 1. Atrial perforation occurred as a complication of right atria1 appendageablation (puppy No. 4). Following delivery of 200J to the baseof the right atria1 appendage,cardiac perforation occurred. Arrows point to a 1.5 mm hole at the site of perforation. This puppy died of cardiac tamponade.
Table
I. Anatomic observationsand complications following electrical ablation of the right atrium Electrical dosage
PUPPY no. Group 1 2 3 4 5 6 7 8 Group 9
Ablation location
(Jl Z-First
II-11
10 11 12 RA = right atrium;
Area of necrosis (mm’)
Outcome
24 hours
weeks
400 400 200 200 loo 200 100 150 after ablation 150 150
RAA Ant RA Ant RA
RAG RAA Ant RA Post Medial RA RAA procedure
150 150 RAA = right atria1 appendage;
RAA
Post = posterior;
electrically selectedfor their ability to withstand current leaking under high voltage stress?‘j and were used only once.A No. 5 French or No. 6 French catheter wasusedin eight and four puppies,respectively. Each puppy received a single shock through the distal pole of the catheter, which served as the cathode. An electrode pad (R2 Corporation) placed on the right anterior chest wall served as the anode. All shockswere R-wave synchronized. We initially beganour experiments with energy dosesof 400 J in two puppies and 200 J in three puppies. Because of the high mortality using these energy levels, we subsequently tested 150 and 100 J doses in five and two puppies, respectively. The following right atrial free wall locations were electrically ablated: right atrial appendage
Alive
Alive Alive
105 95 80 80
Lat RA PostLat RA Ant RA
Post
Ant = anterior;
Died-refractoryVF Died-lowcardiacoutput Died-cardiacperforation Died-cardiacperforation Alive
50 360 84 75 48 285 63 110
Lat = lateral; VF = ventricular
Alive
Alive Alive Alive fibrillation.
(five puppies), anterior-lateral free wall (four puppies), posterior-lateral free walI (two puppies), and posterior-
medial free wall (one puppy). Our experimental protocol con&ted of studying the effects of electrical ablation in two different groups of puppies.In group 1, the early anatomic effects of electrical ablation were studied in eight puppies. Four of theseeight puppies underwent unplanned immediate anatomic assessmentfollowing the ablation procedure becauseof their early death. In the other four puppies, anatomic assessmentwas performed 24 hours after the ablation procedure. Croup 2 consistedof four puppiesin which the anatomic effects of electrical ablation were studied 11 weekslater.
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Atria1 electroablation:
Anatomic observations
1399
Fig. 2. Example of acute anatomic injury produced by right atrial appendageablation-puppy
No. 8. A, Without catheter. Acute atrial necrosiswasevident at three separateand discrete sites. The three sites of atrial necrosisare outlined by arrows. B, After removing the heart from the chest, the electrode catheter usedfor the procedure was repositioned to the location it had held immediately prior to delivery of the ablative shock. Each site of atrial necrosisaligns with one of the three electrode poles of the catheter. IVC = inferior vena cava; RAA = right atrial appendage
Fig. 3. Acute transmural right anterior free wall necrosisproduced during electrical ablation with 200 J-puppy No. 3. A, Epicardial lesion. Arrows outlined area of epicardial hemorrhage overlying the site of endocardial electrical ablation. Acutely, endocardial fulguration of the right atrial free wail produced transmural injury. B, The site of endocardial ablation is outlined by arrows.
Statistical analysis. The data are expressed as the mean + standard deviation. Statistical analysis was performed by the unpaired t test. The statistical significance of differences is expressedin the text. RESULTS
The anatomic effects and outcome of electrical ablation of the right atrial free wall are described in Table I. Early mortality following electrical ablation. Atria1 perforation and cardiac tamponade occurred in two puppies, each of which received one shock of 200 J. Shown in Fig. 1 is the epicardial site of cardiac perforation (puppy No. 3). Outlined by urrows at the base of the right atrial appendage is a 1.5 mm hole corresponding to the site of perforation. At autopsy, blood was found in the pericardial cavity. Transmu-
raI migration of the catheter occurred at the base of the right atrial appendage and at the anterior-lateral right atrium in one puppy each. Puppy No. 1 died of refractory ventricular fibrillation following a single shock of 400 J. This puppy was young (2.5 months) and weighed 4.0 kg. Puppy No. 2 died of low cardiac output following a single shock of 400 J. Early anatomic tion
observations
following
electrlcal
abla-
Area of endocardial necrosis. The area of endocardial necrosis produced during electrical ablation was related to the amount of applied energy. The mean area of endocardial damage for shocks of 100, 150, and 2200 J was 56 f 11, 94 f 14, and 171 2 142 mm2, respectively. The area of myocardial damage following shocks of 150 J was statisticahy larger
1987
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A
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June Heart Journal
RffiHT ATRIAL SEPTUM
Fig. 4. Acute atrial septal necrosis.A, Right atrial septum. Several foci of atria1 necrosiswere apparently produced during electrical ablation of the posterior-medial atrial septum.Atrial injury occurred at the site of contact betweenthe distal pole of the electrode catheter and the atrial wall. In addition, a secondregion of fulguration wasevident in the anterior free wall of the right atrium. Arrows outline right atrial sitesof necrosis.B, Directly opposite the right atrial septal injury, on the left side of the atrial septum, necrosis was present. Electrical ablation produced transseptal injury.
than for shocks of 100 greater than or equal to variability in the amount Electrical ablation with
Fig. 5. Right ventricular myocardial necrosis produced during inferior right atrial free wall ablation. A, Right atrium. Black arrows outline hemorrhagic right ventricular myocardium. Fulguration of the base of the right ventricle occurred inadvertently during electrical ablation of the inferior right atrium. This puppy developed incessant ventricular tachycardia following the ablation procedure. B, View of tqnsmural hemorrhagiclesionat the base of the right ventricle from a different perspective. The endocardium and epicardium are identified by arrows. WC = superior vena cava; other abbreviations as in Fig. 2.
J (p < 0.02). For shocks
200 J, there was a wide of tissue damage. energies of 150 J or more
frequently produced atrial necrosis at several of the electrode poles on the catheter. Fig. 2 demonstrates the endocardial necrosis that occurred in puppy No. 8 following electrical ablation in the right atria1 appendage. Two similar views of the right atrial septum and appendage are presented in this figure. Three discrete lesions of endocardial necrosis are apparent in Fig. 2, A. In Fig. 2, B, a tripolar catheter has been placed in a position simulating that which was observed in vivo. Although all the electrical energy was applied to the distal pole, due to insulation breakdown within the catheter, energy was delivered to all three of the electrode poles, causing tissue damage at each site. Extent of atriab injury. Transmural or transeptal injury occurred following atrial electrical ablation. Fig. 3 demonstrates the acute injury observed following right anterior free wall ablation with a 200 J energy dose. Intense epicardial (Fig. 3, A) and endocardial (Fig. 3, B) necrosis was always observed. Transeptal atrial necrosis is observed in Fig. 4. Following electrical ablation of the posterior-medial right atrial septum, necrosis was observed directly opposite this site, on the left side of the atria1 septum (Fig. 4, B). The atrial tissue injury induced during electrical ablation of the right atrial free wall was frequently multifocal. Tissue injury occurred not only in areas of contact between the catheter and the atrial free wall, but along the pathway of current spread
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Atria1 electroablation:
Anatomic observations
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Fig. 6. Late anatomic findings-intense endocardial fibrosis (puppy No. 10). Endocardial fibrosis occurred in the region of the posterior lateral right atrium, the site of atrial ablation. Arrowheads identify this area. Atria1 fulguration produced multifocal injury. The crista terminalis, anteriorly positioned and in the direct line of current spread between the distal electrode pole of the catheter (cathode) and the anterior chest pad (anode), wasinjured in addition (arrows). To contrast the difference between the early and late anatomic effects of the ablation procedure, compare with Fig. 5, panel A. CT = crista terminalis. Other abbreviations sameas figure 2.
between the cathode and anode. Fig. 4, A demonstrates this phenomenon. Puppy No. 7 underwent
Late anatomic tion. In order
observations
following
electrical
able-
electrode catheter ablation of the posterior-medial right atrium with 100 J. In this puppy, ablation apparently produced two regions of tissue injury. The primary focus of atrial injury occurred at the point of contact between the distal electrode pole and the atrial septum. In addition, necrosis of the right anterior free wall was produced as current spread between the anode and cathode. Ventricular muscle injury. Electrical ablation of the atrial free wall may inadvertently injure the subjacent base of the right ventricle. Ventricular ectopy occurred during the first 24 hours following electrical ablation in five of eight group I puppies. Ventricular ectopy occurred in those animals with associated ventricular injury. Demonstrated in Fig. 5 is an example of acute necrosis of the inferioranterior right atrial free wall following electrical ablation (puppy No. 6). The black arrows in Figure 5, panel A point to the base of the right ventricle. Hemorrhagic necrosis has extended across the atrio-
to assessthe extent of chronic atrial injury, four puppies were followed for 11 weeks after the ablation procedure. The electrical shock was applied to the posterior-lateral right atrium in two, to the right atrial appendage in one, and to the anterior-lateral right atrial free wall in one puppy. Endocardial fibrosis developed at the site of ablation. In three of the puppies, the atrial fibrosis that occurred at this site was nonhomogeneous. In all four puppies there appeared to be several discrete patches of atrial fibrosis within the right atrium. These appeared to represent areas of tissue injury that occurred at multiple electrode poles. Demonstrated in Fig. 6 (puppy No. 10) is a representative example of the endocardial fibrosis that developed late after the atrial ablation procedure. The distal pole of the electrode catheter had been placed in the posterior lateral right atrium. Intense fibrosis occurred in this region. Because the length of the endocardial fibrotic patch was 1.2 cm, it would appear that electrical current had spread
cardium. The hemorrhagic necrosis is viewed from a different perspective in Fig. 5, panel B. Transmural myocardial hemorrhage is demonstrated between the black arrows, outlining the right ventricular endocardium and epicardium.
injurying the atrial tissue between them. In addition, fibrosis was observed anteriorly, along the crista terminalis, presumably in a region not in contact with the catheter. We speculate that the crista terminalis was injured as current spread
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Fig. 7. Transmural atria1fibrosis 11 weeksafter the ablation procedure. High-power photomicrograph of crista terminalis region. In the center of the fulguration scar, on the right-hand side of the figure, fibrosis was transmural. Toward the periphery of the lesion, center of figure, depth of fibrosis was shallower. Further leftward, normal atria1 myocardium wasapparent. Arrows identify the depth of fibrous tissueand atria1 cellular damage(Trichrome stain).
between the posteriorly located cathode and anterior chest wall anode. Atrial muscle fibrosis was transmural in the center of the ablation lesion. Fig. 7 demonstrates, histologically, the transmural fibrosis that developed late after crista terminalis ablation. Centrally, the observed fibrosis was transmural. The depth of fibrosis became less extensive at the periphery of the lesion, where normal atrial muscle was evident. DISCUSSION
Ectopic atrial tachycardia is a frequent mechanism of supraventricular tachycardia in children.’ Suppression of this arrhythmia with currently available antiarrhythmic agents is generally ineffective.2 Surgical resection and cryoablation are highly efficacious in arrhythmia elimination.3 Previous experimental studies’s8 have suggested that electrode cath-
ed both anterior to and posterior to the electrode pole to which the ablative shock was applied. The area of greatest tissue injury was directly under the ablative electrode pole. Late after the procedure, transmural atrial fibrosis developed at the site of maximum injury. The extent of tissue damage ranged from 50 to 360 mmz. As suggested by investigators of low right atrial septal and coronary sinus ablation,7-g we found that there was significantly greater atrial muscle necrosis in the free wall of the right atrium when higher energy doses were used during the ablation procedure. An energy dose 2150 J produced significantly greater tissue damage than an energy dose of 100 J. The energy dose used for right atrial free wall ablation must be chosen carefully. The electrical shock must be of sufiicient intensity to necrose a
minim@ area of tissue damage. We-studied the safety and anatomic effects of electrical ablation on the free wall of the right atrium to assess whether electrode catheter ablation may have applicability in management of atrial ectopic tachycardia. In this study we found that electrode catheter ablation could be used to necrose “small” areas of atria1 muscle in the free walI of the right atrium of young dogs. Acutely, atria1 ablation produced transmural hemorrhage. The field of tissue injury extend-
jj&~~ive area,of tissue1jet not cause
complications-cardiac perforation or arrhythmia induction. What the dimensions of this area should be is complex. It will depend on the size of the arrhythmia circuit, the accuracy of the mapping procedure, the depth within the atrial wall at which the arrhythmia circuit is located, and the orientation of the ablating electrode pole to the arrhythmia circuit. Transmural atrial necrosis may be necessary for atria1 electrical ablation to be effective if the
Volume Number
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arrhythmia circuit is located intramurally or in the epicardium. Acutely, we observed transmural atrial hemorrhage at the site of electrical ablation. Histologic studies, performed 11 weeks after the ablation procedure, demonstrated very localized regions of transmural fibrosis. Normal-appearing atrial myocardium was observed at the periphery of these lesions. If the arrhythmia circuit is located at the periphery of the ablation lesion, the procedure may be unsuccessful. The smallest area of atrial muscle necessary to necrose in order for electrical ablation to be effective is unknown. Surgical cryoablation of 80 mm2, the area under a 1 cm diameter freeze probe, has been effective in controlling ectopic automatic atria1 tachycardia. Unknown is whether a smaller area of tissue damage would suffice. However, our surgical experience would suggest that the minimally effective area necessary to necrose in order to eliminate the automatic focus is at least 80 mm2.3 Attention has been focused on the type and design of catheters used during electrical ablation. The high energy levels used for electrical ablation may injure the catheter and impair its functional and physical integrity. Fischer et al5 have described disruption of the proximal electrical connectors, separation of the tip electrode, intraelectrode pitting, and failure of the internal wiring. These investigators have suggested in vitro testing of the electrode catheter prior to its clinical use. Bardy et al6 have noted a high incidence of current leak between electrode poles when standard tripolar electrode catheters have been tested in vitro with high energy doses. In this study we did not electrically select the catheters used for electrical ablation and noted clinical evidence of current leaking between multiple electrode poles during the ablation. The large variability in tissue damage we found when using energy doses of 200 J or more is best explained by current leaking between the distal electrode and more proximal electrode poles. Current leaking between electrode poles not overlying atrial tissue involved in the arrhythmia circuit may cause potential complications and adverse effects, e.g., sinus or atrioventricular (AV) nodal damage. Atrial perforation occurred in two of five puppies when ablation was attempted with an energy dose of 200 J or more. With the use of similar energy doses, Broadman and Fischer9 observed coronary sinus perforation in larger subjects when ablating with energy doses of 240 J. In addition, large energy doses (400 J) may induce intractable ventricular fibrillation or affect ventricular function in small subjects.
Atria1 electroablation:
Anatomic observations
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Morphologic studies of atrial tissue from patients with chronic atrial fibrillation have demonstrated fibrosis and loss of atria1 muscle cells.‘” Multiple regions of endocardial fibrosis were observed late after right atrial free wall ablation in our studies. Although endocardial atrial ablation may be acutely effective in eliminating an ectopic focus-supraventricular tachycardia or a reentrant atrioventricular tachycardia-our study raises concern about the potential long-term complications of this procedure, i.e., development of atrial flutter or fibrillation. Atrial free wall ablation near the atrioventricular junction may be associated with right ventricular damage. Five of the puppies that had undergone atrial ablation and in which the right ventricle was injured were noted to develop ventricular tachycardia or frequent ventricular ectopy during the first 24 hours after the ablation procedure. No correlation was evident between the energy dose used during the ablation procedure and the subsequent development of ventricular arrhythmias. We conclude that electrode catheter ablation can be used to necrose “small” areas of atria1 muscle in the right atria1 free wall. Because atrial perforation did not occur when an energy dose of 150 J or less was used, we recommend 150 J as a safe upper limit in small subjects. Clinically, atria1 ablation may be successful if lower energy doses are used.‘O The area of tissue necrosis is greater when atrial free wall ablation is performed with higher energy levels (150 J or more), but because of the risk of cardiac perforation, we recommend using multiple shocks at lower energy levels. The authors wish to acknowledge the technical assistance provided by Gregory Clark, Gerry Creager, and Mark Thompson, and also thank Terri Woods for her careful attention to the preparation of this manuscript.
REFERENCES
1. Gillette PC. The mechanisms of supraventricular tachycardia in children. Circulation 1976;54:133. 2. Gillette PC, Garson A. Electrophysiologic and pharmacologic characteristics of automatic ectopic atrial tachycardia. Circulation 1977;56:571. 3. Ott DA, Gillette PC, Garson A, Cooley DA, Reul GJ, McNamara DG. Surgical management of refractory supraventricular tachvcardia in infants and children. J Am Co11 Cardiol 1985;53124. 4. Gillette PC, Wampler DG, Garson A, Zinner A, Ott D, Cooley D. Treatment of atrial automatic tachycardia by ablation procedures. J Am Co11 Cardiol 1985;6:405. 5. Fischer JD, Brodman R, Johnston DR, Waspe LE, Kim SG, Matos JA, Scavin G. Nonsurgical electrical ablation of tachycardias: Importance of prior in vitro testing of catheter leads. PACE 1984;7:74. 6. Bardy GH, Coltori F, Ivey TD, Yerkovich D, Greene HL. Effect of damped sine-wave shocks on catheter dieiectric strength. Am J Cardiol 1985;56:769.
Moak,
Friedman,
and Garson
American
7. Gonzalez R, Scheinman M, Bharati S, Lev M. Closed chest permanent atrioventricular block in dogs. AM HEART J 1983;105:461. 8. Scheinman MM, Bharati S, Wang Y, Shapiro WA, Lev M. Electrophysiologic and anatomic changes in the atrioventricular junction of dogs after direct current shocks through tissue fixation catheters. Am J Cardiol 1985;55:194.
June 1987 Heart Journal
9. Brodman R, Fischer JD. Evaluation of a catheter technique for ablation of accessory pathways near the coronary sinus using a canine model. Circulation 1983;67:923. 10. Silka MJ, Gillette PC, Garson A, Zinner A. Transvenous catheter ablation of a right atria1 automatic ectopic tachycardia. J Am Co11 Cardiol 1985:5:999.
atria Electrical ablation techniques (ECT) have had llmited 8uccoss in achieving control of arrhythmias originating in the rfgM atrial free wall (RAFW). To ascertain determinants for successful ECT, we studied the clnical and cellular etectrophysiologic effects of electrloal abl8tion of the RAFW. After performing electrIcal ablation of the RAFW in 12 beagle Puppies, the fohowing studies were Performed: Hotter monitoring first 24 hours (eight puppies), and Y 1 weeks takr (four pupplea); clinical electrophysiologk study (four puppie@); and microelectrode otudy (&ii!) (etght puppier). Arrhythmias (AR) and conduction disturbaneer (CD) frequentfy occurred tmmedtately following ECT: ventricular tachycerdia (VT) (seven puppie@, junctlonat tachycardle (ona puppy), and asystole or compkte AV block (AVB) (four pupptee). HOlWr monftorlng durtng the flrdt 24 hours after ECT revested VT (four puppies), frequent ventricular premclture Uepderltaiona (one puppy), and type 2 second-degree AVB (four puppies). AR were r8rely 6een I8te 8fter ECT. Durlng clinical EP study 11 weeke after abtation, atrktl f4brHlatlon waa induced In ffiree of tour pupPIer; none had AR prror to ECT. Early ME study revealed a nonhomogeneous atriat infarct-a central zone of “dead” cells surrounded by peripheref idands of depre@eed cellular aotlvity. Cell8 with normal action potential characterlatics were noted in between. We conclude that (1) Electrical ablatton of the RAFW is aaeociated wtth a hleh incidence of early AR and CD. (2) Because of the nonhomogeneous nature of tissue InJury produced during ECT, careful strlal mapping Ls critically Important. (3) l,ocal regions of conductton delay and block may Provide a rub&rate for the late development of atrial arrhythmias. (AM HEAKT J 1987;113:14Cl4.)
Jeffrey P. Moak, Houston, Tex.
M.D., Richard
A. Friedman,
M.D., and Arthur
Electrical ablation techniques have been used to treat medically refractory arrhythmias. Catheter ablation is an accepted experimental technique for interrupting atrioventricular conduction.1-3 Complete atrioventricular (AV) block and control of
From the Lillie Frank Abercrombie Section of Cardiology, Department of Pediatrics, Baylor College of Medicine and Texas Children’s Hospital. Supported in part by Grant RRO5425-23 from the National Institutes of Health Biomedical Research Support Grant, and by Grant No. HL07190 from the National Institutes of Health, United States Public Health Service; and by a Grant from the J. S. Abercrombie Foundation. Received for publication Feb. 10, 1986; accepted Nov. 3, 1986. Reprint requests: Jeffrey P. Moak, M.D., Pediatric Cardiology, Texas Children’s Hospital, 6621 Fannin, Houston, TX 77030.
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Garson, Jr., M.D.
supraventricular arrhythmias can be achieved in 78 % of patients undergoing AV junctional ablation.4 Limited arrhythmia control has been achieved with right atrial free wall or coronary sinus electrical ablation for atrial ectopic tachycardias or accessory atrioventricular connectiona.5~ 6 Few previous investigations have addrmed the possible determinanta of failure of electrical ablation to damage critically imp&ant regions of the arrhythmia circuit. These studies have addressed problems in the delivery of electrical energy to the tissue, i.e., failure of electrode catheter components or electrical current leaking between electrode poles proximal to the cathode.‘v8 The purpose of this report is to describe the early and late clinical and
Jeffrey P. Moak, M.D., Richard A. Friedman, M.D., and Arthur Garson, Jr., M.D. Houston,
Tex.
Atrial ectopic tachycardia is a common mechanism of supraventricular tachycardia in the pediatric population.’ This arrhythmia has proved refractory to treatment with digitalis glycosides, local anesthetic, and slow channel blocking antiarrhythmic agents.2At our institution, we have used the intraoperative cryoablative technique to successfully manage this arrhythmia.3 Direct electrode catheter ablation of the ectopic atrial focus may have similar applicability without requiring cardiothoracic surgery and may avoid the pacemaker dependency inherent in His bundle ablation.4 To be clinically useful, electrode catheter ablation must be free from the complication of atrial perforation, yet effective in necrosing at least 80 mm2 of atrial tissue, the area comparable to a 1 cm diameter cryofreeze lesion. The purpose of this study was twofold: First, to test the safety of electrical shocks applied to the canine right atrial free wall. It is From the Lillie Frank Abercrombie Section of Cardiology, Department of Pediatrics, Baylor College of Medicine and Texas Children’s Hospital. Supported in part by Grant No. RR0542523 from the National Institutes of Health Biomedical Research Support Grant, by Grant No. HL07190 from the National Institutes of Health, United States Public Health Service, and by a grant from the J. S. Abercrombie Foundation. Received for publication Feb. 10, 1986; accepted Nov. 3, 1986. Reprint requests: Jeffrey P. Moak, M.D., Pediatric Cardiology, Texas Children’s Hospital, 6621 Fannin, Houston, TX 77030.
important to establish a range of applied energy to the right atrial free wall that does not result in atria1 perforation. Since puppies have a thinner atrial myocardial wall than humans, we reasoned that the range of applied energies found safe in the immature, thin canine atrium should prove safe for usage in children and adults. The second goal was to assess the early and late anatomic effects of electrical shocks applied to the right atrial free wall. METHODS
Twelve beagle puppies, ranging in age from 2.0 to 7.5 months (median = 2.5 months) and weighing between 2.3 and 8.0 kg (median = 3.0 kg) underwent electrical ablation of the right atrium. The electrode catheters were inserted by the percutaneoustechnique and were positioned under biplane fluroscopic guidance. The electrode catheter was connectedto a Statham defibrillator (model 1210B,Gould Inc. CardiovascularProducts, Oxnard, Calif.) via an isolation unit (R2 Corporation, Skokie, Ill.). The discharge wave form had a rise time of 1.8 msec.The isolation unit wasplaced on the dischargecircuit and allowed triggering
of the electrical defibrillator. The cathode electrode pad was replaced with a pin jack connector to allow the electrode catheter to becomethe cathode in the discharge circuit. No. 5 French or No. 6 French tripolar catheters (USC1 Division of C. R, Bard, Billerica, Mass.) with 1 cm spacing between the electrode poles and 2 mm electrode widths were used for electrical ablation. The catheters were not 1397
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Fig. 1. Atrial perforation occurred as a complication of right atria1 appendageablation (puppy No. 4). Following delivery of 200J to the baseof the right atria1 appendage,cardiac perforation occurred. Arrows point to a 1.5 mm hole at the site of perforation. This puppy died of cardiac tamponade.
Table
I. Anatomic observationsand complications following electrical ablation of the right atrium Electrical dosage
PUPPY no. Group 1 2 3 4 5 6 7 8 Group 9
Ablation location
(Jl Z-First
II-11
10 11 12 RA = right atrium;
Area of necrosis (mm’)
Outcome
24 hours
weeks
400 400 200 200 loo 200 100 150 after ablation 150 150
RAA Ant RA Ant RA
RAG RAA Ant RA Post Medial RA RAA procedure
150 150 RAA = right atria1 appendage;
RAA
Post = posterior;
electrically selectedfor their ability to withstand current leaking under high voltage stress?‘j and were used only once.A No. 5 French or No. 6 French catheter wasusedin eight and four puppies,respectively. Each puppy received a single shock through the distal pole of the catheter, which served as the cathode. An electrode pad (R2 Corporation) placed on the right anterior chest wall served as the anode. All shockswere R-wave synchronized. We initially beganour experiments with energy dosesof 400 J in two puppies and 200 J in three puppies. Because of the high mortality using these energy levels, we subsequently tested 150 and 100 J doses in five and two puppies, respectively. The following right atrial free wall locations were electrically ablated: right atrial appendage
Alive
Alive Alive
105 95 80 80
Lat RA PostLat RA Ant RA
Post
Ant = anterior;
Died-refractoryVF Died-lowcardiacoutput Died-cardiacperforation Died-cardiacperforation Alive
50 360 84 75 48 285 63 110
Lat = lateral; VF = ventricular
Alive
Alive Alive Alive fibrillation.
(five puppies), anterior-lateral free wall (four puppies), posterior-lateral free walI (two puppies), and posterior-
medial free wall (one puppy). Our experimental protocol con&ted of studying the effects of electrical ablation in two different groups of puppies.In group 1, the early anatomic effects of electrical ablation were studied in eight puppies. Four of theseeight puppies underwent unplanned immediate anatomic assessmentfollowing the ablation procedure becauseof their early death. In the other four puppies, anatomic assessmentwas performed 24 hours after the ablation procedure. Croup 2 consistedof four puppiesin which the anatomic effects of electrical ablation were studied 11 weekslater.
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Fig. 2. Example of acute anatomic injury produced by right atrial appendageablation-puppy
No. 8. A, Without catheter. Acute atrial necrosiswasevident at three separateand discrete sites. The three sites of atrial necrosisare outlined by arrows. B, After removing the heart from the chest, the electrode catheter usedfor the procedure was repositioned to the location it had held immediately prior to delivery of the ablative shock. Each site of atrial necrosisaligns with one of the three electrode poles of the catheter. IVC = inferior vena cava; RAA = right atrial appendage
Fig. 3. Acute transmural right anterior free wall necrosisproduced during electrical ablation with 200 J-puppy No. 3. A, Epicardial lesion. Arrows outlined area of epicardial hemorrhage overlying the site of endocardial electrical ablation. Acutely, endocardial fulguration of the right atrial free wail produced transmural injury. B, The site of endocardial ablation is outlined by arrows.
Statistical analysis. The data are expressed as the mean + standard deviation. Statistical analysis was performed by the unpaired t test. The statistical significance of differences is expressedin the text. RESULTS
The anatomic effects and outcome of electrical ablation of the right atrial free wall are described in Table I. Early mortality following electrical ablation. Atria1 perforation and cardiac tamponade occurred in two puppies, each of which received one shock of 200 J. Shown in Fig. 1 is the epicardial site of cardiac perforation (puppy No. 3). Outlined by urrows at the base of the right atrial appendage is a 1.5 mm hole corresponding to the site of perforation. At autopsy, blood was found in the pericardial cavity. Transmu-
raI migration of the catheter occurred at the base of the right atrial appendage and at the anterior-lateral right atrium in one puppy each. Puppy No. 1 died of refractory ventricular fibrillation following a single shock of 400 J. This puppy was young (2.5 months) and weighed 4.0 kg. Puppy No. 2 died of low cardiac output following a single shock of 400 J. Early anatomic tion
observations
following
electrlcal
abla-
Area of endocardial necrosis. The area of endocardial necrosis produced during electrical ablation was related to the amount of applied energy. The mean area of endocardial damage for shocks of 100, 150, and 2200 J was 56 f 11, 94 f 14, and 171 2 142 mm2, respectively. The area of myocardial damage following shocks of 150 J was statisticahy larger
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RffiHT ATRIAL SEPTUM
Fig. 4. Acute atrial septal necrosis.A, Right atrial septum. Several foci of atria1 necrosiswere apparently produced during electrical ablation of the posterior-medial atrial septum.Atrial injury occurred at the site of contact betweenthe distal pole of the electrode catheter and the atrial wall. In addition, a secondregion of fulguration wasevident in the anterior free wall of the right atrium. Arrows outline right atrial sitesof necrosis.B, Directly opposite the right atrial septal injury, on the left side of the atrial septum, necrosis was present. Electrical ablation produced transseptal injury.
than for shocks of 100 greater than or equal to variability in the amount Electrical ablation with
Fig. 5. Right ventricular myocardial necrosis produced during inferior right atrial free wall ablation. A, Right atrium. Black arrows outline hemorrhagic right ventricular myocardium. Fulguration of the base of the right ventricle occurred inadvertently during electrical ablation of the inferior right atrium. This puppy developed incessant ventricular tachycardia following the ablation procedure. B, View of tqnsmural hemorrhagiclesionat the base of the right ventricle from a different perspective. The endocardium and epicardium are identified by arrows. WC = superior vena cava; other abbreviations as in Fig. 2.
J (p < 0.02). For shocks
200 J, there was a wide of tissue damage. energies of 150 J or more
frequently produced atrial necrosis at several of the electrode poles on the catheter. Fig. 2 demonstrates the endocardial necrosis that occurred in puppy No. 8 following electrical ablation in the right atria1 appendage. Two similar views of the right atrial septum and appendage are presented in this figure. Three discrete lesions of endocardial necrosis are apparent in Fig. 2, A. In Fig. 2, B, a tripolar catheter has been placed in a position simulating that which was observed in vivo. Although all the electrical energy was applied to the distal pole, due to insulation breakdown within the catheter, energy was delivered to all three of the electrode poles, causing tissue damage at each site. Extent of atriab injury. Transmural or transeptal injury occurred following atrial electrical ablation. Fig. 3 demonstrates the acute injury observed following right anterior free wall ablation with a 200 J energy dose. Intense epicardial (Fig. 3, A) and endocardial (Fig. 3, B) necrosis was always observed. Transeptal atrial necrosis is observed in Fig. 4. Following electrical ablation of the posterior-medial right atrial septum, necrosis was observed directly opposite this site, on the left side of the atria1 septum (Fig. 4, B). The atrial tissue injury induced during electrical ablation of the right atrial free wall was frequently multifocal. Tissue injury occurred not only in areas of contact between the catheter and the atrial free wall, but along the pathway of current spread
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Fig. 6. Late anatomic findings-intense endocardial fibrosis (puppy No. 10). Endocardial fibrosis occurred in the region of the posterior lateral right atrium, the site of atrial ablation. Arrowheads identify this area. Atria1 fulguration produced multifocal injury. The crista terminalis, anteriorly positioned and in the direct line of current spread between the distal electrode pole of the catheter (cathode) and the anterior chest pad (anode), wasinjured in addition (arrows). To contrast the difference between the early and late anatomic effects of the ablation procedure, compare with Fig. 5, panel A. CT = crista terminalis. Other abbreviations sameas figure 2.
between the cathode and anode. Fig. 4, A demonstrates this phenomenon. Puppy No. 7 underwent
Late anatomic tion. In order
observations
following
electrical
able-
electrode catheter ablation of the posterior-medial right atrium with 100 J. In this puppy, ablation apparently produced two regions of tissue injury. The primary focus of atrial injury occurred at the point of contact between the distal electrode pole and the atrial septum. In addition, necrosis of the right anterior free wall was produced as current spread between the anode and cathode. Ventricular muscle injury. Electrical ablation of the atrial free wall may inadvertently injure the subjacent base of the right ventricle. Ventricular ectopy occurred during the first 24 hours following electrical ablation in five of eight group I puppies. Ventricular ectopy occurred in those animals with associated ventricular injury. Demonstrated in Fig. 5 is an example of acute necrosis of the inferioranterior right atrial free wall following electrical ablation (puppy No. 6). The black arrows in Figure 5, panel A point to the base of the right ventricle. Hemorrhagic necrosis has extended across the atrio-
to assessthe extent of chronic atrial injury, four puppies were followed for 11 weeks after the ablation procedure. The electrical shock was applied to the posterior-lateral right atrium in two, to the right atrial appendage in one, and to the anterior-lateral right atrial free wall in one puppy. Endocardial fibrosis developed at the site of ablation. In three of the puppies, the atrial fibrosis that occurred at this site was nonhomogeneous. In all four puppies there appeared to be several discrete patches of atrial fibrosis within the right atrium. These appeared to represent areas of tissue injury that occurred at multiple electrode poles. Demonstrated in Fig. 6 (puppy No. 10) is a representative example of the endocardial fibrosis that developed late after the atrial ablation procedure. The distal pole of the electrode catheter had been placed in the posterior lateral right atrium. Intense fibrosis occurred in this region. Because the length of the endocardial fibrotic patch was 1.2 cm, it would appear that electrical current had spread
cardium. The hemorrhagic necrosis is viewed from a different perspective in Fig. 5, panel B. Transmural myocardial hemorrhage is demonstrated between the black arrows, outlining the right ventricular endocardium and epicardium.
injurying the atrial tissue between them. In addition, fibrosis was observed anteriorly, along the crista terminalis, presumably in a region not in contact with the catheter. We speculate that the crista terminalis was injured as current spread
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Fig. 7. Transmural atria1fibrosis 11 weeksafter the ablation procedure. High-power photomicrograph of crista terminalis region. In the center of the fulguration scar, on the right-hand side of the figure, fibrosis was transmural. Toward the periphery of the lesion, center of figure, depth of fibrosis was shallower. Further leftward, normal atria1 myocardium wasapparent. Arrows identify the depth of fibrous tissueand atria1 cellular damage(Trichrome stain).
between the posteriorly located cathode and anterior chest wall anode. Atrial muscle fibrosis was transmural in the center of the ablation lesion. Fig. 7 demonstrates, histologically, the transmural fibrosis that developed late after crista terminalis ablation. Centrally, the observed fibrosis was transmural. The depth of fibrosis became less extensive at the periphery of the lesion, where normal atrial muscle was evident. DISCUSSION
Ectopic atrial tachycardia is a frequent mechanism of supraventricular tachycardia in children.’ Suppression of this arrhythmia with currently available antiarrhythmic agents is generally ineffective.2 Surgical resection and cryoablation are highly efficacious in arrhythmia elimination.3 Previous experimental studies’s8 have suggested that electrode cath-
ed both anterior to and posterior to the electrode pole to which the ablative shock was applied. The area of greatest tissue injury was directly under the ablative electrode pole. Late after the procedure, transmural atrial fibrosis developed at the site of maximum injury. The extent of tissue damage ranged from 50 to 360 mmz. As suggested by investigators of low right atrial septal and coronary sinus ablation,7-g we found that there was significantly greater atrial muscle necrosis in the free wall of the right atrium when higher energy doses were used during the ablation procedure. An energy dose 2150 J produced significantly greater tissue damage than an energy dose of 100 J. The energy dose used for right atrial free wall ablation must be chosen carefully. The electrical shock must be of sufiicient intensity to necrose a
minim@ area of tissue damage. We-studied the safety and anatomic effects of electrical ablation on the free wall of the right atrium to assess whether electrode catheter ablation may have applicability in management of atrial ectopic tachycardia. In this study we found that electrode catheter ablation could be used to necrose “small” areas of atria1 muscle in the free walI of the right atrium of young dogs. Acutely, atria1 ablation produced transmural hemorrhage. The field of tissue injury extend-
jj&~~ive area,of tissue1jet not cause
complications-cardiac perforation or arrhythmia induction. What the dimensions of this area should be is complex. It will depend on the size of the arrhythmia circuit, the accuracy of the mapping procedure, the depth within the atrial wall at which the arrhythmia circuit is located, and the orientation of the ablating electrode pole to the arrhythmia circuit. Transmural atrial necrosis may be necessary for atria1 electrical ablation to be effective if the
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arrhythmia circuit is located intramurally or in the epicardium. Acutely, we observed transmural atrial hemorrhage at the site of electrical ablation. Histologic studies, performed 11 weeks after the ablation procedure, demonstrated very localized regions of transmural fibrosis. Normal-appearing atrial myocardium was observed at the periphery of these lesions. If the arrhythmia circuit is located at the periphery of the ablation lesion, the procedure may be unsuccessful. The smallest area of atrial muscle necessary to necrose in order for electrical ablation to be effective is unknown. Surgical cryoablation of 80 mm2, the area under a 1 cm diameter freeze probe, has been effective in controlling ectopic automatic atria1 tachycardia. Unknown is whether a smaller area of tissue damage would suffice. However, our surgical experience would suggest that the minimally effective area necessary to necrose in order to eliminate the automatic focus is at least 80 mm2.3 Attention has been focused on the type and design of catheters used during electrical ablation. The high energy levels used for electrical ablation may injure the catheter and impair its functional and physical integrity. Fischer et al5 have described disruption of the proximal electrical connectors, separation of the tip electrode, intraelectrode pitting, and failure of the internal wiring. These investigators have suggested in vitro testing of the electrode catheter prior to its clinical use. Bardy et al6 have noted a high incidence of current leak between electrode poles when standard tripolar electrode catheters have been tested in vitro with high energy doses. In this study we did not electrically select the catheters used for electrical ablation and noted clinical evidence of current leaking between multiple electrode poles during the ablation. The large variability in tissue damage we found when using energy doses of 200 J or more is best explained by current leaking between the distal electrode and more proximal electrode poles. Current leaking between electrode poles not overlying atrial tissue involved in the arrhythmia circuit may cause potential complications and adverse effects, e.g., sinus or atrioventricular (AV) nodal damage. Atrial perforation occurred in two of five puppies when ablation was attempted with an energy dose of 200 J or more. With the use of similar energy doses, Broadman and Fischer9 observed coronary sinus perforation in larger subjects when ablating with energy doses of 240 J. In addition, large energy doses (400 J) may induce intractable ventricular fibrillation or affect ventricular function in small subjects.
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Morphologic studies of atrial tissue from patients with chronic atrial fibrillation have demonstrated fibrosis and loss of atria1 muscle cells.‘” Multiple regions of endocardial fibrosis were observed late after right atrial free wall ablation in our studies. Although endocardial atrial ablation may be acutely effective in eliminating an ectopic focus-supraventricular tachycardia or a reentrant atrioventricular tachycardia-our study raises concern about the potential long-term complications of this procedure, i.e., development of atrial flutter or fibrillation. Atrial free wall ablation near the atrioventricular junction may be associated with right ventricular damage. Five of the puppies that had undergone atrial ablation and in which the right ventricle was injured were noted to develop ventricular tachycardia or frequent ventricular ectopy during the first 24 hours after the ablation procedure. No correlation was evident between the energy dose used during the ablation procedure and the subsequent development of ventricular arrhythmias. We conclude that electrode catheter ablation can be used to necrose “small” areas of atria1 muscle in the right atria1 free wall. Because atrial perforation did not occur when an energy dose of 150 J or less was used, we recommend 150 J as a safe upper limit in small subjects. Clinically, atria1 ablation may be successful if lower energy doses are used.‘O The area of tissue necrosis is greater when atrial free wall ablation is performed with higher energy levels (150 J or more), but because of the risk of cardiac perforation, we recommend using multiple shocks at lower energy levels. The authors wish to acknowledge the technical assistance provided by Gregory Clark, Gerry Creager, and Mark Thompson, and also thank Terri Woods for her careful attention to the preparation of this manuscript.
REFERENCES
1. Gillette PC. The mechanisms of supraventricular tachycardia in children. Circulation 1976;54:133. 2. Gillette PC, Garson A. Electrophysiologic and pharmacologic characteristics of automatic ectopic atrial tachycardia. Circulation 1977;56:571. 3. Ott DA, Gillette PC, Garson A, Cooley DA, Reul GJ, McNamara DG. Surgical management of refractory supraventricular tachvcardia in infants and children. J Am Co11 Cardiol 1985;53124. 4. Gillette PC, Wampler DG, Garson A, Zinner A, Ott D, Cooley D. Treatment of atrial automatic tachycardia by ablation procedures. J Am Co11 Cardiol 1985;6:405. 5. Fischer JD, Brodman R, Johnston DR, Waspe LE, Kim SG, Matos JA, Scavin G. Nonsurgical electrical ablation of tachycardias: Importance of prior in vitro testing of catheter leads. PACE 1984;7:74. 6. Bardy GH, Coltori F, Ivey TD, Yerkovich D, Greene HL. Effect of damped sine-wave shocks on catheter dieiectric strength. Am J Cardiol 1985;56:769.
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and Garson
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7. Gonzalez R, Scheinman M, Bharati S, Lev M. Closed chest permanent atrioventricular block in dogs. AM HEART J 1983;105:461. 8. Scheinman MM, Bharati S, Wang Y, Shapiro WA, Lev M. Electrophysiologic and anatomic changes in the atrioventricular junction of dogs after direct current shocks through tissue fixation catheters. Am J Cardiol 1985;55:194.
June 1987 Heart Journal
9. Brodman R, Fischer JD. Evaluation of a catheter technique for ablation of accessory pathways near the coronary sinus using a canine model. Circulation 1983;67:923. 10. Silka MJ, Gillette PC, Garson A, Zinner A. Transvenous catheter ablation of a right atria1 automatic ectopic tachycardia. J Am Co11 Cardiol 1985:5:999.
atria Electrical ablation techniques (ECT) have had llmited 8uccoss in achieving control of arrhythmias originating in the rfgM atrial free wall (RAFW). To ascertain determinants for successful ECT, we studied the clnical and cellular etectrophysiologic effects of electrloal abl8tion of the RAFW. After performing electrIcal ablation of the RAFW in 12 beagle Puppies, the fohowing studies were Performed: Hotter monitoring first 24 hours (eight puppies), and Y 1 weeks takr (four pupplea); clinical electrophysiologk study (four puppie@); and microelectrode otudy (&ii!) (etght puppier). Arrhythmias (AR) and conduction disturbaneer (CD) frequentfy occurred tmmedtately following ECT: ventricular tachycerdia (VT) (seven puppie@, junctlonat tachycardle (ona puppy), and asystole or compkte AV block (AVB) (four pupptee). HOlWr monftorlng durtng the flrdt 24 hours after ECT revested VT (four puppies), frequent ventricular premclture Uepderltaiona (one puppy), and type 2 second-degree AVB (four puppies). AR were r8rely 6een I8te 8fter ECT. Durlng clinical EP study 11 weeke after abtation, atrktl f4brHlatlon waa induced In ffiree of tour pupPIer; none had AR prror to ECT. Early ME study revealed a nonhomogeneous atriat infarct-a central zone of “dead” cells surrounded by peripheref idands of depre@eed cellular aotlvity. Cell8 with normal action potential characterlatics were noted in between. We conclude that (1) Electrical ablatton of the RAFW is aaeociated wtth a hleh incidence of early AR and CD. (2) Because of the nonhomogeneous nature of tissue InJury produced during ECT, careful strlal mapping Ls critically Important. (3) l,ocal regions of conductton delay and block may Provide a rub&rate for the late development of atrial arrhythmias. (AM HEAKT J 1987;113:14Cl4.)
Jeffrey P. Moak, Houston, Tex.
M.D., Richard
A. Friedman,
M.D., and Arthur
Electrical ablation techniques have been used to treat medically refractory arrhythmias. Catheter ablation is an accepted experimental technique for interrupting atrioventricular conduction.1-3 Complete atrioventricular (AV) block and control of
From the Lillie Frank Abercrombie Section of Cardiology, Department of Pediatrics, Baylor College of Medicine and Texas Children’s Hospital. Supported in part by Grant RRO5425-23 from the National Institutes of Health Biomedical Research Support Grant, and by Grant No. HL07190 from the National Institutes of Health, United States Public Health Service; and by a Grant from the J. S. Abercrombie Foundation. Received for publication Feb. 10, 1986; accepted Nov. 3, 1986. Reprint requests: Jeffrey P. Moak, M.D., Pediatric Cardiology, Texas Children’s Hospital, 6621 Fannin, Houston, TX 77030.
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supraventricular arrhythmias can be achieved in 78 % of patients undergoing AV junctional ablation.4 Limited arrhythmia control has been achieved with right atrial free wall or coronary sinus electrical ablation for atrial ectopic tachycardias or accessory atrioventricular connectiona.5~ 6 Few previous investigations have addrmed the possible determinanta of failure of electrical ablation to damage critically imp&ant regions of the arrhythmia circuit. These studies have addressed problems in the delivery of electrical energy to the tissue, i.e., failure of electrode catheter components or electrical current leaking between electrode poles proximal to the cathode.‘v8 The purpose of this report is to describe the early and late clinical and