Radiofrequency Catheter Ablation of an Automatic Atrial Tachycardia in an Adult JOHN G. KALL and DAVID J. WILBER From the Section of Cardiology. Loyola University Medical Center, Maywood, Illinois KALL, J.G., ET AL.: Radiofrequency Catheter Ablation of an Automatic Atrial Tachycardia in an Adult.
Automatic atrial tachycardia (AAT) is often refractory to medico] management. While surgical ablation and isolation procedures such as atrioventricular node ablation have been useful in the management 0/ AAT, important limitations remain. Reported experience with catheter ablation of AAT is limited. This report describes the successful appJication of transvenous radiofrequency catheter abJation in an adult ivith AAT. Potential limitations of catheter ablation in the management of AAT are discussed. (PACE, Vol. 15, March 1992)
ectopic atrial tachycardia, electrocoagulation
Introduction Experience with radiofrequency catheter ablation of automatic atrial tachycardias (AATs) is limited. This report describes a case in which transvenous catheter ablation using radiofrequency (RF) energy was successful in ablating an AAT arising from the right atrial appendage. This case is significant in that focal application of RF ablated an AAT in an adult without complication or recurrent atrial arrhythmia. The potential limitations of catheter ablation in the management of AAT are discussed.
Case A 28-year-old woman presented with incessant supraventricular tachycardia during the second trimester of her second pregnancy. Symptoms included palpitations and occasional lightheadedness. There was no history of alcohol ingestion. Physical examination was normal. Transthoracic echocardiography demonstrated normal left ventricular systolic function with a left ventricular
Address for reprints: David |. Wilber, M.D., Section of Cardiology. Loyola University Medical Center. 2160 S. First Ave.. Maywood. IL 60153. Fax: (708) 216-6829. Received May 1. 1991; revision August 1, 1991: revision October 29, 1991; accepted November 26. 1991.
PACE, Vol. 15
diastolic dimension of 46 mm [normal range 42-53 mm) and left ventricular fractional shortening of 0.29 (normal range 0.28-0.42). Thyroid function was normal. Ambulatory electrocardiographic monitoring in the absence of antiarrhythmic therapy demonstrated nearly incessant atrial tachycardia at a rate of 160 beats/min. Therapy with digoxin and propranolol was ineffective in terminating or reducing the rate of the tachycardia. Quinidine and procainamide were also ineffective. Administration of intravenous verapamil resulted in a brief period of 2:1 atrioventricular (AV) block without termination of the tachycardia. Flecainide (300 mg daily) was initially effective in suppressing the tachycardia for > 95% of a 24hour monitoring period, As the pregnancy progressed, symptomatic tachycardia recurred and was suppressed by an increased dose of flecainide and the addition of digoxin. Near term, effective suppression of the tachycardia required combination therapy with flecainide (up to 400 mg daily, flecainide level 0,4 mg/L), digoxin (0.375 mg daily, digoxin level 1,6 ng/mL), and verapamil (320 mg daily). Two weeks after an uncomplicated Caesarean delivery of a healthy infant, antiarrhythmic therapy was discontinued in the hospital and incessant atrial tachycardia returned. Since the patient initially refused nonpharmacological intervention, the regimen of flecainide, digoxin, and verapamil was continued. An-
March 1992
281
KALL, ET AL.
tiarrhythmic therapy was intermittently withdrawn over the ensuing 4 years with prompt recurrence of symptomatic tachycardia. In the months prior to ablation, symptomatic tachycardia became more frequent despite combination antiarrhythmic therapy. Due to incomplete efficacy and a diminishing tolerance of antiarrhythmic therapy, the patient elected to pursue an attempt at catheter ablation of the atrial automatic focus. Catheter Ablation
The patient was admitted to the hospital and antiarrhythmic therapy was discontinued for 48 hours prior to electrophysiology study and catheter ablation. Incessant atrial tachycardia ensued at a rate of 190 beats/min (Fig. 1). After informed consent, 6 French quadripolar catheters were positioned at the AV junction and in the right ventricular apex. A 6 French hexapolar catheter with a Conrnand curve and 2-mm interelectrode spacing (Bard Electrophysiology, CR. Bard, Inc., Tewksbury, MA, USA) was positioned in the right atrium and used for initial endocardial mapping. Intracardiac electrograms from the right atrium, AV junc-
tion, right ventricular apex, and surface electrocardiographic leads I, II. Ill, aVF, Vi, and VQ were continuously monitored and recorded. Electrical stimulation was performed with a programmable stimulator (Bloom Associates, Ltd., Narberth, PA, USA). Intravenous midazolam 4 mg and morphine sulphate 2 mg were administered for anxiety and mild chest discomfort encountered during application of RF and intravenous heparin 2,000 units was administered for thrombosis prophylaxis. Atrial stimulation including burst pacing (to cycle lengths of 200 msec) and atrial extrastimuli failed to terminate or reset the tachycardia. Adenosine administration did not influence the atrial rate. However, AV block was produced and revealed an inferior P wave axis during tachycardia (Fig. 2]. Initial right atrial endocardial mapping demonstrated earliest atrial endocardial activation to be in the right atrial appendage. The 6 French catheter positioned at the AV junction was exchanged for a steerable quadripolar catheter with a 4-mm tip electrode (Polaris, Mansfield/Webster, Boston Scientific Corp., Watertown, MA, USA) that was subsequently used for mapping and ablating. This catheter was positioned in the right atrial
Figure 1. Baseline 12-lead electrocardiogram demonstrating supraventricuiar tachycardia at a rate of 190 beats/min.
282
March 1992
PACE, VoL 15
RADIOFREQUENCY CATHETER ABLATION
H.M. 1 - 2 1 - 9 1
after adenosine
Figure 2. Electrocardiogram obtained after adenosine administration demonstrating afriai tachycardia at a rate of 190 beats/min, transient AV block, and an in/erior P wave axis suggesting a high right atrial tachycardia focus. The atrial rate was not influenced by adeno-
sine.
appendage and localized earliest atrial activation to the tip of the right atrial appendage. Ablation was performed using a RF lesion generator (Radionics, Inc., Burlington, MA, USA) delivering RF at 300 kHz (40 Watts [W] maximum output). RF pulses were delivered through the ablating catheter with the distal electrode as cathode and a surface patch electrode as anode. RF lesion generator output (volts) and delivered current (mAj were continuously monitored during RF application to detect any rise in impedance consistent with clot formation at the tip of the ablating catheter. All RF applications were of 15 seconds maximum duration. Following positioning of the ablating catheter near the site of earliest activation, three initial applications of RF (28 W) during atrial tachycardia were without effect. After catheter repositioning of approximately 1-mm displacement (Fig. 3), a fourth application of RF (22 W) resulted in termination of the atrial tachycardia (Fig. 4). Three additional applications of RF during sinus
PACE, Vol. 15
rhythm were then performed (22-28 W] at closely adjacent sites (within 1-2 mm). Following intravenous isoproterenol infusion (2 mcg/min), atrial tachycardia returned without alteration in baseline cycle length or atrial activation sequence. After five additional unsuccessful applications of RF (22-28 W] at the initial catheter position, the ablating catheter was withdrawn 3-mm caudal and two subsequent RF applications (28 W) resulted in transient and then permanent termination of the atrial tachycardia. Continued infusion of isoproterenol (up to 3 mcg/min) failed to reinitiate the tachycardia. Two additional RF applications were administered during sinus rhythm at the final location. A total of 16 applications of RF was administered (22-28 W maximum) over a 58-minute period. All lesions were performed with minimal catheter manipulation (within approximately 1 cm^). There were no complications. After the procedure, heparin 5,000 units was administered subcutaneously every 6 hours for 24 hours.
March 1992
283
KALL, ET AL.
Figure 3. Right anterior obJique projection demonstrating CQtheferpo.sifions. Both Ihe hexapolar and steerable quadripolar catheters are in the right atrial appendage (RAA). The steerabJe quadripolar catheter was used for radio/requency ablation and is positioned in fhe apex of the RAA.
FoUow-Up
After the ablation procedure, telemetry for 48 hours demonstrated only sinus rhythm. Transesophageal echocardiography performed the day following the procedure demonstrated opacification at the tip of the right atrial appendage consistent with thrombus. The patient was discharged on aspirin 325 mg daily. Twenty-four hour ambulatory electrocardiography performed 3 weeks after the ablation procedure demonstrated only sinus rhythm. The patient remains asymptomatic and is in good health 12 months after the ablation.
Discussion The clinical and electrophysiological characteristics of AAT have been previously described in children and in adults.^"'' Despite reports of spontaneous resolution,*"^ AAT is most often chronic, incessant, and associated with significant symptoms. Though pharmacological suppression
284
of presumed AAT is sometimes possible, these atrial tachycardias are frequently refractory to medical therapy.^'^"^ Although the patient's arrhythmia was initially controlled during pregnancy with antiarrhythmic medication, her course was eventually complicated by intolerance of antiarrhythmic medication and inadequate suppression despite combination drug therapy. Nonpharmacological approaches to the management of patients with medically refractory automatic atriai tachycardias include isolation techniques such as AV nodal ablation, and surgical extirpation or cryoablation procedures directed at the tachycardia focus. Direct surgical ablation of automatic atrial tacbycardia has been reported to be uhimately successful in 82%-100%.^-^" While surgery is generally safe in the absence of congestive heart failure, important limitations exist. Despite often extensive resection of atrial tissue, up to 50% of surgical ablations for AAT have been complicated by the intraoperative or late (up to 1 year) appearance of previously undocumented
March 1992
PACE, VoL 15
RADIOFREQUENCY CATHETER ABLATION
SURFACE LEAD 11
fH+fftm co(itinuou5 s t r i p
-
Figure 4. Electrocardiographic recording of surface lead II and infracardiac electrograms from the distal electrode pair of the ablating catheter and the low right afrium (RA) during radiofrequency energy application to the atrial tachycardia focus (1 sec/division). Sinus rhythm appears after 2 seconds of radiofrequency energy appJication.
atrial tachycardia foci, often remote from the site of primary ablation.^"^° Surgical experience demonstrating the potential multifocal origin of AAT suggests that focal ablative techniques may have limited application. Occasional success has been reported with catheter ablation using direct current (DC) shocks ranging from 50-400 joules (J)/'^" While no complications have been reported in man, refractory ventricular fibrillation, low cardiac output, atrial perforation, cardiac tamponade, and transient arrhythmias and conduction disturbances have been described in canines receiving 200-400 J DC shocks to the atrium.^^^ Failure of ablation has been most commonly attributed to multiple tachycardia origins, technical difficulties inherent to
PACE. Vol. 15
catheter ablation (inadequate control of lesion size with DC shock, insufficient catheter contact and stability), and imprecision of catheter mapping of the atrium. Frequent primary failure of DC catheter shock and tachycardia recurrences have led some centers to recommend a direct surgical approach for medically refractory AAT^^ or indirect isolation procedures such as AV nodal ablation.^^ Due to the appearance of new atrial tachycardias after a relatively wide surgical excision (up to 10 ± 6 cm^)^ for AAT, it has been suggested that a diffuse pathological process, acquired or congenital, may involve the atrium in some patients witb AAT.^^ It is also possible that surgical manipulation or DC shocks produce new arrhythmogenic foci in the
March 1992
285
KALL, ET AL.
atrium. Diffuse atrial pathology may account for some tachycardia recurrences. Histologic findings in atrial tissue removed during ablative therapy for AAT have been variable, including normal histology, focal and diffuse fibrosis, and focal and diffuse cellular infiltration (usually leukocytic)."'^^*^^ In vitro electrophysiological studies of explanted atrial tissue of patients with AAT are limited. ^**-^^ Nonetheless, the occassional success of DC shock ablation suggests that some AAT may he amenable to RF catheter ablation. RF lesions are generally smaller and more discrete than lesions obtained through the use of DC shocks, and are not associated with the potentially adverse remote effects of barotrauma."'^"'^^ By permitting increased control of delivered energy and lesion size, application of RF energy may accomplish ablation with minimal risk and patient discomfort. In this patient, multiple applications of RF and minor catheter repositioning were ultimately required to ablate the tachycardia. Although 16 applications of RF were performed, applications were limited to < 30 W for 15 sec/application in a closely circumscribed area, Use of higher energy for a more prolonged period may have permitted effective ablation with a smaller number of RF applications. Energy application was initially limited to avoid extensive injury to the thin walled atrial appendage, The requirement for catheter repositioning may reflect imprecision of tachycardia localization or the presence of a sufficiently large
amount of arrhythmogenic tissue that exceeded the volume of one RF lesion. While reinitiation of a tachycardia following isoproterenol infusion in this patient may have represented failure to ablate the primary focus, it is possible that a new focus appeared in response to catecholamine stimulation of catheter mediated atrial injury.^^ The presence of intraatrial thrombus has been documented in animal models of atrial RF catheter ablation.^' With the suggestion of thrombus in the atrial appendage in our patient, anticoagnlation after an uncomplicated catheter ablation may be prudent, especially if a procedure in the left atrium is contemplated. This successful application of RF catheter ablation suggests that in some patients, AATs may arise from sufficiently discrete foci to permit endocardial RF catheter ablation. The right atrial appendage was the site of successful catheter ablation in this case and in another report of two patients receiving DC shock ablation.^ Specific atrial locations may be more amenable to transvenous catheter approaches to ablation, either by permitting better catheter contact with atrial endocardium, or by allowing more precise atrial mapping. Preliminary data suggest that left atrial foci may also be amenable to RF ablation.^** Transvenous RF catheter ablation should be considered as a viable option in the management of medically refractory AAT. Factors influencing patient selection and procedural success warrant further investigation.
References 1. Goldreyer BN, Gallagher JJ, Damato AN. The electrophysiologic demonstration of atrial ectopic tachycardia in man. Am Heart J 1973; 85(2):205-215. 2. Scheinman MM, Basu D, Hollenberg M. Electrophysiologic studies in patients with persistent atrial tachycardia. Circulation 1974; 50:266-273. 3. Gillette PC, Garson A Jr. Electrophysiologic and pharmacologic characteristics of automatic ectopic atrial tachycardia, Circulation 1977; 56(4):571-575. 4. Mehta AV, Sanchez GR, Sacks EJ, et al. Ectopic automatic atrial tachycardia in children: Clinical characteristics, management and follow-up. J Am Coll Cardiol 1988; 11:379-385. 5. Mehta AV, Ewing L, Sacks EJ, et al. Automatic ectopic atriai tachycardia in children: Is ablation needed? J Am Coll Cardiol 1986; 7(2):S-119A. 6. Benson DW Jr, Dunnigan A, Overhoit ED, et aL Electrophysiologic features and treatment of pri-
286
12.
mary atrial tachycardia in ostensibly healthy children. Circulation 1985; 72(SuppL ni):III-339. Gillette PC, Wampler DG, Garson A Jr. et al. Treatment of atrial automatic tachycardia by ablation procedures. J Am Coll Cardiol 1985; 6:405-409, McGuire MA, Johnson DC, Nunn GR, et al. Surgical therapy for atrial tachycardia in adults. J Am Coll Cardiol 1989; 14:1777-1782. Hendry PJ, Packer DL, Anstadt MP, et al. Surgical treatment of automatic atrial tachycardias. Ann Thorac Surg 1990; 49:253-260. Garson A Jr, Smith RT, Moak JP, et al. Supraventricular tachycardia due to multiple atrial ectopic foci: A relatively common problem, (abstract) J Am Coll Cardiol 1986; 7(2);119A. Silka MJ, Gillette PC, Carson A Jr, et aL Transvenous catheter ablation of a right atrial automatic ectopic tachycardia. J Am Coll Cardiol 1985; 5:999-1004. Moak JP, Friedman RA, Garson A Jr. Electrical ab-
March 1992
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7. 8. 9. 10.
11.
RADIOFREQUENCY CATHETER ABLATION
13.
14.
15.
16. 17.
18.
lation of atrial muscle. L Early and late anatomic observations in canine atria. Am Heart J 1987; 113:1397-1404. Moak JP, Friedman RA, Garson A Jr. Electrical ablation of atrial muscle. II. Early and late electrophysiologic observations in canine atria. Am Heart J 1987; 113:1404-1413. Garson A Jr, Smith RT, Moak JP, et al. Atrial automatic ectopic tachycardia in children. In AL Waldo, P Toubol (eds.): Atrial Arrhythmias: Current Concepts and Management. St. Louis, MO, Mosby-Year Book, 1990, pp. 282-287. Scheinman MM. Catheter ablation for atrial tachycardia. In AL Waldo, P Toubol (eds.): Atriai Arrhythmias: Current Concepts and Management. St. Louis, MO, Mosby-Year Book, 1990, pp. 458-461. Garson A Jr. Atrial tachycardia: A rare disease sheds light on common questions. J Am Coll Cardiol 1989; 14{7):1783-1784. Davis J, Scheinman MM, Ruder MA, et al. Ablation of cardiac tissues by an electrode catheter technique for the treatment of ectopic supraventricular tachycardia in adults. Circulation 1986; 74(5):1044-l'053. Wyndbam CRC, Arnsdorf MF, Levitsky S, et al.
PACE. Vol. 15
Successful surgical excision of focal paroxysmal atrial tachycardia. Observations in vivo and in vitro. Circulation 1980: 62(6):1365-1373. 19. Josepbsen ME, Spear JE, Harken AH, et al. Surgical excision of automatic atrial tachycardia: Anatomic and electropbysiologic correlates. Am Heart J 1982; 104:1076-1085. 20. Hauer RNW, Freericks MP, Wittkampf FHM. Lesion size after DC shock ablation: Variability at identical delivered energy, (abstract) PACE 1988; ll(Suppl.):908. 21. Wittkampf EHM, Hauer RNW, Robles de Medina EO. Control of radiofrequency lesion size by power regulation. Circulation 1989; 80:962-968. 22. Moore EN, Spear JF, Kadisb A, et al. Cellular electrophysiologic effects of ablation on cardiac tissue, (abstract) PACE 1988; ll(Suppl.):9a7. 23. Chauvin M, Dumont P, Di Francesco G. Trans-catheter radio frequency ablation of atrial myocardium: An anatomic examination in dogs, (abstract) PACE 1988; 11:523. 24, Walsh PW, Saul JP, Hulse JE, et al. Successful transcatheter ablation of ectopic atrial tacbycardia using radiofrequency energy, (abstract) PACE 1991; 14:656.
March 1992
287
Automatic atrial tachycardia (AAT) is often refractory to medico] management. While surgical ablation and isolation procedures such as atrioventricular node ablation have been useful in the management 0/ AAT, important limitations remain. Reported experience with catheter ablation of AAT is limited. This report describes the successful appJication of transvenous radiofrequency catheter abJation in an adult ivith AAT. Potential limitations of catheter ablation in the management of AAT are discussed. (PACE, Vol. 15, March 1992)
ectopic atrial tachycardia, electrocoagulation
Introduction Experience with radiofrequency catheter ablation of automatic atrial tachycardias (AATs) is limited. This report describes a case in which transvenous catheter ablation using radiofrequency (RF) energy was successful in ablating an AAT arising from the right atrial appendage. This case is significant in that focal application of RF ablated an AAT in an adult without complication or recurrent atrial arrhythmia. The potential limitations of catheter ablation in the management of AAT are discussed.
Case A 28-year-old woman presented with incessant supraventricular tachycardia during the second trimester of her second pregnancy. Symptoms included palpitations and occasional lightheadedness. There was no history of alcohol ingestion. Physical examination was normal. Transthoracic echocardiography demonstrated normal left ventricular systolic function with a left ventricular
Address for reprints: David |. Wilber, M.D., Section of Cardiology. Loyola University Medical Center. 2160 S. First Ave.. Maywood. IL 60153. Fax: (708) 216-6829. Received May 1. 1991; revision August 1, 1991: revision October 29, 1991; accepted November 26. 1991.
PACE, Vol. 15
diastolic dimension of 46 mm [normal range 42-53 mm) and left ventricular fractional shortening of 0.29 (normal range 0.28-0.42). Thyroid function was normal. Ambulatory electrocardiographic monitoring in the absence of antiarrhythmic therapy demonstrated nearly incessant atrial tachycardia at a rate of 160 beats/min. Therapy with digoxin and propranolol was ineffective in terminating or reducing the rate of the tachycardia. Quinidine and procainamide were also ineffective. Administration of intravenous verapamil resulted in a brief period of 2:1 atrioventricular (AV) block without termination of the tachycardia. Flecainide (300 mg daily) was initially effective in suppressing the tachycardia for > 95% of a 24hour monitoring period, As the pregnancy progressed, symptomatic tachycardia recurred and was suppressed by an increased dose of flecainide and the addition of digoxin. Near term, effective suppression of the tachycardia required combination therapy with flecainide (up to 400 mg daily, flecainide level 0,4 mg/L), digoxin (0.375 mg daily, digoxin level 1,6 ng/mL), and verapamil (320 mg daily). Two weeks after an uncomplicated Caesarean delivery of a healthy infant, antiarrhythmic therapy was discontinued in the hospital and incessant atrial tachycardia returned. Since the patient initially refused nonpharmacological intervention, the regimen of flecainide, digoxin, and verapamil was continued. An-
March 1992
281
KALL, ET AL.
tiarrhythmic therapy was intermittently withdrawn over the ensuing 4 years with prompt recurrence of symptomatic tachycardia. In the months prior to ablation, symptomatic tachycardia became more frequent despite combination antiarrhythmic therapy. Due to incomplete efficacy and a diminishing tolerance of antiarrhythmic therapy, the patient elected to pursue an attempt at catheter ablation of the atrial automatic focus. Catheter Ablation
The patient was admitted to the hospital and antiarrhythmic therapy was discontinued for 48 hours prior to electrophysiology study and catheter ablation. Incessant atrial tachycardia ensued at a rate of 190 beats/min (Fig. 1). After informed consent, 6 French quadripolar catheters were positioned at the AV junction and in the right ventricular apex. A 6 French hexapolar catheter with a Conrnand curve and 2-mm interelectrode spacing (Bard Electrophysiology, CR. Bard, Inc., Tewksbury, MA, USA) was positioned in the right atrium and used for initial endocardial mapping. Intracardiac electrograms from the right atrium, AV junc-
tion, right ventricular apex, and surface electrocardiographic leads I, II. Ill, aVF, Vi, and VQ were continuously monitored and recorded. Electrical stimulation was performed with a programmable stimulator (Bloom Associates, Ltd., Narberth, PA, USA). Intravenous midazolam 4 mg and morphine sulphate 2 mg were administered for anxiety and mild chest discomfort encountered during application of RF and intravenous heparin 2,000 units was administered for thrombosis prophylaxis. Atrial stimulation including burst pacing (to cycle lengths of 200 msec) and atrial extrastimuli failed to terminate or reset the tachycardia. Adenosine administration did not influence the atrial rate. However, AV block was produced and revealed an inferior P wave axis during tachycardia (Fig. 2]. Initial right atrial endocardial mapping demonstrated earliest atrial endocardial activation to be in the right atrial appendage. The 6 French catheter positioned at the AV junction was exchanged for a steerable quadripolar catheter with a 4-mm tip electrode (Polaris, Mansfield/Webster, Boston Scientific Corp., Watertown, MA, USA) that was subsequently used for mapping and ablating. This catheter was positioned in the right atrial
Figure 1. Baseline 12-lead electrocardiogram demonstrating supraventricuiar tachycardia at a rate of 190 beats/min.
282
March 1992
PACE, VoL 15
RADIOFREQUENCY CATHETER ABLATION
H.M. 1 - 2 1 - 9 1
after adenosine
Figure 2. Electrocardiogram obtained after adenosine administration demonstrating afriai tachycardia at a rate of 190 beats/min, transient AV block, and an in/erior P wave axis suggesting a high right atrial tachycardia focus. The atrial rate was not influenced by adeno-
sine.
appendage and localized earliest atrial activation to the tip of the right atrial appendage. Ablation was performed using a RF lesion generator (Radionics, Inc., Burlington, MA, USA) delivering RF at 300 kHz (40 Watts [W] maximum output). RF pulses were delivered through the ablating catheter with the distal electrode as cathode and a surface patch electrode as anode. RF lesion generator output (volts) and delivered current (mAj were continuously monitored during RF application to detect any rise in impedance consistent with clot formation at the tip of the ablating catheter. All RF applications were of 15 seconds maximum duration. Following positioning of the ablating catheter near the site of earliest activation, three initial applications of RF (28 W) during atrial tachycardia were without effect. After catheter repositioning of approximately 1-mm displacement (Fig. 3), a fourth application of RF (22 W) resulted in termination of the atrial tachycardia (Fig. 4). Three additional applications of RF during sinus
PACE, Vol. 15
rhythm were then performed (22-28 W] at closely adjacent sites (within 1-2 mm). Following intravenous isoproterenol infusion (2 mcg/min), atrial tachycardia returned without alteration in baseline cycle length or atrial activation sequence. After five additional unsuccessful applications of RF (22-28 W] at the initial catheter position, the ablating catheter was withdrawn 3-mm caudal and two subsequent RF applications (28 W) resulted in transient and then permanent termination of the atrial tachycardia. Continued infusion of isoproterenol (up to 3 mcg/min) failed to reinitiate the tachycardia. Two additional RF applications were administered during sinus rhythm at the final location. A total of 16 applications of RF was administered (22-28 W maximum) over a 58-minute period. All lesions were performed with minimal catheter manipulation (within approximately 1 cm^). There were no complications. After the procedure, heparin 5,000 units was administered subcutaneously every 6 hours for 24 hours.
March 1992
283
KALL, ET AL.
Figure 3. Right anterior obJique projection demonstrating CQtheferpo.sifions. Both Ihe hexapolar and steerable quadripolar catheters are in the right atrial appendage (RAA). The steerabJe quadripolar catheter was used for radio/requency ablation and is positioned in fhe apex of the RAA.
FoUow-Up
After the ablation procedure, telemetry for 48 hours demonstrated only sinus rhythm. Transesophageal echocardiography performed the day following the procedure demonstrated opacification at the tip of the right atrial appendage consistent with thrombus. The patient was discharged on aspirin 325 mg daily. Twenty-four hour ambulatory electrocardiography performed 3 weeks after the ablation procedure demonstrated only sinus rhythm. The patient remains asymptomatic and is in good health 12 months after the ablation.
Discussion The clinical and electrophysiological characteristics of AAT have been previously described in children and in adults.^"'' Despite reports of spontaneous resolution,*"^ AAT is most often chronic, incessant, and associated with significant symptoms. Though pharmacological suppression
284
of presumed AAT is sometimes possible, these atrial tachycardias are frequently refractory to medical therapy.^'^"^ Although the patient's arrhythmia was initially controlled during pregnancy with antiarrhythmic medication, her course was eventually complicated by intolerance of antiarrhythmic medication and inadequate suppression despite combination drug therapy. Nonpharmacological approaches to the management of patients with medically refractory automatic atriai tachycardias include isolation techniques such as AV nodal ablation, and surgical extirpation or cryoablation procedures directed at the tachycardia focus. Direct surgical ablation of automatic atrial tacbycardia has been reported to be uhimately successful in 82%-100%.^-^" While surgery is generally safe in the absence of congestive heart failure, important limitations exist. Despite often extensive resection of atrial tissue, up to 50% of surgical ablations for AAT have been complicated by the intraoperative or late (up to 1 year) appearance of previously undocumented
March 1992
PACE, VoL 15
RADIOFREQUENCY CATHETER ABLATION
SURFACE LEAD 11
fH+fftm co(itinuou5 s t r i p
-
Figure 4. Electrocardiographic recording of surface lead II and infracardiac electrograms from the distal electrode pair of the ablating catheter and the low right afrium (RA) during radiofrequency energy application to the atrial tachycardia focus (1 sec/division). Sinus rhythm appears after 2 seconds of radiofrequency energy appJication.
atrial tachycardia foci, often remote from the site of primary ablation.^"^° Surgical experience demonstrating the potential multifocal origin of AAT suggests that focal ablative techniques may have limited application. Occasional success has been reported with catheter ablation using direct current (DC) shocks ranging from 50-400 joules (J)/'^" While no complications have been reported in man, refractory ventricular fibrillation, low cardiac output, atrial perforation, cardiac tamponade, and transient arrhythmias and conduction disturbances have been described in canines receiving 200-400 J DC shocks to the atrium.^^^ Failure of ablation has been most commonly attributed to multiple tachycardia origins, technical difficulties inherent to
PACE. Vol. 15
catheter ablation (inadequate control of lesion size with DC shock, insufficient catheter contact and stability), and imprecision of catheter mapping of the atrium. Frequent primary failure of DC catheter shock and tachycardia recurrences have led some centers to recommend a direct surgical approach for medically refractory AAT^^ or indirect isolation procedures such as AV nodal ablation.^^ Due to the appearance of new atrial tachycardias after a relatively wide surgical excision (up to 10 ± 6 cm^)^ for AAT, it has been suggested that a diffuse pathological process, acquired or congenital, may involve the atrium in some patients witb AAT.^^ It is also possible that surgical manipulation or DC shocks produce new arrhythmogenic foci in the
March 1992
285
KALL, ET AL.
atrium. Diffuse atrial pathology may account for some tachycardia recurrences. Histologic findings in atrial tissue removed during ablative therapy for AAT have been variable, including normal histology, focal and diffuse fibrosis, and focal and diffuse cellular infiltration (usually leukocytic)."'^^*^^ In vitro electrophysiological studies of explanted atrial tissue of patients with AAT are limited. ^**-^^ Nonetheless, the occassional success of DC shock ablation suggests that some AAT may he amenable to RF catheter ablation. RF lesions are generally smaller and more discrete than lesions obtained through the use of DC shocks, and are not associated with the potentially adverse remote effects of barotrauma."'^"'^^ By permitting increased control of delivered energy and lesion size, application of RF energy may accomplish ablation with minimal risk and patient discomfort. In this patient, multiple applications of RF and minor catheter repositioning were ultimately required to ablate the tachycardia. Although 16 applications of RF were performed, applications were limited to < 30 W for 15 sec/application in a closely circumscribed area, Use of higher energy for a more prolonged period may have permitted effective ablation with a smaller number of RF applications. Energy application was initially limited to avoid extensive injury to the thin walled atrial appendage, The requirement for catheter repositioning may reflect imprecision of tachycardia localization or the presence of a sufficiently large
amount of arrhythmogenic tissue that exceeded the volume of one RF lesion. While reinitiation of a tachycardia following isoproterenol infusion in this patient may have represented failure to ablate the primary focus, it is possible that a new focus appeared in response to catecholamine stimulation of catheter mediated atrial injury.^^ The presence of intraatrial thrombus has been documented in animal models of atrial RF catheter ablation.^' With the suggestion of thrombus in the atrial appendage in our patient, anticoagnlation after an uncomplicated catheter ablation may be prudent, especially if a procedure in the left atrium is contemplated. This successful application of RF catheter ablation suggests that in some patients, AATs may arise from sufficiently discrete foci to permit endocardial RF catheter ablation. The right atrial appendage was the site of successful catheter ablation in this case and in another report of two patients receiving DC shock ablation.^ Specific atrial locations may be more amenable to transvenous catheter approaches to ablation, either by permitting better catheter contact with atrial endocardium, or by allowing more precise atrial mapping. Preliminary data suggest that left atrial foci may also be amenable to RF ablation.^** Transvenous RF catheter ablation should be considered as a viable option in the management of medically refractory AAT. Factors influencing patient selection and procedural success warrant further investigation.
References 1. Goldreyer BN, Gallagher JJ, Damato AN. The electrophysiologic demonstration of atrial ectopic tachycardia in man. Am Heart J 1973; 85(2):205-215. 2. Scheinman MM, Basu D, Hollenberg M. Electrophysiologic studies in patients with persistent atrial tachycardia. Circulation 1974; 50:266-273. 3. Gillette PC, Garson A Jr. Electrophysiologic and pharmacologic characteristics of automatic ectopic atrial tachycardia, Circulation 1977; 56(4):571-575. 4. Mehta AV, Sanchez GR, Sacks EJ, et al. Ectopic automatic atrial tachycardia in children: Clinical characteristics, management and follow-up. J Am Coll Cardiol 1988; 11:379-385. 5. Mehta AV, Ewing L, Sacks EJ, et al. Automatic ectopic atriai tachycardia in children: Is ablation needed? J Am Coll Cardiol 1986; 7(2):S-119A. 6. Benson DW Jr, Dunnigan A, Overhoit ED, et aL Electrophysiologic features and treatment of pri-
286
12.
mary atrial tachycardia in ostensibly healthy children. Circulation 1985; 72(SuppL ni):III-339. Gillette PC, Wampler DG, Garson A Jr. et al. Treatment of atrial automatic tachycardia by ablation procedures. J Am Coll Cardiol 1985; 6:405-409, McGuire MA, Johnson DC, Nunn GR, et al. Surgical therapy for atrial tachycardia in adults. J Am Coll Cardiol 1989; 14:1777-1782. Hendry PJ, Packer DL, Anstadt MP, et al. Surgical treatment of automatic atrial tachycardias. Ann Thorac Surg 1990; 49:253-260. Garson A Jr, Smith RT, Moak JP, et al. Supraventricular tachycardia due to multiple atrial ectopic foci: A relatively common problem, (abstract) J Am Coll Cardiol 1986; 7(2);119A. Silka MJ, Gillette PC, Carson A Jr, et aL Transvenous catheter ablation of a right atrial automatic ectopic tachycardia. J Am Coll Cardiol 1985; 5:999-1004. Moak JP, Friedman RA, Garson A Jr. Electrical ab-
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