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Catheter radiofrequency ablation of slow pathway in patients with atrioventricular nodal re-entrant tachycardia
International Journal of Cardiology, 39 (1993) 203-208 @ 1993 Elsevier Scientific Publishers Ireland Ltd. All rights reserved. 016%5273/93/$06.00
203
CARD10 01694
Catheter radiofrequency ablation of slow pathway in patients with atrioventricular nodal re-entrant tachycardia Da-yi Hu and Le-Xin Wang Eiectrophysiologic Section, Division of Cardiology, First Teaching Hospital of Beijing Medical University, Beijing 100034, P.R. China
(Received 19 October 1992; revision accepted 7 Janurary 1993)
Selective ablation of slow pathway by radiofrequency current in 12 patients with atrioventricular (AV) nodal dual pathway and tachycardia was performed in our section. A large-tip ablation catheter was positioned around the ostium of the coronary sinus. The slow pathways of all the 12 patients were abolished permanently. Both the antegrade and retrograde conduction of fast pathway was not affected. There was no recurrence after 178 days follow-up. Key words: Atrionodal tachycardia; Radiofrequency
Introduction Catheter radiofrequency current ablation was first introduced clinically to block AV conduction of patients with supraventricular tachycardia 7 years ago [ 1,2]. Now some studies have shown that it can be used also to cure AV nodal re-entrant tachycardia by modification [3,4]. Retrograde conduction of fast pathway can be ablated selectively by this procedure. However, first or higher degree AV-conduction block may occur. The purpose of the study is to evaluate the effects and safety of selective slow pathway ablation.
Correspondence to: Le-Xin Wang M.D., Division of Cardiology, First Teaching Hospital of Beijing Medical University, Beijing 100034, P.R. China.
ablation
Patients and Methods
Study patients From October, 1991 to July, 1992, 12 consecutive patients (six males and six females, mean age 38 f 14 years, range 21-63 years) with a usual slow-fast form of AV nodal re-entrant tachycardia were referred to our division for modification of the AV node with radiofrequency current. All of them had more than 5 years’ history of symptomatic tachycardia. Mean 2.1 f 1.8 antiarrhythmic agents were administered but the tachycardia could not be controled satisfactorily before the referal. Routine physical examination, X-ray chest film, echocardiography and 24-h Holter monitoring were performed but no organic heart diseases were found.
204
Electrophysiologic study
Catheter ablation
The diagnosis of AV nodal re-entrant tachycardia was made according to previously described criteria [5]. Antiarrhythmic agents were withdrawn for at least five half-lives before ablation. Informed written consent was obtained. Three 6F quadripolar electrode catheters (USCI) were introduced through the femoral vein to the high right atrium, the bundle of His area, and the right ventricular apex, respectively. A 6F quadripolar electrode catheter was introduced through the right internal jugular or left subclavin vein and advanced to the coronary sinus. Electrocardiographic (ECG) leads I, aVF and Vl as well as intracardiac electrograms were simultaneously displayed and recorded on a multichannel oscilloscopic recorder (Mingograph 7, SIMENS) at a paper speed of 100 mm/s. The pacing stimulli were approximately twice the diastolic threshold in strength and 2 ms in duration, and were provided by a digital programmable stimulator (Biotronic). All the patients underwent complete antegrade and retrograde electrophysiologic study using incremental pacing and extrastimulus testing techniques before and after ablation.
Radiofrequency energy was provided by a generator kindly provided by Dr Osypka HAT, 200 s at a frequency of 750 kHz. A large-tip ablation catheter (Mansfieldwebster) was introduced into the right femoral vein, advanced to the right atrium and positioned around the ostium of the coronary sinus, at the base of the triangle of Koch (Fig. la). A small atria1 and a large ventricular electrogram (Fig. 2) were recorded by the distal paired electrodes of the large-tip catheter. The radiofrequency current was delivered initially at this site during sinus rhythm. The current was usually at 30-35 W lasting 30 s. Electrophysiologic study was repeated after each current delivery. If the slow pathway still existed, then the ablation catheter was moved upward and anteriorly in stepwise fashion along the area between the coronary sinus ostium and the bundle His of catheter, until the compact node was reached (Fig. lb). Successful ablation was defined as follows (1) no evidence of antegrade slow pathway conduction. (2) slow-fast form of AV nodal re-entrant tachycardia is not inducible by atria1 and ventricular pacing and extrastimulation.
a
b
Fig. 1. Radiograph of ablation catheter (arrow) position during ablation of slow pathway. Right anterior oblique projection in left panel (a) shows the ablation catheter is placed anteriorly to the coronary sinus ostium. In right panel (b), the ablation catheter is between the coronary sinus ostium and the bundle of His catheter.
205
The patients were kept in the hospital for 3-4 days with multiple measurements of serum creatine kinase, 24-h Holtor monitoring and echocardiography. This monitoring was followed up in the clinic every month.
Fig. 2. Simultaneous
Data analysis The data were expressed as mean value + standard deviation and paired data were compared by Student’s t-test.
recordings of surface ieads I. II together with proxismal coronary sinus (CSp), high right atrium the possible area of slow pathway recorded by ablation catheter (ABL).
WRAP and
206
Fig. 3. Tracings of surface ECG leads I, II, and bundle of His (HB), proxismal coronary sinus (CSp), high right atrium (HRA), distal coronary sinus (CSd) and ablation catheter (ABL) placed anteriorly to the coronary sinus ostium. On the ABL tracing. the second and third beat shows a sharp monophasic deflection 30 MS after atria1 electrogram. It is the slow pathway potential (SP). It still existed after the abolishing of slow pathway.
Results Electrophysiologic findings
Dual AV node physiology was noted in all the 12 patients. It was present as a discontinuous AA-, AH-curve by incremental atria1 pacing in six patients and as a discontinuous AlA2-, A2H2-curve
by atria1 extrastimulus testing in 11 patients. The earliest atria1 activation during AV nodal reentrant tachycardia occured at the bundle of His recording site in all 12 patients. Slow pathway potential Slow pathway potential
was recorded
in the
207
anterior aspect of the ostium of the coronary sinus in four patients. These potentials are characterised by a monophasic spike within 30 ms after the atria1 deflection (Fig. 3). Radiofrequency ablation A mean of 14 f 6 applications was delivered at a power level of 38 f 5 W with a duration of 40 f 10 s. The mean accumulated energy was 19 330 f 16 098 J and the mean procedure was 1.8 f 0.7 h. The slow pathways in 12 patients were ablated successfully. The shortest atria1 paced cycle lengths that sustained a 1:1 fastpathway conduction were 366 + 54 and 389 i 78 ms, before and after the ablation, respectively (P-value not significant), and the longest atria1 paced cycle lengths for the second degree AV node block were 3 15 f 66 and 355 f 71 ms, before and after the ablation, respectively. The antegrade effective refractory periods of the fast pathway could be measured in 11 patients and were 346 f 45 and 367 f 67 ms before and after the ablation, respectively (P-value not significant). Antegrade and retrograde slow pathway conduction was not noted in all the patients after the ablation. AV nodal re-entrant echoes or tachycardias were also not induced. Follow-up No follow-up electrophysiologic studies were performed. However, there were no recurrences of proxysmal palpitation in these 12 patients during a period of 178 f 77 days. Complication Incomplete right bundle branch block occured in one patient after the ablation and recovered 1 week later. Discussion The traditional therapy for AV nodal re-entrant tachycardia is antiarrhythmic agents. However, the long-term effects of these agents is poor. Surgical modification of the AV node re-entrant circuit was inadvertently achieved by Pritchett et al. [5] in
1979. Subsequently Ross et al. [6] and Cox [7] developed the dissection of perinodal tissue and a cryosurgical procedure for ablating the perinodal tissue. These two procedures abolish the slow pathway and maintain antegrade conduction of the fast pathway. Modification of the AV node by direct current shock was introduced by Haissaguerre [8] 3 years ago. It usually results in abolition of the retrograde fast pathway conduction and causes a variable degree of damage to the antegrade fast and slow pathway conduction. Catheter ablation by radiofrequency current was used to block the AV node completely to cure refractory AV re-entrant tachycardia when the procedure was introduced. The method was used for the first time by Goy et al. [9] to modify the AV node in 1989. The advantage of this energy source is the ability to produce a small dense and well delineated leision. Therefore, ablation could be more selective and safe. This procedure could cause retrograde conduction block of the fast pathway [3,10], antegrade conduction block of the slow pathway [4,10], or both. Several studies have demonstrated that the site of ablation is correlated to the success rate and complication. Recently Wu et al. [lo] described three methods of localizing the ablation site in detail. The slow pathway is composed of a posterior input of a transitional cell to the compact node and the compact node itself. Therefore, the procedure we used in this study could ablate the slow pathway. All 12 patients were ablated successfully. The result is little different from that of Wu et al. [lo], in which a 50% success rate only was achieved at the site. The electrophysiologic significance of slow pathway potential is not clear [4]. The potential could be recorded on sinus rhythm or during AV nodal re-entrant tachycardia. Four of the 12 patients in our study had this kind of potential. It is usually a monophasic upstroke deflection and within 30 ms after atria1 deflection. Radiofrequency current delivery at the site where slow pathway potential was recorded abolished three of four slow pathways. These potentials disappeared after blocking of the pathways. Since the transitional cells (AN cells) have a fully developed action potential with a rounded peak, whereas the compact node cells (N cell) have a small action potential with a slow upstroke
208 [ 11,121, the slow pathway potential we recorded around the ostium of coronary sinus may represent the posterior input of transitional cells. Ablation at this site will abolish slow pathway.
6
7
References 8 Lavergne T, Guiz.e L, Le Heuzey JY, et al. Closed-chest atrioventricualr junction ablation by high-frequency energy transcatheter desiccation. Lancet 1986; 2: 858-859. Budde T, Breithardt G, Borggrefe M et al. Initial experiences with high-frequency electric ablation of the AV conduction system in the human. 2 Kardiol 1987; 76: 204-210. Lee MA, Morady F, Kadish A et al. Catheter modilication of the atrioventricular junction with radiofrequency energy for control of atrioventricular nodal reentrant tachycardia. Circulation 1991; 83: 827-835. Hu DY, Wang LS, Kuck KH et al. Clinical application of radiofrequency ablation. I. Patients with WolffParkinson-White syndrom. II. Patients with AV nodal dual pathway. Chin J Cardiol 1992: 4: 207-212. Pritchett ELC, Anderson RW, Benditt DG et al. Reentry within the atrioventricular node: surgical cure with preservation of atrioventricular conduction. Circulation 1979; 60: 440-450.
Ross DL, Johnson DC, Denniss AR, Cooper MJ, Richards DA, Uther JB. Curative surgery for atrioventricular junctional (“AV nodal”) reentrant tachycardia. J Am Coil Cardiol 1985; 6: 1383-1392. Cox JL, Holman WL, Cain ME. Cryosurgical treatment of atrioventricular conduction. Circulation 1987; 76: 1329-1336. Haissaquerre M, Warin JF, Lemetayer P, Saoudi N, Guillem JP, Blanchot P. Closed-chest ablation of retrograde conduction in the patients with atrioventricular nodal reentrant tachycardia. N Engl J Med 1989; 320: 426-433. Goy JJ, Fromer M, Schlaepfer J, Kappenberger L. Clinical efficacy of radiofrequency current in the treatment of patients with atrioventricular node reentrant tachycardia. J Am Coil Cardiol 1990; 16: 418-423. Wu D, Yeh SJ, Wang CC, Wen MS, Chang HJ, Lin FC. Nature of dual atrioventricular node pathways and the tachycardia circuit as defined by radiofrequency ablation technique. J Am COB Cardiol 1992; 20: 884-895. Anderson RH, Janse MJ, Van Capelle FJL, Billette J, Becker AE, Durrer D. A combined morphological and electrophysiologoical study of the atrioventricular node of the rabbit heart. Circ Res 1974; 35: 909-922. Paes de Carvaiho A, de Almeda DF. Spread of activity through the atrioventricular node. Circ Res 1960; 8: 801-809.
203
CARD10 01694
Catheter radiofrequency ablation of slow pathway in patients with atrioventricular nodal re-entrant tachycardia Da-yi Hu and Le-Xin Wang Eiectrophysiologic Section, Division of Cardiology, First Teaching Hospital of Beijing Medical University, Beijing 100034, P.R. China
(Received 19 October 1992; revision accepted 7 Janurary 1993)
Selective ablation of slow pathway by radiofrequency current in 12 patients with atrioventricular (AV) nodal dual pathway and tachycardia was performed in our section. A large-tip ablation catheter was positioned around the ostium of the coronary sinus. The slow pathways of all the 12 patients were abolished permanently. Both the antegrade and retrograde conduction of fast pathway was not affected. There was no recurrence after 178 days follow-up. Key words: Atrionodal tachycardia; Radiofrequency
Introduction Catheter radiofrequency current ablation was first introduced clinically to block AV conduction of patients with supraventricular tachycardia 7 years ago [ 1,2]. Now some studies have shown that it can be used also to cure AV nodal re-entrant tachycardia by modification [3,4]. Retrograde conduction of fast pathway can be ablated selectively by this procedure. However, first or higher degree AV-conduction block may occur. The purpose of the study is to evaluate the effects and safety of selective slow pathway ablation.
Correspondence to: Le-Xin Wang M.D., Division of Cardiology, First Teaching Hospital of Beijing Medical University, Beijing 100034, P.R. China.
ablation
Patients and Methods
Study patients From October, 1991 to July, 1992, 12 consecutive patients (six males and six females, mean age 38 f 14 years, range 21-63 years) with a usual slow-fast form of AV nodal re-entrant tachycardia were referred to our division for modification of the AV node with radiofrequency current. All of them had more than 5 years’ history of symptomatic tachycardia. Mean 2.1 f 1.8 antiarrhythmic agents were administered but the tachycardia could not be controled satisfactorily before the referal. Routine physical examination, X-ray chest film, echocardiography and 24-h Holter monitoring were performed but no organic heart diseases were found.
204
Electrophysiologic study
Catheter ablation
The diagnosis of AV nodal re-entrant tachycardia was made according to previously described criteria [5]. Antiarrhythmic agents were withdrawn for at least five half-lives before ablation. Informed written consent was obtained. Three 6F quadripolar electrode catheters (USCI) were introduced through the femoral vein to the high right atrium, the bundle of His area, and the right ventricular apex, respectively. A 6F quadripolar electrode catheter was introduced through the right internal jugular or left subclavin vein and advanced to the coronary sinus. Electrocardiographic (ECG) leads I, aVF and Vl as well as intracardiac electrograms were simultaneously displayed and recorded on a multichannel oscilloscopic recorder (Mingograph 7, SIMENS) at a paper speed of 100 mm/s. The pacing stimulli were approximately twice the diastolic threshold in strength and 2 ms in duration, and were provided by a digital programmable stimulator (Biotronic). All the patients underwent complete antegrade and retrograde electrophysiologic study using incremental pacing and extrastimulus testing techniques before and after ablation.
Radiofrequency energy was provided by a generator kindly provided by Dr Osypka HAT, 200 s at a frequency of 750 kHz. A large-tip ablation catheter (Mansfieldwebster) was introduced into the right femoral vein, advanced to the right atrium and positioned around the ostium of the coronary sinus, at the base of the triangle of Koch (Fig. la). A small atria1 and a large ventricular electrogram (Fig. 2) were recorded by the distal paired electrodes of the large-tip catheter. The radiofrequency current was delivered initially at this site during sinus rhythm. The current was usually at 30-35 W lasting 30 s. Electrophysiologic study was repeated after each current delivery. If the slow pathway still existed, then the ablation catheter was moved upward and anteriorly in stepwise fashion along the area between the coronary sinus ostium and the bundle His of catheter, until the compact node was reached (Fig. lb). Successful ablation was defined as follows (1) no evidence of antegrade slow pathway conduction. (2) slow-fast form of AV nodal re-entrant tachycardia is not inducible by atria1 and ventricular pacing and extrastimulation.
a
b
Fig. 1. Radiograph of ablation catheter (arrow) position during ablation of slow pathway. Right anterior oblique projection in left panel (a) shows the ablation catheter is placed anteriorly to the coronary sinus ostium. In right panel (b), the ablation catheter is between the coronary sinus ostium and the bundle of His catheter.
205
The patients were kept in the hospital for 3-4 days with multiple measurements of serum creatine kinase, 24-h Holtor monitoring and echocardiography. This monitoring was followed up in the clinic every month.
Fig. 2. Simultaneous
Data analysis The data were expressed as mean value + standard deviation and paired data were compared by Student’s t-test.
recordings of surface ieads I. II together with proxismal coronary sinus (CSp), high right atrium the possible area of slow pathway recorded by ablation catheter (ABL).
WRAP and
206
Fig. 3. Tracings of surface ECG leads I, II, and bundle of His (HB), proxismal coronary sinus (CSp), high right atrium (HRA), distal coronary sinus (CSd) and ablation catheter (ABL) placed anteriorly to the coronary sinus ostium. On the ABL tracing. the second and third beat shows a sharp monophasic deflection 30 MS after atria1 electrogram. It is the slow pathway potential (SP). It still existed after the abolishing of slow pathway.
Results Electrophysiologic findings
Dual AV node physiology was noted in all the 12 patients. It was present as a discontinuous AA-, AH-curve by incremental atria1 pacing in six patients and as a discontinuous AlA2-, A2H2-curve
by atria1 extrastimulus testing in 11 patients. The earliest atria1 activation during AV nodal reentrant tachycardia occured at the bundle of His recording site in all 12 patients. Slow pathway potential Slow pathway potential
was recorded
in the
207
anterior aspect of the ostium of the coronary sinus in four patients. These potentials are characterised by a monophasic spike within 30 ms after the atria1 deflection (Fig. 3). Radiofrequency ablation A mean of 14 f 6 applications was delivered at a power level of 38 f 5 W with a duration of 40 f 10 s. The mean accumulated energy was 19 330 f 16 098 J and the mean procedure was 1.8 f 0.7 h. The slow pathways in 12 patients were ablated successfully. The shortest atria1 paced cycle lengths that sustained a 1:1 fastpathway conduction were 366 + 54 and 389 i 78 ms, before and after the ablation, respectively (P-value not significant), and the longest atria1 paced cycle lengths for the second degree AV node block were 3 15 f 66 and 355 f 71 ms, before and after the ablation, respectively. The antegrade effective refractory periods of the fast pathway could be measured in 11 patients and were 346 f 45 and 367 f 67 ms before and after the ablation, respectively (P-value not significant). Antegrade and retrograde slow pathway conduction was not noted in all the patients after the ablation. AV nodal re-entrant echoes or tachycardias were also not induced. Follow-up No follow-up electrophysiologic studies were performed. However, there were no recurrences of proxysmal palpitation in these 12 patients during a period of 178 f 77 days. Complication Incomplete right bundle branch block occured in one patient after the ablation and recovered 1 week later. Discussion The traditional therapy for AV nodal re-entrant tachycardia is antiarrhythmic agents. However, the long-term effects of these agents is poor. Surgical modification of the AV node re-entrant circuit was inadvertently achieved by Pritchett et al. [5] in
1979. Subsequently Ross et al. [6] and Cox [7] developed the dissection of perinodal tissue and a cryosurgical procedure for ablating the perinodal tissue. These two procedures abolish the slow pathway and maintain antegrade conduction of the fast pathway. Modification of the AV node by direct current shock was introduced by Haissaguerre [8] 3 years ago. It usually results in abolition of the retrograde fast pathway conduction and causes a variable degree of damage to the antegrade fast and slow pathway conduction. Catheter ablation by radiofrequency current was used to block the AV node completely to cure refractory AV re-entrant tachycardia when the procedure was introduced. The method was used for the first time by Goy et al. [9] to modify the AV node in 1989. The advantage of this energy source is the ability to produce a small dense and well delineated leision. Therefore, ablation could be more selective and safe. This procedure could cause retrograde conduction block of the fast pathway [3,10], antegrade conduction block of the slow pathway [4,10], or both. Several studies have demonstrated that the site of ablation is correlated to the success rate and complication. Recently Wu et al. [lo] described three methods of localizing the ablation site in detail. The slow pathway is composed of a posterior input of a transitional cell to the compact node and the compact node itself. Therefore, the procedure we used in this study could ablate the slow pathway. All 12 patients were ablated successfully. The result is little different from that of Wu et al. [lo], in which a 50% success rate only was achieved at the site. The electrophysiologic significance of slow pathway potential is not clear [4]. The potential could be recorded on sinus rhythm or during AV nodal re-entrant tachycardia. Four of the 12 patients in our study had this kind of potential. It is usually a monophasic upstroke deflection and within 30 ms after atria1 deflection. Radiofrequency current delivery at the site where slow pathway potential was recorded abolished three of four slow pathways. These potentials disappeared after blocking of the pathways. Since the transitional cells (AN cells) have a fully developed action potential with a rounded peak, whereas the compact node cells (N cell) have a small action potential with a slow upstroke
208 [ 11,121, the slow pathway potential we recorded around the ostium of coronary sinus may represent the posterior input of transitional cells. Ablation at this site will abolish slow pathway.
6
7
References 8 Lavergne T, Guiz.e L, Le Heuzey JY, et al. Closed-chest atrioventricualr junction ablation by high-frequency energy transcatheter desiccation. Lancet 1986; 2: 858-859. Budde T, Breithardt G, Borggrefe M et al. Initial experiences with high-frequency electric ablation of the AV conduction system in the human. 2 Kardiol 1987; 76: 204-210. Lee MA, Morady F, Kadish A et al. Catheter modilication of the atrioventricular junction with radiofrequency energy for control of atrioventricular nodal reentrant tachycardia. Circulation 1991; 83: 827-835. Hu DY, Wang LS, Kuck KH et al. Clinical application of radiofrequency ablation. I. Patients with WolffParkinson-White syndrom. II. Patients with AV nodal dual pathway. Chin J Cardiol 1992: 4: 207-212. Pritchett ELC, Anderson RW, Benditt DG et al. Reentry within the atrioventricular node: surgical cure with preservation of atrioventricular conduction. Circulation 1979; 60: 440-450.
Ross DL, Johnson DC, Denniss AR, Cooper MJ, Richards DA, Uther JB. Curative surgery for atrioventricular junctional (“AV nodal”) reentrant tachycardia. J Am Coil Cardiol 1985; 6: 1383-1392. Cox JL, Holman WL, Cain ME. Cryosurgical treatment of atrioventricular conduction. Circulation 1987; 76: 1329-1336. Haissaquerre M, Warin JF, Lemetayer P, Saoudi N, Guillem JP, Blanchot P. Closed-chest ablation of retrograde conduction in the patients with atrioventricular nodal reentrant tachycardia. N Engl J Med 1989; 320: 426-433. Goy JJ, Fromer M, Schlaepfer J, Kappenberger L. Clinical efficacy of radiofrequency current in the treatment of patients with atrioventricular node reentrant tachycardia. J Am Coil Cardiol 1990; 16: 418-423. Wu D, Yeh SJ, Wang CC, Wen MS, Chang HJ, Lin FC. Nature of dual atrioventricular node pathways and the tachycardia circuit as defined by radiofrequency ablation technique. J Am COB Cardiol 1992; 20: 884-895. Anderson RH, Janse MJ, Van Capelle FJL, Billette J, Becker AE, Durrer D. A combined morphological and electrophysiologoical study of the atrioventricular node of the rabbit heart. Circ Res 1974; 35: 909-922. Paes de Carvaiho A, de Almeda DF. Spread of activity through the atrioventricular node. Circ Res 1960; 8: 801-809.