- Email: [email protected]
Atrioventricular nodal or atriojunctional reentrant tachycardia?
1393
lAce Vol. O. No. 0 Decemher 19H5: 1393··4
Editorial Comment
Atrioventricular Nodal or Atriojunctional Reentrant Tachycardia? * MELVIN M. SCHEINMAN, MD, FACC San Francisco, Ca/!/
Ross et al. (1) in this issue of the Journal are to be con· gratulated on furnishing a bold and imaginative innovation in the surgical management of patients with drug-resistant "atrioventricular (A V) nodal" reentrant tachycardia. Their seminal approach has wide implications both in terms of therapy and as potentially providing insights into the mech• anism of this arrhythmia in humans. Although the diagnostic features of the arrhythmia have been defined, the basic mechanisms are still unclear.
Mechanisms Role of atrial link in the tachycardia circuit versus intranodal reentry. Mendez and Moe (2) in 1966 pre• sented cogent evidence for the existence of a dual A V nodal conduction system to explain atrial echoes in the isolated rabbit heart. These investigators also hypothesized the need for an atrial link in the tachycardia circuit. These obser• vations were further supported by the studies of Wit et al. (3), in which an in vitro animal preparation was used. A series of both clinical and laboratory observations raised serious questions relative to the need for an atrial link in the tachycardia circuit. The experimental observations of Mignone and Wallace (4), together with those of Janse et al. (5), were interpreted as showing intranodal reentry. In addition, a series of invasive clinical electrophysiologic studies (6-9) in patients with "A V nodal" reentry supported the concept that the atrium was not a critical link in the tachy• cardia circuit. Denes et al. (6) demonstrated the presence of dual A V nodal curves in the majority of patients with paroxysmal supraventricular tachycardia. Josephson and Kastor (7) elegantly demonstrated that the mass of atrial tissue could be dissociated from the tachycardia. These ex• perimental and clinical observations painted a rather tidy
*Editorials published in Journal of the American Col/eRe ofCardioloRV rellect the views of the author and do not necessarily represent the opinions of lACC or the American College of Cardiology. From the Department of Medicine and Cardiovascular Research Insti• tute, University of California, San Francisco, California. Address for reprints: Melvin M. Scheinman, MD. Room 312. Moffitt Hospital, University of California. San Francisco. California 94143. 01985 hy the American College of Cardiology
schema of A V nodal reentrant tachycardia, namely, dual A V nodal conduction with reciprocation within the A V node. These observations gave birth to the term A V nodal reentrant tachycardia (a designation interestingly used by Ross et al. [ I ]). Role of atrial perinodal fibers. The concept of sole reentry within the A V node was challenged by a number of subsequent observations. Gomes et al. (10) in a masterful, reasoned essay pointed out the consistent relation of the His deflection to the retrogradely conducted atrial impulse and suggested that this consistency was related to impulse prop• agation by way of an extranodal retrograde pathway. This consistency was corroborated by other investigators (9, II ). In addition, linuma et al. (12), using an isolated rabbit heart prerJaration, emphasized the critical role of the atrial peri• nodal flbers in sustaining A V nodal reentrant tachycardia. In addition, the histologic basis for arrhythmias related to atrioHisian flbers was clearly confirmed by the studies of Brechenmacher (13). Effect of surgery. In the report by Ross et al. (I), an imaginative approach is used to both cure the tachycardia and implicate the essential role of atrial fibers in clinical arrhythmias. Have the authors actually proved that a portion of the atrium is an essential portion of the tachycardia cir• cuit? I think not. The surgical dissection used to expose the A V node and its approaches was rather extensive and may have produced nonspecific "curative" trauma to the node itself. Such nonspecific damage may result from interruption of the neurovascular supply of the node incident to surgical trauma. The data provided could equally well be interpreted as showing nonspeciflc trauma to the node. While all pa• tients showed disturbance of retrograde ventriculoatrial con• duction, most also showed altered anterograde conduction. Could the latter reflect nonspecific trauma to the node with relative sparing of the fast pathway owing to its anatomic position relative to the dissection? The strongest supporting argument for atrial involvement in the tachycardia is detailed in Case 4, in which clearly A V nodal function remains intact but the tachycardia is no longer inducible. In the vast ma• jority of patients (8 of 10) the critical AH interval required for preoperative initiation of the tachycardia could not be achieved!
Intranodal Versus Atrionodal Tachycardia The careful observations of Ross et al. (I) notwithstand• ing, the fundamental mechanism of this fascinating tachy• cardia in humans still remains a mystery. The ultimate so• lution to this important riddle may finally be clarified by three different approaches. I) One approach may be the use of pharmacologic agents that have selective action on A V nodal cells. Neither verapamil nor beta-adrenergic blocking 0735-1097/H5/$3.30
1394
SCHEINMAN EDITORIAL COMMENT
agents would appear suitable, but preliminary studies (14) suggest that adenosine may, in fact, be such a drug. 2) Careful operative multielectrode mapping and atrial stim• ulation studies to discern the tachycardia pathway before and after selective atrial dissection should provide an ex• cellent approach. 3) Although many patients with this ar• rhythmia have undergone careful electrophysiologic studies, there is a paucity of anatomic information. Because these patients age and die (hopefully of causes other than tachy• cardia), efforts should be made to obtain histologic evidence for or against the presence of extranodal pathways. Role of surgery and other therapy. If the initial fa• vorable results are maintained, then clearly the authors have provided an important new approach to the nonpharmacol• ogic management of patients with so-called A V nodal reen• try tachycardia. The authors are to be further commended for providing the details of their postoperative complica• tions. Clinicians sorely need these data to best assess the benefit versus risk from among a variety of available non• pharmacologic approaches. These approaches include an• titachycardia pacing (15) as well as catheter ablation of the AV junction (16). Once again, a surgical approach has appeared to pave the way for a potential breakthrough in the management of patients with a frequently troublesome arrhythmia. Surely, the nimble-fingered catheter ablators will not be far behind.
References I. Ross DL, Johnson DC, Denniss AR, Cooper MJ, Richards DA, Uther JB. Curative surgery for atrioventricular junctional ("AV nodal") reentrant tachycardia. J Am Coli Cardiol 1985;6:1383-92. 2. Mendez C. Moe GK. Demonstration of a dual AV nodal conduction system in the isolated rabbit heart. Circ Res 1966;19:378-93.
lACC Vol. 6. No.6
December 1985: 1393-4
3. Wit AL. Goldreyer BN, Damato AN. An in vitro model of paroxysmal supraventricular tachycardia. Circulation 1981 ;43:862-75. 4. Mignone RJ. Wallace AG. Ventricular echoes: evidence for dissocia• tion of conduction and reentry within the AV node. Circ Res 1966; 19:638-49. 5. Janse MJ. Van Capelle FJL, Freud GE. Durrer D. Circus movement within the A V node as a basis for supraventricular tachycardia as shown by multiple microelectrode recording in the isolated rabbit heart. Circ Res 1971;28:403-14. 6. Denes P, WU D. Dhingra RC. Chuquimia R, Rosen KM. Demon• stration of dual A V nodal pathways in patients with supraventricular tachycardia. Circulation 1973;48:549-55. 7. Josephson ME. Kastor JA. Paroxysmal supraventricular tachycardia. Is the atrium a necessary link? Circulation 1976;54:430-5. 8. Scheinman MM, Gonzalez R, Thomas A, Ullyot D, Bharati S, Lev M. Reentry confined to the atrioventricular node: electrophysiologic and anatomic findings. Am J Cardiol 1982;49:1814-8. 9. Kerr CR, Benson DW, Gallagher JJ. Role of specialized conducting fibers in the genesis of "A V nodal" reentry tachycardia. PACE 1983;6: 171-84.
10. Gomes JAC. Dhatt MS. Damato AN, Akhtar M. Holder CA. Inci• dence. determinants and significance of fixed retrograde conduction in the region of the atrioventricular node: evidence for retrograde atrioventricular nodal bypass tracts. Am J Cardiol 1979;44: 1089-98. II. Ross DL. Uther lB. Diagnosis of concealed accessory pathways in supraventricular tachycardia. PACE 1984;7: 1069-85.
12. !inuma H. Dreifus LS. Mazgalev T. Price R, Michelson EL. Role of the peri nodal region in atrioventricular nodal reentry: evidence in an isolated rabbit heart preparation. J Am Coli Cardiol 1983;2:465-73. 13. BrechenmacherC. Atrio-His bundle tracts. Br Heart J 1975;37:853-5. 14. DiMarco JP. Sellers TD. Berne RM, West GA. Belardinelli L. Aden• osine: electrophysiologic effects and therapeutic use of terminating paroxysmal supraventricular tachycardia. Circulation 1983;68: 1254-63. 15. Spurrel RAJ. Nathan AW. Bexton RS. Hellestrand KJ, Nappholz T. Camm AJ. Implantable automatic scanning pacemaker for termination of supraventricular tachycardia. Am J Cardiol 1982;49:755-60. 16. Scheinman MM, Evans-Bell T. The Executive Committee of the Per• cutaneous Cardiac Mapping and Ablation Registry. Catheter ablation of the atrioventricular junction: a report of the percutaneous mapping and ablation registry. Circulation 1984;70: 1024-9.
lAce Vol. O. No. 0 Decemher 19H5: 1393··4
Editorial Comment
Atrioventricular Nodal or Atriojunctional Reentrant Tachycardia? * MELVIN M. SCHEINMAN, MD, FACC San Francisco, Ca/!/
Ross et al. (1) in this issue of the Journal are to be con· gratulated on furnishing a bold and imaginative innovation in the surgical management of patients with drug-resistant "atrioventricular (A V) nodal" reentrant tachycardia. Their seminal approach has wide implications both in terms of therapy and as potentially providing insights into the mech• anism of this arrhythmia in humans. Although the diagnostic features of the arrhythmia have been defined, the basic mechanisms are still unclear.
Mechanisms Role of atrial link in the tachycardia circuit versus intranodal reentry. Mendez and Moe (2) in 1966 pre• sented cogent evidence for the existence of a dual A V nodal conduction system to explain atrial echoes in the isolated rabbit heart. These investigators also hypothesized the need for an atrial link in the tachycardia circuit. These obser• vations were further supported by the studies of Wit et al. (3), in which an in vitro animal preparation was used. A series of both clinical and laboratory observations raised serious questions relative to the need for an atrial link in the tachycardia circuit. The experimental observations of Mignone and Wallace (4), together with those of Janse et al. (5), were interpreted as showing intranodal reentry. In addition, a series of invasive clinical electrophysiologic studies (6-9) in patients with "A V nodal" reentry supported the concept that the atrium was not a critical link in the tachy• cardia circuit. Denes et al. (6) demonstrated the presence of dual A V nodal curves in the majority of patients with paroxysmal supraventricular tachycardia. Josephson and Kastor (7) elegantly demonstrated that the mass of atrial tissue could be dissociated from the tachycardia. These ex• perimental and clinical observations painted a rather tidy
*Editorials published in Journal of the American Col/eRe ofCardioloRV rellect the views of the author and do not necessarily represent the opinions of lACC or the American College of Cardiology. From the Department of Medicine and Cardiovascular Research Insti• tute, University of California, San Francisco, California. Address for reprints: Melvin M. Scheinman, MD. Room 312. Moffitt Hospital, University of California. San Francisco. California 94143. 01985 hy the American College of Cardiology
schema of A V nodal reentrant tachycardia, namely, dual A V nodal conduction with reciprocation within the A V node. These observations gave birth to the term A V nodal reentrant tachycardia (a designation interestingly used by Ross et al. [ I ]). Role of atrial perinodal fibers. The concept of sole reentry within the A V node was challenged by a number of subsequent observations. Gomes et al. (10) in a masterful, reasoned essay pointed out the consistent relation of the His deflection to the retrogradely conducted atrial impulse and suggested that this consistency was related to impulse prop• agation by way of an extranodal retrograde pathway. This consistency was corroborated by other investigators (9, II ). In addition, linuma et al. (12), using an isolated rabbit heart prerJaration, emphasized the critical role of the atrial peri• nodal flbers in sustaining A V nodal reentrant tachycardia. In addition, the histologic basis for arrhythmias related to atrioHisian flbers was clearly confirmed by the studies of Brechenmacher (13). Effect of surgery. In the report by Ross et al. (I), an imaginative approach is used to both cure the tachycardia and implicate the essential role of atrial fibers in clinical arrhythmias. Have the authors actually proved that a portion of the atrium is an essential portion of the tachycardia cir• cuit? I think not. The surgical dissection used to expose the A V node and its approaches was rather extensive and may have produced nonspecific "curative" trauma to the node itself. Such nonspecific damage may result from interruption of the neurovascular supply of the node incident to surgical trauma. The data provided could equally well be interpreted as showing nonspeciflc trauma to the node. While all pa• tients showed disturbance of retrograde ventriculoatrial con• duction, most also showed altered anterograde conduction. Could the latter reflect nonspecific trauma to the node with relative sparing of the fast pathway owing to its anatomic position relative to the dissection? The strongest supporting argument for atrial involvement in the tachycardia is detailed in Case 4, in which clearly A V nodal function remains intact but the tachycardia is no longer inducible. In the vast ma• jority of patients (8 of 10) the critical AH interval required for preoperative initiation of the tachycardia could not be achieved!
Intranodal Versus Atrionodal Tachycardia The careful observations of Ross et al. (I) notwithstand• ing, the fundamental mechanism of this fascinating tachy• cardia in humans still remains a mystery. The ultimate so• lution to this important riddle may finally be clarified by three different approaches. I) One approach may be the use of pharmacologic agents that have selective action on A V nodal cells. Neither verapamil nor beta-adrenergic blocking 0735-1097/H5/$3.30
1394
SCHEINMAN EDITORIAL COMMENT
agents would appear suitable, but preliminary studies (14) suggest that adenosine may, in fact, be such a drug. 2) Careful operative multielectrode mapping and atrial stim• ulation studies to discern the tachycardia pathway before and after selective atrial dissection should provide an ex• cellent approach. 3) Although many patients with this ar• rhythmia have undergone careful electrophysiologic studies, there is a paucity of anatomic information. Because these patients age and die (hopefully of causes other than tachy• cardia), efforts should be made to obtain histologic evidence for or against the presence of extranodal pathways. Role of surgery and other therapy. If the initial fa• vorable results are maintained, then clearly the authors have provided an important new approach to the nonpharmacol• ogic management of patients with so-called A V nodal reen• try tachycardia. The authors are to be further commended for providing the details of their postoperative complica• tions. Clinicians sorely need these data to best assess the benefit versus risk from among a variety of available non• pharmacologic approaches. These approaches include an• titachycardia pacing (15) as well as catheter ablation of the AV junction (16). Once again, a surgical approach has appeared to pave the way for a potential breakthrough in the management of patients with a frequently troublesome arrhythmia. Surely, the nimble-fingered catheter ablators will not be far behind.
References I. Ross DL, Johnson DC, Denniss AR, Cooper MJ, Richards DA, Uther JB. Curative surgery for atrioventricular junctional ("AV nodal") reentrant tachycardia. J Am Coli Cardiol 1985;6:1383-92. 2. Mendez C. Moe GK. Demonstration of a dual AV nodal conduction system in the isolated rabbit heart. Circ Res 1966;19:378-93.
lACC Vol. 6. No.6
December 1985: 1393-4
3. Wit AL. Goldreyer BN, Damato AN. An in vitro model of paroxysmal supraventricular tachycardia. Circulation 1981 ;43:862-75. 4. Mignone RJ. Wallace AG. Ventricular echoes: evidence for dissocia• tion of conduction and reentry within the AV node. Circ Res 1966; 19:638-49. 5. Janse MJ. Van Capelle FJL, Freud GE. Durrer D. Circus movement within the A V node as a basis for supraventricular tachycardia as shown by multiple microelectrode recording in the isolated rabbit heart. Circ Res 1971;28:403-14. 6. Denes P, WU D. Dhingra RC. Chuquimia R, Rosen KM. Demon• stration of dual A V nodal pathways in patients with supraventricular tachycardia. Circulation 1973;48:549-55. 7. Josephson ME. Kastor JA. Paroxysmal supraventricular tachycardia. Is the atrium a necessary link? Circulation 1976;54:430-5. 8. Scheinman MM, Gonzalez R, Thomas A, Ullyot D, Bharati S, Lev M. Reentry confined to the atrioventricular node: electrophysiologic and anatomic findings. Am J Cardiol 1982;49:1814-8. 9. Kerr CR, Benson DW, Gallagher JJ. Role of specialized conducting fibers in the genesis of "A V nodal" reentry tachycardia. PACE 1983;6: 171-84.
10. Gomes JAC. Dhatt MS. Damato AN, Akhtar M. Holder CA. Inci• dence. determinants and significance of fixed retrograde conduction in the region of the atrioventricular node: evidence for retrograde atrioventricular nodal bypass tracts. Am J Cardiol 1979;44: 1089-98. II. Ross DL. Uther lB. Diagnosis of concealed accessory pathways in supraventricular tachycardia. PACE 1984;7: 1069-85.
12. !inuma H. Dreifus LS. Mazgalev T. Price R, Michelson EL. Role of the peri nodal region in atrioventricular nodal reentry: evidence in an isolated rabbit heart preparation. J Am Coli Cardiol 1983;2:465-73. 13. BrechenmacherC. Atrio-His bundle tracts. Br Heart J 1975;37:853-5. 14. DiMarco JP. Sellers TD. Berne RM, West GA. Belardinelli L. Aden• osine: electrophysiologic effects and therapeutic use of terminating paroxysmal supraventricular tachycardia. Circulation 1983;68: 1254-63. 15. Spurrel RAJ. Nathan AW. Bexton RS. Hellestrand KJ, Nappholz T. Camm AJ. Implantable automatic scanning pacemaker for termination of supraventricular tachycardia. Am J Cardiol 1982;49:755-60. 16. Scheinman MM, Evans-Bell T. The Executive Committee of the Per• cutaneous Cardiac Mapping and Ablation Registry. Catheter ablation of the atrioventricular junction: a report of the percutaneous mapping and ablation registry. Circulation 1984;70: 1024-9.