- Email: [email protected]
Is there an upper common pathway in AVNRT?
Letters to the Editor
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Lawrie TDV, eds. Comprehensive Electrocardiography, Volume 2. New York: Pergamon Press, 1989:1267–1329. 18. Coronel R, Opthof T, Plotnikov AN, Wilms-Schopman FJG, Shlapakova IN, Danilo P Jr, Sosunov EA, Anyukhovsky EP, Janse MJ, Rosen MR. Long-term cardiac memory in canine heart is associated with the evolution of a transmural repolarization gradient. Cardiovasc Res 2007;74:416 – 425. 19. Xia Y, Yuan S. In vivo validation of the T-peak to T-end interval: implications for the genesis of the T wave. Heart Rhythm 2007;4:349 –350.
Is there an upper common pathway in AVNRT? To the Editor: In their recent interesting article on atrioventricular nodal reentrant tachycardia (AVNRT), Otomo et al1 provide data on the “upper common pathway.” In early studies and sporadic case reports, ventriculoatrial block patterns and variable His– atrial conduction times have been interpreted as suggesting the presence of a common pathway with decremental conduction properties.2– 4 However, no histologic data supporting such a notion have ever been produced. Subsequent evidence, derived from high-resolution mapping in animal hearts5 as well as human electrophysiology6,7 and intraoperative8 studies, also has clearly argued against the notion of a separate entity connecting the AVNRT circuit with the atria. The majority of patients with slow–fast AVNRT have multiple heterogeneous sites of early atrial activation during the arrhythmia rather than a focal breakthrough site,6 whereas earliest retrograde activation may be recorded in both the right and left atria.9 It seems that, if anything, upper and perhaps even lower common pathways represent concepts for which, as Valderrábano stated in his thoughtful editorial commentary in the same issue of Heart Rhythm,10 “the mechanisms and relevance . . . remain speculative.” Perhaps now is the time to abandon this rather unsupported speculation? Demosthenes G. Katritsis, MD, PhD, FRCP [email protected] Department of Cardiology Athens Euroclinic Athens, Greece
References 1. Otomo K, Nagata Y, Uno K, Fujiwara H, Iesaka Y. Atypical atrioventricular nodal reentrant tachycardia with eccentric coronary sinus activation: electrophysiological characteristics and essential effects of left-sided ablation inside the coronary sinus. Heart Rhythm 2007;4:421– 432. 2. Miller JM, Rosenthal ME, Vassalo JA, Josephson ME. Atrioventricular nodal reentrant tachycardia: studies on upper and lower “common pathways.” Circulation 1987;75:930 –940. 3. Chinushi M, Aizawa Y, Ogawa Y, Fujita S, Kusano Y, Miyajima S, Shibata A. Successful slow pathway ablation in a patient with atrioventricular nodal reentrant tachycardia having a proximal common pathway. Pacing Clin Electrophysiol 1998;21:1316 –1318. 4. Guo HM, Nerheim P, Olshansky B. Irregular atrial activation during atrioventricular nodal re-entrant tachycardia: evidence of an upper common pathway. J Cardiovasc Electrophysiol 2003;14:309 –313. 5. Loh P, de Bakker JM, Hocini M, Thibault B, Hauer RN, Janse MJ. Reentrant pathway during ventricular echoes is confined to the atrioventricular node: high-resolution mapping and dissection of the triangle of Koch in isolated, perfused canine hearts. Circulation 1999;100:1346 –1353. 6. Anselme F, Hook B, Monahan K, Frederiks J, Callans D, Zardini M, Epstein LM, Zebede J, Josephson ME. Heterogeneity of retrograde fast-pathway con-
7.
8.
9.
10.
duction pattern in patients with atrioventricular nodal reentry tachycardia: observations by simultaneous multisite catheter mapping of Koch’s triangle. Circulation 1996;93:960 –968. McGuire MA, Lau K-C, Johnson DC, Richards DA, Uther JB, Ross DL. Patients with two types of atrioventricular junctional (AV nodal) reentrant tachycardia. Evidence that a common pathway of nodal tissue is not present above the reentrant circuit. Circulation 1991;83:1232–1246. Keim S, Werner P, Jazayeri M, Akhtar M, Tchou P. Localization of the fast and slow pathways in atrioventricular nodal re-entrant tachycardia by intraoperative ice mapping. Circulation 1992;86:919 –925. Katritsis DG, Ellenbogen KA, Becker AE. Atrial activation during atrioventricular nodal reentrant tachycardia: studies on retrograde fast pathway conduction. Heart Rhythm 2006;3:993–1000. Valderrábano M. Atypical atrioventricular nodal reentry with eccentric atrial activation. Is the right target on the left? Heart Rhythm 2007;4:433– 434.
To the Editor—Response: We appreciate Dr. Katritsis’s interest in our article on atypical atrioventricular (AV) nodal reentrant tachycardia (AVNRT) with eccentric coronary sinus activation,1 which suggested the presence of an upper common pathway (UCP) in 4 (1%) of the 340 cases with all forms of AVNRT. In his letter to the editor, Dr. Katritsis points out that the concept of a UCP was only speculative and should be abandoned because data2– 6 in the literature argue against the presence of a UCP. Nevertheless, we still believe that, in at least some AVNRT cases, the tachycardia circuit would be subatrial and the concept of a UCP would be required to explain the unusual phenomena, including ventriculoatrial (VA) dissociation. Before discussing whether or not the tachycardia circuit of AVNRT was confined to the AV node (“subatrial”) and connected to the atrium via a UCP, it seems crucial to define the extent of the “AV node.” Previous morphologic studies of the AV node have demonstrated a superior dense network of nodal tissue (compact AV node), an inferior portion of the AV node into which atrial bands gradually merged (transitional cell zone), and superficial transitional cells along the anterior limbus of the fossa ovalis.7,8 This threedimensional reconstruction demonstrates that AV nodal tissue occupies the bulk of the triangle of Koch. Therefore, much of the disagreement on the role of the atrium in the genesis of the tachycardia circuit seems to be derived from the definition of the extent of the AV node, especially from the failure to recognize the transitional cell zone as a specialized tissue that is part of the AV node. As described in our previous9 as well as recent report1 on the UCP, the tachycardia circuit was considered to be subatrial and connected to the atrium via a functional UCP in at least some rare cases with atypical AVNRT. The electrophysiologic evidence for a subatrial reentrant circuit and UCP included VA dissociation during a tachycardia, Wenckebach, 2:1 VA block without any tachycardia interruption, and variations in the H-A interval and/or retrograde atrial activation sequence during a stable tachycardia cycle length. An intraatrial conduction block between the perinodal atrium within the tachycardia circuit and the rest of the atrium cannot be excluded as a possible mechanism for those unusual phenomena; however, an intraatrial Wenckebach or 2:1 conduction block would be an extremely rare phenomenon at a tachycardia cycle length as long as 350 –500 ms in patients without any organic heart disease. In
1119
Lawrie TDV, eds. Comprehensive Electrocardiography, Volume 2. New York: Pergamon Press, 1989:1267–1329. 18. Coronel R, Opthof T, Plotnikov AN, Wilms-Schopman FJG, Shlapakova IN, Danilo P Jr, Sosunov EA, Anyukhovsky EP, Janse MJ, Rosen MR. Long-term cardiac memory in canine heart is associated with the evolution of a transmural repolarization gradient. Cardiovasc Res 2007;74:416 – 425. 19. Xia Y, Yuan S. In vivo validation of the T-peak to T-end interval: implications for the genesis of the T wave. Heart Rhythm 2007;4:349 –350.
Is there an upper common pathway in AVNRT? To the Editor: In their recent interesting article on atrioventricular nodal reentrant tachycardia (AVNRT), Otomo et al1 provide data on the “upper common pathway.” In early studies and sporadic case reports, ventriculoatrial block patterns and variable His– atrial conduction times have been interpreted as suggesting the presence of a common pathway with decremental conduction properties.2– 4 However, no histologic data supporting such a notion have ever been produced. Subsequent evidence, derived from high-resolution mapping in animal hearts5 as well as human electrophysiology6,7 and intraoperative8 studies, also has clearly argued against the notion of a separate entity connecting the AVNRT circuit with the atria. The majority of patients with slow–fast AVNRT have multiple heterogeneous sites of early atrial activation during the arrhythmia rather than a focal breakthrough site,6 whereas earliest retrograde activation may be recorded in both the right and left atria.9 It seems that, if anything, upper and perhaps even lower common pathways represent concepts for which, as Valderrábano stated in his thoughtful editorial commentary in the same issue of Heart Rhythm,10 “the mechanisms and relevance . . . remain speculative.” Perhaps now is the time to abandon this rather unsupported speculation? Demosthenes G. Katritsis, MD, PhD, FRCP [email protected] Department of Cardiology Athens Euroclinic Athens, Greece
References 1. Otomo K, Nagata Y, Uno K, Fujiwara H, Iesaka Y. Atypical atrioventricular nodal reentrant tachycardia with eccentric coronary sinus activation: electrophysiological characteristics and essential effects of left-sided ablation inside the coronary sinus. Heart Rhythm 2007;4:421– 432. 2. Miller JM, Rosenthal ME, Vassalo JA, Josephson ME. Atrioventricular nodal reentrant tachycardia: studies on upper and lower “common pathways.” Circulation 1987;75:930 –940. 3. Chinushi M, Aizawa Y, Ogawa Y, Fujita S, Kusano Y, Miyajima S, Shibata A. Successful slow pathway ablation in a patient with atrioventricular nodal reentrant tachycardia having a proximal common pathway. Pacing Clin Electrophysiol 1998;21:1316 –1318. 4. Guo HM, Nerheim P, Olshansky B. Irregular atrial activation during atrioventricular nodal re-entrant tachycardia: evidence of an upper common pathway. J Cardiovasc Electrophysiol 2003;14:309 –313. 5. Loh P, de Bakker JM, Hocini M, Thibault B, Hauer RN, Janse MJ. Reentrant pathway during ventricular echoes is confined to the atrioventricular node: high-resolution mapping and dissection of the triangle of Koch in isolated, perfused canine hearts. Circulation 1999;100:1346 –1353. 6. Anselme F, Hook B, Monahan K, Frederiks J, Callans D, Zardini M, Epstein LM, Zebede J, Josephson ME. Heterogeneity of retrograde fast-pathway con-
7.
8.
9.
10.
duction pattern in patients with atrioventricular nodal reentry tachycardia: observations by simultaneous multisite catheter mapping of Koch’s triangle. Circulation 1996;93:960 –968. McGuire MA, Lau K-C, Johnson DC, Richards DA, Uther JB, Ross DL. Patients with two types of atrioventricular junctional (AV nodal) reentrant tachycardia. Evidence that a common pathway of nodal tissue is not present above the reentrant circuit. Circulation 1991;83:1232–1246. Keim S, Werner P, Jazayeri M, Akhtar M, Tchou P. Localization of the fast and slow pathways in atrioventricular nodal re-entrant tachycardia by intraoperative ice mapping. Circulation 1992;86:919 –925. Katritsis DG, Ellenbogen KA, Becker AE. Atrial activation during atrioventricular nodal reentrant tachycardia: studies on retrograde fast pathway conduction. Heart Rhythm 2006;3:993–1000. Valderrábano M. Atypical atrioventricular nodal reentry with eccentric atrial activation. Is the right target on the left? Heart Rhythm 2007;4:433– 434.
To the Editor—Response: We appreciate Dr. Katritsis’s interest in our article on atypical atrioventricular (AV) nodal reentrant tachycardia (AVNRT) with eccentric coronary sinus activation,1 which suggested the presence of an upper common pathway (UCP) in 4 (1%) of the 340 cases with all forms of AVNRT. In his letter to the editor, Dr. Katritsis points out that the concept of a UCP was only speculative and should be abandoned because data2– 6 in the literature argue against the presence of a UCP. Nevertheless, we still believe that, in at least some AVNRT cases, the tachycardia circuit would be subatrial and the concept of a UCP would be required to explain the unusual phenomena, including ventriculoatrial (VA) dissociation. Before discussing whether or not the tachycardia circuit of AVNRT was confined to the AV node (“subatrial”) and connected to the atrium via a UCP, it seems crucial to define the extent of the “AV node.” Previous morphologic studies of the AV node have demonstrated a superior dense network of nodal tissue (compact AV node), an inferior portion of the AV node into which atrial bands gradually merged (transitional cell zone), and superficial transitional cells along the anterior limbus of the fossa ovalis.7,8 This threedimensional reconstruction demonstrates that AV nodal tissue occupies the bulk of the triangle of Koch. Therefore, much of the disagreement on the role of the atrium in the genesis of the tachycardia circuit seems to be derived from the definition of the extent of the AV node, especially from the failure to recognize the transitional cell zone as a specialized tissue that is part of the AV node. As described in our previous9 as well as recent report1 on the UCP, the tachycardia circuit was considered to be subatrial and connected to the atrium via a functional UCP in at least some rare cases with atypical AVNRT. The electrophysiologic evidence for a subatrial reentrant circuit and UCP included VA dissociation during a tachycardia, Wenckebach, 2:1 VA block without any tachycardia interruption, and variations in the H-A interval and/or retrograde atrial activation sequence during a stable tachycardia cycle length. An intraatrial conduction block between the perinodal atrium within the tachycardia circuit and the rest of the atrium cannot be excluded as a possible mechanism for those unusual phenomena; however, an intraatrial Wenckebach or 2:1 conduction block would be an extremely rare phenomenon at a tachycardia cycle length as long as 350 –500 ms in patients without any organic heart disease. In