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A narrow complex tachycardia with atrioventricular dissociation: What is the mechanism?
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A narrow complex tachycardia with atrioventricular dissociation: What is the mechanism? Reginald T. Ho, MD, FHRS From the Department of Medicine, Division of Cardiology, Thomas Jefferson University Hospital, Philadelphia, Pennsylvania.
Case Presentation A 74-year-old woman underwent diagnostic electrophysiologic study because of recurrent, symptomatic supraventricular tachycardia. Baseline atrio-His and His-ventricular intervals measured 75 ms and 50 ms, respectively. Programmed atrial extrastimulation elicited dual atrioventricular (AV) nodal physiology and ventricular pacing showed no ventriculoatrial conduction despite isoproterenol. Figure 1 shows her clinical tachycardia. The response of tachycardia to a His-refractory ventricular premature depolarization (VPD) is shown in the top section of Figure 2, while its induction twice by rapid ventricular pacing (340 ms) is shown in the middle and bottom sections of Figure 2. Based on these observations, what is the mechanism of tachycardia?
Discussion Figure 1 shows a narrow complex tachycardia with AV dissociation, the differential diagnosis of which includes the following: (1) junctional ectopic tachycardia (JET) with junctional-atrial block, (2) AV nodal reentrant tachycardia (AVNRT) with upper common final pathway block, (3) orthodromic reentrant tachycardia (ORT) using either a nodofascicular (NF) or nodoventricular (NV) bypass tract (BPT) with nodal-atrial block, and (4) intra-Hisian reentrant tachycardia. The absence of split His bundle potentials excludes intra-Hisian reentry. Tachycardia also shows cycle length alternans, which can be explained by JET with 3:2 exit block from an automatic focus or alternating antegrade conduction over 2 AV nodal pathways during ORT-NF/NV (eg, fast [FP] and slow [SP]) or during AVNRT. Another narrow complex tachycardia associated with cycle length alternans is dual
KEYWORDS Nodofascicular; Nodoventricular; Bypass tract; Orthodromic reciprocating tachycardia; Atrioventricular nodal reentrant tachycardia; Atrioventricular dissociation (Heart Rhythm 2017;14:1570–1573) Address reprint requests and correspondence: Dr. Reginald T. Ho, Department of Medicine, Division of Cardiology, Thomas Jefferson University Hospital, 925 Chestnut Street, Mezzanine Level, Philadelphia, PA 19107. E-mail address: [email protected].
1547-5271/$-see front matter © 2017 Heart Rhythm Society. All rights reserved.
antegrade response tachycardia resulting from simultaneous conduction over the FP and SP of the AV node after each sinus beat (“double fire”), but the wide variability in “AH” intervals that do not reliably precede and predict His-His intervals argues against this diagnosis. Although atrial overdrive pacing and the delivery of single atrial premature depolarizations can differentiate JET from AVNRT, these maneuvers are limited in the presence of complete AV dissociation. Figure 2 (Top) shows a His-refractory VPD that resets tachycardia with delay of the subsequent His bundle (indicated by an asterisk), proving the presence of a concealed NF/NV BPT but not necessarily its participation in tachycardia. Such a finding, however, effectively excludes pure JET, AVNRT, and dual antegrade response tachycardia. Though the delay could occur retrogradely in the BPT, it might also occur antegradely in the SP. This is then followed by 1 additional cycle of tachycardia with antegrade conduction over the FP, resulting in the shortest His-His interval on the tracing followed by tachycardia termination. (Alternatively, the second VPD [spontaneous, but also Hisrefractory] advances the His bundle over the BPT–FP). Further proof of the existence of a BPT is shown with tachycardia induction (Figure 2, Middle). During pacing, 2 consecutive His bundle electrograms occur at the pacing cycle length shortly after the second and third pacing stimuli. Although these could be retrograde His bundle potentials, the His bundle’s absence after the fourth pacing stimulus would make AVNRT unlikely, as it is not possible to penetrate the AV node and initiate AVNRT without prior retrograde activation of the His bundle. Additionally, the morphology of these His bundle electrograms is identical to those during tachycardia, indicating that they are activated antegradely. A more likely explanation is that these His bundle electrograms are orthodromically activated after long stimulus-His (St-H) intervals (385 ms). Further support for orthodromic activation of the His bundle is that initiation of tachycardia after the last paced complex is associated with a similarly long St-H interval. Orthodromic activation of the His bundle can only occur in the presence of a BPT. Tachycardia induction, however, is associated with a long postpacing interval (PPI) relative to the tachycardia cycle length http://dx.doi.org/10.1016/j.hrthm.2017.06.011
Ho
Narrow Complex Tachycardia With AV Dissociation
Figure 1
1571
Narrow complex tachycardia with atrioventricular dissociation.
(TCL) (138 ms) raising the possibility that the mechanism of tachycardia is AVNRT with upper common final pathway block in the presence of a bystander NF/NV pathway that inserts into 1 limb of the AV nodal circuit. A long PPI– TCL, however, can also result from pacing-induced retrograde delay over the nodal portion of the BPT or antegrade delay over the AV node, particularly the SP.1,2 The latter explanation supports the findings of the second tachycardia induction (Figure 2, Bottom). The first 2 pacing stimuli orthodromically activate the His bundle over the NF/NV BPT–SP, generating a long St-H interval. The last paced complex, however, orthodromically activates the His bundle with a shorter St-H interval (346 ms) because of NF/NV BPT–FP conduction (thereby also explaining the cycle length alternans during tachycardia), producing a short PPI–TCL (102
ms), which excludes AVNRT and establishes a diagnosis of ORT-NF/NV. Figure 3 depicts the orthodromic activation of the His bundle (arrows) during rapid ventricular pacing by retrograde conduction over a concealed NF/NV BPT and then antegradely over the SP (longer St-H interval) or FP (shorter St-H interval). The distal insertion (fascicular or ventricular) of the nodal fiber could not be identified. Para-Hisian pacing might differentiate between an NF and NV BPT by demonstrating its dependence upon His-Purkinje vs ventricular activation, respectively, but would be difficult in the absence of ventriculoatrial conduction. Entrainment with manifest fusion (particularly mild or progressive fusion) might favor an NV BPT because entrainment involving an NF BPT requires that paced antidromic wavefronts
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Figure 2 Top: Response of tachycardia to a His-refractory ventricular premature depolarization. Middle, Bottom: Induction of tachycardia by rapid ventricular pacing (340 ms).
penetrate the distal Purkinje system to reach the circuit. It is theoretically possible, however, to entrain ORT-NF with manifest fusion if the collision point between antidromic and orthodromic wavefronts occurs in the proximal right
bundle between the bifurcation of the His bundle and take-off of the NF BPT from the distal right bundle. In such a situation, paced antidromic wavefronts from the right ventricle would fuse with orthodromic activation of the His
Ho
Narrow Complex Tachycardia With AV Dissociation
1573
Figure 3 Induction of tachycardia by right ventricular pacing with arrows depicting orthodromic activation of the His bundle (H) over a concealed nodofascicular/nodoventricular bypass tract (BPT) and the slow pathway (SP) (longer stimulus-His interval) or fast pathway (FP) (shorter stimulus-His interval).
bundle–left bundle–left ventricle axis. Manifest fusion was not observed in this case. In summary, the patient had ORT using a concealed NF/ NV BPT with both (1) nodal-atrial block and AV dissociation and (2) dual AV nodal physiology with cycle length alternans. Although the NF/NV BPT could not be mapped, anecdotal cases have shown that its proximal insertion can be in the SP; and, therefore, the patient underwent SP ablation in the right posteroseptal region.3–5 During radiofrequency delivery, the integrity of the AV node was monitored by atrial pacing because junctional ectopy was associated with junctional-atrial block. After SP ablation, the patient had no further tachycardia and has remained symptom-free.
References 1. Ho RT, Frisch DF, Pavri BB, Levi SA, Greenspon AJ. Electrophysiologic features differentiating the atypical atrioventricular node-dependent long RP supraventricular tachycardia. Circ Arrhythm Electrophysiol 2013; 6(3):597–605. 2. Gonzalez-Torrecilla E, Arenal A, Atienza F, Osca J, Garcia-Fernandez J, Puchol A, Sanchez A, Almendra J. First postpacing interval after tachycardia entrainment with correction for atrioventricular node delay: a simple maneuver for differential diagnosis of atrioventricular nodal reentrant tachycardias versus orthodromic reciprocating tachycardias. Heart Rhythm 2006; 3:674–679. 3. Ho RT, Fischman DL. Entrainment versus resetting of a long RP tachycardia: what is the diagnosis? Heart Rhythm 2012;9(2):312–314. 4. Ho RT, Levi SA. An atypical long RP tachycardia: what is the mechanism? Heart Rhythm 2013;10(7):1089–1090. 5. Ho RT, Pavri BB. A long RP interval tachycardia: what is the mechanism? Heart Rhythm 2013;10(3):456–458.
A narrow complex tachycardia with atrioventricular dissociation: What is the mechanism? Reginald T. Ho, MD, FHRS From the Department of Medicine, Division of Cardiology, Thomas Jefferson University Hospital, Philadelphia, Pennsylvania.
Case Presentation A 74-year-old woman underwent diagnostic electrophysiologic study because of recurrent, symptomatic supraventricular tachycardia. Baseline atrio-His and His-ventricular intervals measured 75 ms and 50 ms, respectively. Programmed atrial extrastimulation elicited dual atrioventricular (AV) nodal physiology and ventricular pacing showed no ventriculoatrial conduction despite isoproterenol. Figure 1 shows her clinical tachycardia. The response of tachycardia to a His-refractory ventricular premature depolarization (VPD) is shown in the top section of Figure 2, while its induction twice by rapid ventricular pacing (340 ms) is shown in the middle and bottom sections of Figure 2. Based on these observations, what is the mechanism of tachycardia?
Discussion Figure 1 shows a narrow complex tachycardia with AV dissociation, the differential diagnosis of which includes the following: (1) junctional ectopic tachycardia (JET) with junctional-atrial block, (2) AV nodal reentrant tachycardia (AVNRT) with upper common final pathway block, (3) orthodromic reentrant tachycardia (ORT) using either a nodofascicular (NF) or nodoventricular (NV) bypass tract (BPT) with nodal-atrial block, and (4) intra-Hisian reentrant tachycardia. The absence of split His bundle potentials excludes intra-Hisian reentry. Tachycardia also shows cycle length alternans, which can be explained by JET with 3:2 exit block from an automatic focus or alternating antegrade conduction over 2 AV nodal pathways during ORT-NF/NV (eg, fast [FP] and slow [SP]) or during AVNRT. Another narrow complex tachycardia associated with cycle length alternans is dual
KEYWORDS Nodofascicular; Nodoventricular; Bypass tract; Orthodromic reciprocating tachycardia; Atrioventricular nodal reentrant tachycardia; Atrioventricular dissociation (Heart Rhythm 2017;14:1570–1573) Address reprint requests and correspondence: Dr. Reginald T. Ho, Department of Medicine, Division of Cardiology, Thomas Jefferson University Hospital, 925 Chestnut Street, Mezzanine Level, Philadelphia, PA 19107. E-mail address: [email protected].
1547-5271/$-see front matter © 2017 Heart Rhythm Society. All rights reserved.
antegrade response tachycardia resulting from simultaneous conduction over the FP and SP of the AV node after each sinus beat (“double fire”), but the wide variability in “AH” intervals that do not reliably precede and predict His-His intervals argues against this diagnosis. Although atrial overdrive pacing and the delivery of single atrial premature depolarizations can differentiate JET from AVNRT, these maneuvers are limited in the presence of complete AV dissociation. Figure 2 (Top) shows a His-refractory VPD that resets tachycardia with delay of the subsequent His bundle (indicated by an asterisk), proving the presence of a concealed NF/NV BPT but not necessarily its participation in tachycardia. Such a finding, however, effectively excludes pure JET, AVNRT, and dual antegrade response tachycardia. Though the delay could occur retrogradely in the BPT, it might also occur antegradely in the SP. This is then followed by 1 additional cycle of tachycardia with antegrade conduction over the FP, resulting in the shortest His-His interval on the tracing followed by tachycardia termination. (Alternatively, the second VPD [spontaneous, but also Hisrefractory] advances the His bundle over the BPT–FP). Further proof of the existence of a BPT is shown with tachycardia induction (Figure 2, Middle). During pacing, 2 consecutive His bundle electrograms occur at the pacing cycle length shortly after the second and third pacing stimuli. Although these could be retrograde His bundle potentials, the His bundle’s absence after the fourth pacing stimulus would make AVNRT unlikely, as it is not possible to penetrate the AV node and initiate AVNRT without prior retrograde activation of the His bundle. Additionally, the morphology of these His bundle electrograms is identical to those during tachycardia, indicating that they are activated antegradely. A more likely explanation is that these His bundle electrograms are orthodromically activated after long stimulus-His (St-H) intervals (385 ms). Further support for orthodromic activation of the His bundle is that initiation of tachycardia after the last paced complex is associated with a similarly long St-H interval. Orthodromic activation of the His bundle can only occur in the presence of a BPT. Tachycardia induction, however, is associated with a long postpacing interval (PPI) relative to the tachycardia cycle length http://dx.doi.org/10.1016/j.hrthm.2017.06.011
Ho
Narrow Complex Tachycardia With AV Dissociation
Figure 1
1571
Narrow complex tachycardia with atrioventricular dissociation.
(TCL) (138 ms) raising the possibility that the mechanism of tachycardia is AVNRT with upper common final pathway block in the presence of a bystander NF/NV pathway that inserts into 1 limb of the AV nodal circuit. A long PPI– TCL, however, can also result from pacing-induced retrograde delay over the nodal portion of the BPT or antegrade delay over the AV node, particularly the SP.1,2 The latter explanation supports the findings of the second tachycardia induction (Figure 2, Bottom). The first 2 pacing stimuli orthodromically activate the His bundle over the NF/NV BPT–SP, generating a long St-H interval. The last paced complex, however, orthodromically activates the His bundle with a shorter St-H interval (346 ms) because of NF/NV BPT–FP conduction (thereby also explaining the cycle length alternans during tachycardia), producing a short PPI–TCL (102
ms), which excludes AVNRT and establishes a diagnosis of ORT-NF/NV. Figure 3 depicts the orthodromic activation of the His bundle (arrows) during rapid ventricular pacing by retrograde conduction over a concealed NF/NV BPT and then antegradely over the SP (longer St-H interval) or FP (shorter St-H interval). The distal insertion (fascicular or ventricular) of the nodal fiber could not be identified. Para-Hisian pacing might differentiate between an NF and NV BPT by demonstrating its dependence upon His-Purkinje vs ventricular activation, respectively, but would be difficult in the absence of ventriculoatrial conduction. Entrainment with manifest fusion (particularly mild or progressive fusion) might favor an NV BPT because entrainment involving an NF BPT requires that paced antidromic wavefronts
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Heart Rhythm, Vol 14, No 10, October 2017
Figure 2 Top: Response of tachycardia to a His-refractory ventricular premature depolarization. Middle, Bottom: Induction of tachycardia by rapid ventricular pacing (340 ms).
penetrate the distal Purkinje system to reach the circuit. It is theoretically possible, however, to entrain ORT-NF with manifest fusion if the collision point between antidromic and orthodromic wavefronts occurs in the proximal right
bundle between the bifurcation of the His bundle and take-off of the NF BPT from the distal right bundle. In such a situation, paced antidromic wavefronts from the right ventricle would fuse with orthodromic activation of the His
Ho
Narrow Complex Tachycardia With AV Dissociation
1573
Figure 3 Induction of tachycardia by right ventricular pacing with arrows depicting orthodromic activation of the His bundle (H) over a concealed nodofascicular/nodoventricular bypass tract (BPT) and the slow pathway (SP) (longer stimulus-His interval) or fast pathway (FP) (shorter stimulus-His interval).
bundle–left bundle–left ventricle axis. Manifest fusion was not observed in this case. In summary, the patient had ORT using a concealed NF/ NV BPT with both (1) nodal-atrial block and AV dissociation and (2) dual AV nodal physiology with cycle length alternans. Although the NF/NV BPT could not be mapped, anecdotal cases have shown that its proximal insertion can be in the SP; and, therefore, the patient underwent SP ablation in the right posteroseptal region.3–5 During radiofrequency delivery, the integrity of the AV node was monitored by atrial pacing because junctional ectopy was associated with junctional-atrial block. After SP ablation, the patient had no further tachycardia and has remained symptom-free.
References 1. Ho RT, Frisch DF, Pavri BB, Levi SA, Greenspon AJ. Electrophysiologic features differentiating the atypical atrioventricular node-dependent long RP supraventricular tachycardia. Circ Arrhythm Electrophysiol 2013; 6(3):597–605. 2. Gonzalez-Torrecilla E, Arenal A, Atienza F, Osca J, Garcia-Fernandez J, Puchol A, Sanchez A, Almendra J. First postpacing interval after tachycardia entrainment with correction for atrioventricular node delay: a simple maneuver for differential diagnosis of atrioventricular nodal reentrant tachycardias versus orthodromic reciprocating tachycardias. Heart Rhythm 2006; 3:674–679. 3. Ho RT, Fischman DL. Entrainment versus resetting of a long RP tachycardia: what is the diagnosis? Heart Rhythm 2012;9(2):312–314. 4. Ho RT, Levi SA. An atypical long RP tachycardia: what is the mechanism? Heart Rhythm 2013;10(7):1089–1090. 5. Ho RT, Pavri BB. A long RP interval tachycardia: what is the mechanism? Heart Rhythm 2013;10(3):456–458.