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A narrow complex tachycardia with intermittent atrioventricular dissociation: What is the mechanism?
A narrow complex tachycardia with intermittent atrioventricular dissociation: What is the mechanism? Reginald T. Ho, MD, FHRS, Grzegorz Pietrasik, MD, Arnold J. Greenspon, MD From the From the Department of Medicine, Division of Cardiology, Thomas Jefferson University Hospital, Philadelphia, Pennsylvania.
Case presentation A 57-year-old woman underwent diagnostic electrophysiology study because of recurrent symptomatic supraventricular tachycardia refractory to combination therapy with metoprolol and Cardizem. Her resting 12-lead electrocardiogram and transthoracic echocardiogram were normal. Baseline atrio-His and His-ventricular intervals measured 59 and 52 ms, respectively. Dual antegrade atrioventricular (AV) node physiology was observed during programmed atrial extrastimulation. Ventriculoatrial conduction was midline but only intermittent at a paced cycle length of 500 ms. Multiple episodes of tachycardia initiated and terminated spontaneously (Figure 1). Right ventricular (RV) premature depolarizations delivered when the His bundle was refractory failed to affect the tachycardia. The response of tachycardia to overdrive RV and coronary sinus (CS) pacing as well as atrial premature depolarizations (APDs) delivered during His bundle refractoriness are shown in Figure 2. Based on these observations, what is the mechanism of tachycardia?
Discussion The top panel of Figure 1 shows 2 sinus complexes followed by the initiation of tachycardia with an “AHH” response. During tachycardia, there is midline retrograde conduction (earliest at the His bundle region) that demonstrates delay and then block (Wenckebach) followed by AV dissociation and sinus rhythm. During AV dissociation, both early (Figure 1, middle panel) and late (Figure 1, bottom panel) coupled sinus complexes (see the asterisk in the figure) KEYWORDS Supraventricular tachycardia; Atrioventricular dissociation; Junctional ectopic tachycardia; Atrioventricular nodal reentrant tachycardia ABBREVIATIONS APD ¼ atrial premature depolarization; AV ¼ atrioventricular; AVNRT ¼ atrioventricular nodal reentrant tachycardia; CS ¼ coronary sinus; FP ¼ fast pathway; JET ¼ junctional ectopic tachycardia; RV ¼ right ventricular; SP ¼ slow pathway (Heart Rhythm 2014;0:1–4) Address reprint requests and correspondence: Dr Reginald T. Ho, Department of Medicine, Division of Cardiology, Thomas Jefferson University Hospital, 925 Chestnut St, Mezzanine Level, Philadelphia, PA 19107. E-mail address: [email protected].
1547-5271/$-see front matter B 2014 Heart Rhythm Society. All rights reserved.
conduct over the AV node to the ventricle and terminate or reset tachycardia, respectively—the latter also with an AHH response. The differential diagnosis of supraventricular tachycardia with AV dissociation is short and includes (1) atrioventricular nodal reentrant tachycardia (AVNRT) with upper common final pathway block, (2) junctional ectopic tachycardia (JET) with junctional-atrial (JA) block, (3) orthodromic reentrant tachycardia using a concealed nodofascicular accessory pathway with nodal atrial block, and (4) intrahisian reentrant tachycardia with His-atrial block.1 The absence of split His bundle potentials during sinus rhythm excludes intrahisian reentry. The top panel of Figure 2 shows rapid RV pacing that retrogradely captures the His bundle but fails to accelerate the atrium. The 155-ms longer postpacing interval relative to tachycardia cycle length and failure of His-refractory RV premature depolarizations to affect tachycardia argue against nodofascicular accessory pathway, which leaves AVNRT and JET as the 2 remaining possibilities. The middle panel of Figure 2 shows rapid CS pacing that accelerates the His bundle to the paced cycle length and produces an AHH response upon pacing cessation, while the bottom panel of Figure 2 shows a Hisrefractory APD delivered from the CS that resets tachycardia with the delay of the His bundle and shortening of the subsequent HA interval. Three pacing maneuvers that can be used to differentiate AVNRT from JET are (1) ventricular pacing at the tachycardia cycle length, (2) overdrive atrial pacing, and (3) single atrial extrastimulation.2–5 A negative (AVNRT)/positive (JET) ΔHA (HApacing HASVT) value with ventricular pacing at the tachycardia cycle length was found by some, but not others, to be a useful criterion distinguishing these 2 diagnoses.2,3 The inability of ventricular pacing to accelerate the atrium despite retrograde capture of the His bundle made this criterion not applicable in this case. Another criterion is an “AHA” (AVNRT)/“AHH” (JET) response to atrial overdrive pacing.4 The AHH response accompanying rapid CS pacing along with multiple AHH responses during tachycardia initiation and resetting favor JET. However, a third criterion (any perturbation [resetting or termination] of tachycardia by a His-refractory APD) has been considered diagnostic of AVNRT, thereby excluding JET.5 Which then
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Figure 1 Spontaneous initiation (top), termination (middle), and resetting (bottom) of tachycardia. CS ¼ coronary sinus; ds ¼ distal; HRA ¼ high right atrium; md ¼ mid; px ¼ proximal; RV ¼ right ventricular.
is the correct diagnosis? The one and most likely diagnosis that can explain all these findings is AVNRT with repetitive dual antegrade responses (“double fire” phenomenon). Simultaneous conduction over the fast pathway (FP) and slow pathway (SP) during initiation, resetting, and entrainment can produce multiple AHH responses resembling JET. After resetting of AVNRT by a His-refractory APD, the unexpected 25-ms prolongation of the HA interval without any change in tachycardia rate results from exposure of the
upper common final pathway to a long-short sequence, rendering it relatively refractory with ongoing tachycardia. One theoretical alternative, however, is JET arising from the proximal SP. While the third criterion may be true for JET originating close to the His bundle (eg, compact AV node or FP) where the junctional focus and surrounding tissue remain refractory when the His bundle is depolarized, it may not be so for JET arising from the proximal SP distant from the His bundle. In such a scenario, an ectopic focus near
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Tachycardia With Intermittent Atrioventricular Dissociation
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Figure 2 Response of tachycardia to overdrive ventricular (top) and atrial (middle) pacing as well as an atrial extrastimulus delivered during His bundle refractoriness (bottom). CS ¼ coronary sinus; ds ¼ distal; HRA ¼ high right atrium; md ¼ mid; px ¼ proximal; RV ¼ right ventricular.
the atrial insertion site of the SP might fail to propagate retrogradely and conduct antegradely over the SP reaching the lower turnaround point of the AV node from where it conducts further antegradely to activate the His bundle and retrogradely to activate the FP. Depolarization of the His bundle, therefore, occurs long after discharge of the focus such that an APD delivered near the SP (CS) when the preceding wavefront reaches the His bundle might find the SP again excitable and capable of conduction. Slow pathway
conduction resets tachycardia followed by a long AH interval. Resetting of the ectopic focus with slight delay in recovery but not discharging rate could find the SP in a less refractory state. Faster SP conduction that then encroaches upon relative refractoriness of the FP accounts for longer HA values without any change in the tachycardia rate (Figure 3). While JET arising specifically from the SP cannot be definitively excluded, its diagnosis is remote compared to dual AV node physiology and AVNRT. Radiofrequency energy
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Figure 3 Figure 2 bottom panel (shown again) and its corresponding ladder diagram of a resetting atrial extrastimulus during a theoretical case of junctional ectopic tachycardia arising from the proximal slow pathway and mimicking slow-fast atrioventricular nodal reentrant tachycardia. Black dots denote the discharging junctional focus. The open white dot denotes the anticipated discharge had the focus not been reset. AVN ¼ atrioventricular nodal; CS ¼ coronary sinus; ds ¼ distal; HRA ¼ high right atrium; md ¼ mid; px ¼ proximal; RV ¼ right ventricular.
delivery to the SP resulted in a slow junctional rhythm isorhythmic with the sinus rate, subsequent loss of all AHH responses, and noninducibility of tachycardia despite isoproterenol provocation.
References 1. Hamdan MH, Kalman JM, Lesh MD, Lee RJ, Saxon LA, Dorostkar P, Scheinman M. Narrow complex tachycardia with VA block: diagnostic and therapeutic implications. Pacing Clin Electrophysiol 1998;21:1196–1206. 2. Srivathsan K, Gami AS, Barrett R, Monahan K, Packer DL, Asirvatham SJ. Differentiating atrioventricular nodal reentrant tachycardia from junctional
tachycardia: novel application of the delta H-A interval. J Cardiovasc Electrophysiol 2008;19:1–6. 3. Luebbert J, Greenspon AJ, Pavri BB, Frisch DR, Ho RT. Do ΔHA values differentiate slow-fast atrio-ventricular nodal reentrant tachycardia from automatic junctional tachycardia arising from the slow pathway of the AV node? Heart Rhythm 2011;8:S302. 4. Fan R, Tardos JG, Almasry I, Barbera S, Rashba EJ, Iwai S. Novel use of atrial overdrive pacing to rapidly differentiate junctional tachycardia from atrioventricular nodal reentrant tachycardia. Heart Rhythm 2011;8:840–844. 5. Padanilam BJ, Manfredi JA, Steinberg LA, Olson JA, Fogel RI, Prystowsky EN. Differentiating junctional tachycardia and atrioventricular node re-entry tachycardia based on response to atrial extrastimulus pacing. J Am Coll Cardiol 2008;52: 1711–1717.
Case presentation A 57-year-old woman underwent diagnostic electrophysiology study because of recurrent symptomatic supraventricular tachycardia refractory to combination therapy with metoprolol and Cardizem. Her resting 12-lead electrocardiogram and transthoracic echocardiogram were normal. Baseline atrio-His and His-ventricular intervals measured 59 and 52 ms, respectively. Dual antegrade atrioventricular (AV) node physiology was observed during programmed atrial extrastimulation. Ventriculoatrial conduction was midline but only intermittent at a paced cycle length of 500 ms. Multiple episodes of tachycardia initiated and terminated spontaneously (Figure 1). Right ventricular (RV) premature depolarizations delivered when the His bundle was refractory failed to affect the tachycardia. The response of tachycardia to overdrive RV and coronary sinus (CS) pacing as well as atrial premature depolarizations (APDs) delivered during His bundle refractoriness are shown in Figure 2. Based on these observations, what is the mechanism of tachycardia?
Discussion The top panel of Figure 1 shows 2 sinus complexes followed by the initiation of tachycardia with an “AHH” response. During tachycardia, there is midline retrograde conduction (earliest at the His bundle region) that demonstrates delay and then block (Wenckebach) followed by AV dissociation and sinus rhythm. During AV dissociation, both early (Figure 1, middle panel) and late (Figure 1, bottom panel) coupled sinus complexes (see the asterisk in the figure) KEYWORDS Supraventricular tachycardia; Atrioventricular dissociation; Junctional ectopic tachycardia; Atrioventricular nodal reentrant tachycardia ABBREVIATIONS APD ¼ atrial premature depolarization; AV ¼ atrioventricular; AVNRT ¼ atrioventricular nodal reentrant tachycardia; CS ¼ coronary sinus; FP ¼ fast pathway; JET ¼ junctional ectopic tachycardia; RV ¼ right ventricular; SP ¼ slow pathway (Heart Rhythm 2014;0:1–4) Address reprint requests and correspondence: Dr Reginald T. Ho, Department of Medicine, Division of Cardiology, Thomas Jefferson University Hospital, 925 Chestnut St, Mezzanine Level, Philadelphia, PA 19107. E-mail address: [email protected].
1547-5271/$-see front matter B 2014 Heart Rhythm Society. All rights reserved.
conduct over the AV node to the ventricle and terminate or reset tachycardia, respectively—the latter also with an AHH response. The differential diagnosis of supraventricular tachycardia with AV dissociation is short and includes (1) atrioventricular nodal reentrant tachycardia (AVNRT) with upper common final pathway block, (2) junctional ectopic tachycardia (JET) with junctional-atrial (JA) block, (3) orthodromic reentrant tachycardia using a concealed nodofascicular accessory pathway with nodal atrial block, and (4) intrahisian reentrant tachycardia with His-atrial block.1 The absence of split His bundle potentials during sinus rhythm excludes intrahisian reentry. The top panel of Figure 2 shows rapid RV pacing that retrogradely captures the His bundle but fails to accelerate the atrium. The 155-ms longer postpacing interval relative to tachycardia cycle length and failure of His-refractory RV premature depolarizations to affect tachycardia argue against nodofascicular accessory pathway, which leaves AVNRT and JET as the 2 remaining possibilities. The middle panel of Figure 2 shows rapid CS pacing that accelerates the His bundle to the paced cycle length and produces an AHH response upon pacing cessation, while the bottom panel of Figure 2 shows a Hisrefractory APD delivered from the CS that resets tachycardia with the delay of the His bundle and shortening of the subsequent HA interval. Three pacing maneuvers that can be used to differentiate AVNRT from JET are (1) ventricular pacing at the tachycardia cycle length, (2) overdrive atrial pacing, and (3) single atrial extrastimulation.2–5 A negative (AVNRT)/positive (JET) ΔHA (HApacing HASVT) value with ventricular pacing at the tachycardia cycle length was found by some, but not others, to be a useful criterion distinguishing these 2 diagnoses.2,3 The inability of ventricular pacing to accelerate the atrium despite retrograde capture of the His bundle made this criterion not applicable in this case. Another criterion is an “AHA” (AVNRT)/“AHH” (JET) response to atrial overdrive pacing.4 The AHH response accompanying rapid CS pacing along with multiple AHH responses during tachycardia initiation and resetting favor JET. However, a third criterion (any perturbation [resetting or termination] of tachycardia by a His-refractory APD) has been considered diagnostic of AVNRT, thereby excluding JET.5 Which then
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Figure 1 Spontaneous initiation (top), termination (middle), and resetting (bottom) of tachycardia. CS ¼ coronary sinus; ds ¼ distal; HRA ¼ high right atrium; md ¼ mid; px ¼ proximal; RV ¼ right ventricular.
is the correct diagnosis? The one and most likely diagnosis that can explain all these findings is AVNRT with repetitive dual antegrade responses (“double fire” phenomenon). Simultaneous conduction over the fast pathway (FP) and slow pathway (SP) during initiation, resetting, and entrainment can produce multiple AHH responses resembling JET. After resetting of AVNRT by a His-refractory APD, the unexpected 25-ms prolongation of the HA interval without any change in tachycardia rate results from exposure of the
upper common final pathway to a long-short sequence, rendering it relatively refractory with ongoing tachycardia. One theoretical alternative, however, is JET arising from the proximal SP. While the third criterion may be true for JET originating close to the His bundle (eg, compact AV node or FP) where the junctional focus and surrounding tissue remain refractory when the His bundle is depolarized, it may not be so for JET arising from the proximal SP distant from the His bundle. In such a scenario, an ectopic focus near
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Figure 2 Response of tachycardia to overdrive ventricular (top) and atrial (middle) pacing as well as an atrial extrastimulus delivered during His bundle refractoriness (bottom). CS ¼ coronary sinus; ds ¼ distal; HRA ¼ high right atrium; md ¼ mid; px ¼ proximal; RV ¼ right ventricular.
the atrial insertion site of the SP might fail to propagate retrogradely and conduct antegradely over the SP reaching the lower turnaround point of the AV node from where it conducts further antegradely to activate the His bundle and retrogradely to activate the FP. Depolarization of the His bundle, therefore, occurs long after discharge of the focus such that an APD delivered near the SP (CS) when the preceding wavefront reaches the His bundle might find the SP again excitable and capable of conduction. Slow pathway
conduction resets tachycardia followed by a long AH interval. Resetting of the ectopic focus with slight delay in recovery but not discharging rate could find the SP in a less refractory state. Faster SP conduction that then encroaches upon relative refractoriness of the FP accounts for longer HA values without any change in the tachycardia rate (Figure 3). While JET arising specifically from the SP cannot be definitively excluded, its diagnosis is remote compared to dual AV node physiology and AVNRT. Radiofrequency energy
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Figure 3 Figure 2 bottom panel (shown again) and its corresponding ladder diagram of a resetting atrial extrastimulus during a theoretical case of junctional ectopic tachycardia arising from the proximal slow pathway and mimicking slow-fast atrioventricular nodal reentrant tachycardia. Black dots denote the discharging junctional focus. The open white dot denotes the anticipated discharge had the focus not been reset. AVN ¼ atrioventricular nodal; CS ¼ coronary sinus; ds ¼ distal; HRA ¼ high right atrium; md ¼ mid; px ¼ proximal; RV ¼ right ventricular.
delivery to the SP resulted in a slow junctional rhythm isorhythmic with the sinus rate, subsequent loss of all AHH responses, and noninducibility of tachycardia despite isoproterenol provocation.
References 1. Hamdan MH, Kalman JM, Lesh MD, Lee RJ, Saxon LA, Dorostkar P, Scheinman M. Narrow complex tachycardia with VA block: diagnostic and therapeutic implications. Pacing Clin Electrophysiol 1998;21:1196–1206. 2. Srivathsan K, Gami AS, Barrett R, Monahan K, Packer DL, Asirvatham SJ. Differentiating atrioventricular nodal reentrant tachycardia from junctional
tachycardia: novel application of the delta H-A interval. J Cardiovasc Electrophysiol 2008;19:1–6. 3. Luebbert J, Greenspon AJ, Pavri BB, Frisch DR, Ho RT. Do ΔHA values differentiate slow-fast atrio-ventricular nodal reentrant tachycardia from automatic junctional tachycardia arising from the slow pathway of the AV node? Heart Rhythm 2011;8:S302. 4. Fan R, Tardos JG, Almasry I, Barbera S, Rashba EJ, Iwai S. Novel use of atrial overdrive pacing to rapidly differentiate junctional tachycardia from atrioventricular nodal reentrant tachycardia. Heart Rhythm 2011;8:840–844. 5. Padanilam BJ, Manfredi JA, Steinberg LA, Olson JA, Fogel RI, Prystowsky EN. Differentiating junctional tachycardia and atrioventricular node re-entry tachycardia based on response to atrial extrastimulus pacing. J Am Coll Cardiol 2008;52: 1711–1717.