Broad complex tachycardia in a structurally normal heart
Richard Ang M.B.B.S. , Lola Villagraz Tecedor M.D., Mark J. Earley M.D. *
Department of Arrhythmia Services, Bart’s Heart Centre, St Bartholomew’s Hospital, Barts Health NHS Trust, London, UK.
* Corresponding author: [email protected] Tel: +442034656763 Fax: +442034655771
Disclosures: None
This article has been accepted for publication and undergone full peer review but has not been through the copyediting, typesetting, pagination and proofreading process, which may lead to differences between this version and the Version of Record. Please cite this article as doi: 10.1111/jce.12703. This article is protected by copyright. All rights reserved.
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Keywords: WPW syndrome; AV reentry; antidromic tachycardia; preexcited tachycardia; catheter ablation
Case Summary A 29-year-old man presented with palpitations after running. He was found to be in a regular broad complex tachycardia but spontaneously cardioverted in hospital with ventricular preexcitation on his electrocardiogram (Figure 1). He had a structurally normal heart on echocardiogram and underwent electrophysiological study. Tachycardia was easily inducible with atrial extrastimuli and spontaneous termination of tachycardia was observed (Figure 2). What is the mechanism of the tachycardia?
Commentary Figure 1(A) shows a regular broad complex tachycardia with the QRS morphology consistent with ventricular activation from the anterior left ventricular free wall. The differential diagnosis is antidromic atrioventricular reentrant tachycardia (AVRT) with anterograde conduction down a left-sided accessory pathway (AP), preexcited atrioventricular nodal reentrant tachycardia (AVNRT) or an atrial tachycardia (AT) with anterograde conduction down a bystander left-sided AP, or ventricular tachycardia (VT) arising from the left ventricular basal anterolateral wall. The baseline ECG (Figure 1(B)) shows evidence of ventricular preexcitation at an entirely different location (superior paraseptal or anteroseptal). This AP may be part of the tachycardia mechanism or a bystander. During tachycardia (Figure 2), the earliest activation of the atrium was at the His catheter and the earliest activation of the ventricle was at the distal coronary sinus.
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The septal V-A interval was 104ms and did not vary, making atrial tachycardia unlikely. The His electrogram was always seen preceding the local ventricular electrogram but with 2:1 AV nodal block, so the AV node is unlikely to have any role in the tachycardia mechanism. The last beat of the tachycardia is clearly conducted down the AV node with an identical retrograde activation to the atrium and a prolongation of the A-A interval (300ms to 340ms) consistent with conduction delay through the His-Purkinje system. Tachycardia terminates in the atrium due to block in the left-sided accessory pathway and the AV node. As this termination in the atria was seen repeatedly, atrial tachycardia is extremely unlikely. During tachycardia, atrial premature beats advanced ventricular activation without changing QRS morphology excluding VT. The only feasible tachycardia mechanism is a pathway to pathway AVRT utilizing a left free wall accessory pathway for anterograde conduction and a paraseptal accessory pathway for retrograde conduction.
Using an F curve Celsius Thermocool ablation catheter (Biosense Webster, Diamond Bar, CA, USA) the tricuspid annulus was mapped during tachycardia and earliest activation was found at approximately 11 o’clock on the TV annulus (Figure 3). Ablation here terminated tachycardia to reveal sinus rhythm with ventricular preexcitation consistent with a left-sided AP. Further testing revealed no retrograde conduction via the AV node or the L sided pathway and very short pathway anterograde refractory period of less than 300ms. A transseptal puncture was made and the left-sided pathway was successfully ablated using the same catheter. Further testing revealed normal anterograde conduction via the AV node. Spontaneous antidromic AVRT is rare, occurring in about 1-4% of two large cohorts of patients with Wolff-Parkinson-White syndrome1,2. Antidromic AVRT is often associated with multiple accessory pathways and is seen more frequently in patients with structural heart disease, especially Ebstein’s anomaly3. Atrial fibrillation is more easily inducible in this group of patients with the resulting higher risk of malignant forms of arrhythmia, although they appear to do well post ablation in the absence of structural heart disease.
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References 1. Bardy, G. H., Packer, D. L., German, L. D., and Gallagher, J. J. Preexcited reciprocating tachycardia in patients with Wolff-Parkinson-White syndrome: incidence and mechanisms. Circulation 1984;70:377–391. 2. Brembilla-Perrot, B., Pauriah, M., Sellal, J.-M., Zinzius, P. Y., Schwartz, J., de Chillou, C., Cismaru, G., Beurrier, D., Voilliot, D., Selton, O., et a. Incidence and prognostic significance of spontaneous and inducible antidromic tachycardia. Europace 2013;15:871–876. 3. Zachariah, J. P., Walsh, E. P., Triedman, J. K., Berul, C. I., Cecchin, F., Alexander, M. E., and Bevilacqua, L. M. Multiple accessory pathways in the young: the impact of structural heart disease. Am Heart J 2013;165:87–92.
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Figure 1. Surface electrogram showing: (A) a regular broad complex tachycardia with QRS morphology consistent with ventricular activation from the basal left ventricular antero lateral wall; and (B) sinus rhythm with ventricular preexcitation and delta waves suggestive of a superior paraseptal or anteroseptal AP.
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Figure 2. Intracardiac electrograms of the clinical tachycardia spontaneously terminating into sinus rhythm. See text for explanation. HIS = His bundle, CS = coronary sinus. The catheters are positioned as seen in Figure 3.
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Figure 3. Mapping the paraseptal AP along the TV annulus during tachycardia with the intracardiac electrograms on the left panel and a fluroscopic image of the catheters in the left anterior oblique 300 projection on the right panel. The ablation catheter is positioned at the 11 o'clock position of the TV annulus and the earliest atrial electrogram was recorded. A fused V-A signal is seen on the distal pole of the catheter. Map = mapping catheter, HIS = His bundle, CS = coronary sinus.
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Richard Ang M.B.B.S. , Lola Villagraz Tecedor M.D., Mark J. Earley M.D. *
Department of Arrhythmia Services, Bart’s Heart Centre, St Bartholomew’s Hospital, Barts Health NHS Trust, London, UK.
* Corresponding author: [email protected] Tel: +442034656763 Fax: +442034655771
Disclosures: None
This article has been accepted for publication and undergone full peer review but has not been through the copyediting, typesetting, pagination and proofreading process, which may lead to differences between this version and the Version of Record. Please cite this article as doi: 10.1111/jce.12703. This article is protected by copyright. All rights reserved.
1
Keywords: WPW syndrome; AV reentry; antidromic tachycardia; preexcited tachycardia; catheter ablation
Case Summary A 29-year-old man presented with palpitations after running. He was found to be in a regular broad complex tachycardia but spontaneously cardioverted in hospital with ventricular preexcitation on his electrocardiogram (Figure 1). He had a structurally normal heart on echocardiogram and underwent electrophysiological study. Tachycardia was easily inducible with atrial extrastimuli and spontaneous termination of tachycardia was observed (Figure 2). What is the mechanism of the tachycardia?
Commentary Figure 1(A) shows a regular broad complex tachycardia with the QRS morphology consistent with ventricular activation from the anterior left ventricular free wall. The differential diagnosis is antidromic atrioventricular reentrant tachycardia (AVRT) with anterograde conduction down a left-sided accessory pathway (AP), preexcited atrioventricular nodal reentrant tachycardia (AVNRT) or an atrial tachycardia (AT) with anterograde conduction down a bystander left-sided AP, or ventricular tachycardia (VT) arising from the left ventricular basal anterolateral wall. The baseline ECG (Figure 1(B)) shows evidence of ventricular preexcitation at an entirely different location (superior paraseptal or anteroseptal). This AP may be part of the tachycardia mechanism or a bystander. During tachycardia (Figure 2), the earliest activation of the atrium was at the His catheter and the earliest activation of the ventricle was at the distal coronary sinus.
This article is protected by copyright. All rights reserved.
2
The septal V-A interval was 104ms and did not vary, making atrial tachycardia unlikely. The His electrogram was always seen preceding the local ventricular electrogram but with 2:1 AV nodal block, so the AV node is unlikely to have any role in the tachycardia mechanism. The last beat of the tachycardia is clearly conducted down the AV node with an identical retrograde activation to the atrium and a prolongation of the A-A interval (300ms to 340ms) consistent with conduction delay through the His-Purkinje system. Tachycardia terminates in the atrium due to block in the left-sided accessory pathway and the AV node. As this termination in the atria was seen repeatedly, atrial tachycardia is extremely unlikely. During tachycardia, atrial premature beats advanced ventricular activation without changing QRS morphology excluding VT. The only feasible tachycardia mechanism is a pathway to pathway AVRT utilizing a left free wall accessory pathway for anterograde conduction and a paraseptal accessory pathway for retrograde conduction.
Using an F curve Celsius Thermocool ablation catheter (Biosense Webster, Diamond Bar, CA, USA) the tricuspid annulus was mapped during tachycardia and earliest activation was found at approximately 11 o’clock on the TV annulus (Figure 3). Ablation here terminated tachycardia to reveal sinus rhythm with ventricular preexcitation consistent with a left-sided AP. Further testing revealed no retrograde conduction via the AV node or the L sided pathway and very short pathway anterograde refractory period of less than 300ms. A transseptal puncture was made and the left-sided pathway was successfully ablated using the same catheter. Further testing revealed normal anterograde conduction via the AV node. Spontaneous antidromic AVRT is rare, occurring in about 1-4% of two large cohorts of patients with Wolff-Parkinson-White syndrome1,2. Antidromic AVRT is often associated with multiple accessory pathways and is seen more frequently in patients with structural heart disease, especially Ebstein’s anomaly3. Atrial fibrillation is more easily inducible in this group of patients with the resulting higher risk of malignant forms of arrhythmia, although they appear to do well post ablation in the absence of structural heart disease.
This article is protected by copyright. All rights reserved.
3
References 1. Bardy, G. H., Packer, D. L., German, L. D., and Gallagher, J. J. Preexcited reciprocating tachycardia in patients with Wolff-Parkinson-White syndrome: incidence and mechanisms. Circulation 1984;70:377–391. 2. Brembilla-Perrot, B., Pauriah, M., Sellal, J.-M., Zinzius, P. Y., Schwartz, J., de Chillou, C., Cismaru, G., Beurrier, D., Voilliot, D., Selton, O., et a. Incidence and prognostic significance of spontaneous and inducible antidromic tachycardia. Europace 2013;15:871–876. 3. Zachariah, J. P., Walsh, E. P., Triedman, J. K., Berul, C. I., Cecchin, F., Alexander, M. E., and Bevilacqua, L. M. Multiple accessory pathways in the young: the impact of structural heart disease. Am Heart J 2013;165:87–92.
This article is protected by copyright. All rights reserved.
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Figure 1. Surface electrogram showing: (A) a regular broad complex tachycardia with QRS morphology consistent with ventricular activation from the basal left ventricular antero lateral wall; and (B) sinus rhythm with ventricular preexcitation and delta waves suggestive of a superior paraseptal or anteroseptal AP.
This article is protected by copyright. All rights reserved.
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Figure 2. Intracardiac electrograms of the clinical tachycardia spontaneously terminating into sinus rhythm. See text for explanation. HIS = His bundle, CS = coronary sinus. The catheters are positioned as seen in Figure 3.
This article is protected by copyright. All rights reserved.
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Figure 3. Mapping the paraseptal AP along the TV annulus during tachycardia with the intracardiac electrograms on the left panel and a fluroscopic image of the catheters in the left anterior oblique 300 projection on the right panel. The ablation catheter is positioned at the 11 o'clock position of the TV annulus and the earliest atrial electrogram was recorded. A fused V-A signal is seen on the distal pole of the catheter. Map = mapping catheter, HIS = His bundle, CS = coronary sinus.
This article is protected by copyright. All rights reserved.
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