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Narrow Complex Tachycardia
N a r ro w C o m p l e x Tac h yc ardia What is the Mechanism? Marwan M. Refaat, MD, FHRS, FESCa,*, Melvin M. Scheinman, MD, FHRSb, Nitish Badhwar, MBBS, FHRSb KEYWORDS Catheter ablation Junctional tachycardia Atrioventricular nodal reentrant tachycardia
KEY POINTS This article presents a diagnostic dilemma in which atrioventricular nodal reentrant tachycardia (AVNRT) and junctional tachycardia (JT) were differentiated based on tachycardia initiation with atrial extrastimulus as well as on the response to progressive decremental atrial extrastimuli. The progressive increase in A2H20 (Atrial His interval) and H2H20 (His-His interval) in response to atrial extrastimuli favors reentry as the mechanism of the tachycardia. This is a novel mechanistic differentiation of AVNRT from focal JT.
A 51-year-old man presented with incessant supraventricular tachycardia (SVT) despite treatment with b-blockers. He was referred for electrophysiology study and catheter ablation. SVT initiation was characterized by dual ventricular response to the programmed premature atrial complex (PAC) and the atrial depolarization was linked to the second ventricular response (Fig. 1). Hisrefractory premature ventricular contraction (PVC) had no effect on the SVT and ventricular overdrive pacing during SVT did not preexcite or postexcite the first fused beat. Atrial overdrive pacing (AOD) during SVT led to an AHHA response. As shown in Fig. 2, with AOD from the proximal coronary sinus at 600 milliseconds, progressively tighter extrastimuli (360 milliseconds in Fig. 2A, 340 milliseconds in Fig. 2B,
320 milliseconds in Fig. 2C) lead to longer A2H20 and H2H20 .
QUESTION What is the diagnosis of the narrow complex tachycardia?
DISCUSSION An A-on-V SVT with septal VA timing less than 70 milliseconds rules out extranodal accessory pathway–mediated SVT. The differential diagnosis of an A-on-V SVT is typical slow-fast atrioventricular (AV) nodal reentrant tachycardia (AVNRT), atrial tachycardia, focal junctional tachycardia (JT), concealed nodofascicular/nodoventricular tachycardia, as well as intrahisian reentrant tachycardia. Because His-refractory PVC had no effect
Disclosures: None. a Section of Cardiac Electrophysiology, Division of Cardiology, Department of Medicine, Faculty of Medicine and Medical Center, American University of Beirut, PO Box 11-0236, Riad El-Solh, Beirut 1107 2020, Lebanon; b Section of Cardiac Electrophysiology, Division of Cardiology, Department of Medicine, University of California, 500 Parnassus Avenue, San Francisco, CA 94143, USA * Corresponding author. Cardiology/Cardiac Electrophysiology, Departments of Internal Medicine and Biochemistry and Molecular Genetics, Faculty of Medicine and Medical Center, American University of Beirut, PO Box 11-0236, Riad El-Solh, Beirut 1107 2020, Lebanon. E-mail address: [email protected] Card Electrophysiol Clin - (2015) -–http://dx.doi.org/10.1016/j.ccep.2015.10.006 1877-9182/15/$ – see front matter Ó 2015 Elsevier Inc. All rights reserved.
cardiacEP.theclinics.com
CLINICAL PRESENTATION
2
Refaat et al
Fig. 1. SVT initiation with atrial extrastimulus that leads to AHHA response. This finding is consistent with junctional tachycardia as well as atrioventricular nodal reentrant tachycardia initiating with double fire.
Fig. 2. AOD from the proximal coronary sinus at 600 milliseconds, progressive tighter extrastimuli (360 milliseconds in [A], 340 milliseconds in [B], 320 milliseconds in [C]) lead to longer A2H20 and H2H20 . HBE, His Bundle electrogram; HRA, high right atrium; CSd, distal coronary sinus electrogram; CSp, proximal coronary sinus electrogram; RVA, right ventricular apex electrogram.
Narrow Complex Tachycardia on the SVT, and ventricular overdrive pacing during SVT did not preexcite or postexcite the first fused beat, a concealed nodofascicular or nodoventricular reentrant tachycardia is less likely. VA linking argues against atrial tachycardia. An extranodal accessory pathway is excluded by the short VA interval (<70 milliseconds). AOD during SVT led to an AHHA response, which could be caused by JT or AVNRT termination with AOD and reinduction with a 2:1 response to atrial pacing.1 Thus, the main differential diagnosis was between JT and AVNRT initiating with double fire. AVNRT involves a reentrant circuit within the AV node, whereas the mechanism of JT in adults is enhanced automaticity or triggered activity. As shown in Fig. 2, progressively tighter extrastimuli (360 milliseconds in [A] to 320 milliseconds in [C]) lead to longer A2H20 and H2H20 that favors a reentrant mechanism (AVNRT). A focus with triggered activity (JT) would have yielded a shorter A2H20 and H2H20 with tighter extrastimuli. A late PAC induced during His bundle refractoriness delayed the next His and A. These findings exclude focal JT and favor AVNRT as the diagnosis.2,3 Following determination of the SVT mechanism, a deflectable-tip mapping/ablation catheter was maneuvered into position along the medial tricuspid annulus at the traditional slow pathway region, to about one-third of the way between the coronary sinus os and the His recording position; this latter distance comprised about 5 mm fluoroscopically. The patient had a small circuit with a narrow distance from the coronary sinus to the His catheter. At this location, the local
electrogram showed a configuration consistent with an AV nodal slow-pathway potential. The bipolar signal in sinus rhythm had a small atrial component ending in a small upward deflection, and a larger ventricular component. Catheter ablation at this site led to junctional beats and made SVT noninducible. The patient has been symptom free for 18 months. This article presents a diagnostic dilemma in that AVNRT and JT were differentiated based on tachycardia initiation with atrial extrastimulus as well as on the response to progressive decremental atrial extrastimuli. The progressive increase in A2H20 and H2H20 in response to atrial extrastimuli favors reentry as the mechanism of the tachycardia, which is a novel mechanistic differentiation of AVNRT from focal JT.
REFERENCES 1. Fan R, Tardos JG, Almasry I, et al. Novel use of atrial overdrive pacing to rapidly differentiate junctional tachycardia from atrioventricular nodal reentrant tachycardia. Heart Rhythm 2011;8:840–4. 2. Viswanatham MN, Scheinman MM, Badhwar N. A new diagnostic maneuver to differentiate atrioventricular nodal reentrant tachycardia from junctional tachycardia: a difficult distinction. Heart Rhythm 2007;4(5):S288. 3. Padanilam BJ, Manfredi JA, Steinberg LA, et al. Differentiating junctional tachycardia and atrioventricular node re-entry tachycardia based on response to atrial extrastimulus pacing. J Am Coll Cardiol 2008; 52(21):1711–7.
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KEY POINTS This article presents a diagnostic dilemma in which atrioventricular nodal reentrant tachycardia (AVNRT) and junctional tachycardia (JT) were differentiated based on tachycardia initiation with atrial extrastimulus as well as on the response to progressive decremental atrial extrastimuli. The progressive increase in A2H20 (Atrial His interval) and H2H20 (His-His interval) in response to atrial extrastimuli favors reentry as the mechanism of the tachycardia. This is a novel mechanistic differentiation of AVNRT from focal JT.
A 51-year-old man presented with incessant supraventricular tachycardia (SVT) despite treatment with b-blockers. He was referred for electrophysiology study and catheter ablation. SVT initiation was characterized by dual ventricular response to the programmed premature atrial complex (PAC) and the atrial depolarization was linked to the second ventricular response (Fig. 1). Hisrefractory premature ventricular contraction (PVC) had no effect on the SVT and ventricular overdrive pacing during SVT did not preexcite or postexcite the first fused beat. Atrial overdrive pacing (AOD) during SVT led to an AHHA response. As shown in Fig. 2, with AOD from the proximal coronary sinus at 600 milliseconds, progressively tighter extrastimuli (360 milliseconds in Fig. 2A, 340 milliseconds in Fig. 2B,
320 milliseconds in Fig. 2C) lead to longer A2H20 and H2H20 .
QUESTION What is the diagnosis of the narrow complex tachycardia?
DISCUSSION An A-on-V SVT with septal VA timing less than 70 milliseconds rules out extranodal accessory pathway–mediated SVT. The differential diagnosis of an A-on-V SVT is typical slow-fast atrioventricular (AV) nodal reentrant tachycardia (AVNRT), atrial tachycardia, focal junctional tachycardia (JT), concealed nodofascicular/nodoventricular tachycardia, as well as intrahisian reentrant tachycardia. Because His-refractory PVC had no effect
Disclosures: None. a Section of Cardiac Electrophysiology, Division of Cardiology, Department of Medicine, Faculty of Medicine and Medical Center, American University of Beirut, PO Box 11-0236, Riad El-Solh, Beirut 1107 2020, Lebanon; b Section of Cardiac Electrophysiology, Division of Cardiology, Department of Medicine, University of California, 500 Parnassus Avenue, San Francisco, CA 94143, USA * Corresponding author. Cardiology/Cardiac Electrophysiology, Departments of Internal Medicine and Biochemistry and Molecular Genetics, Faculty of Medicine and Medical Center, American University of Beirut, PO Box 11-0236, Riad El-Solh, Beirut 1107 2020, Lebanon. E-mail address: [email protected] Card Electrophysiol Clin - (2015) -–http://dx.doi.org/10.1016/j.ccep.2015.10.006 1877-9182/15/$ – see front matter Ó 2015 Elsevier Inc. All rights reserved.
cardiacEP.theclinics.com
CLINICAL PRESENTATION
2
Refaat et al
Fig. 1. SVT initiation with atrial extrastimulus that leads to AHHA response. This finding is consistent with junctional tachycardia as well as atrioventricular nodal reentrant tachycardia initiating with double fire.
Fig. 2. AOD from the proximal coronary sinus at 600 milliseconds, progressive tighter extrastimuli (360 milliseconds in [A], 340 milliseconds in [B], 320 milliseconds in [C]) lead to longer A2H20 and H2H20 . HBE, His Bundle electrogram; HRA, high right atrium; CSd, distal coronary sinus electrogram; CSp, proximal coronary sinus electrogram; RVA, right ventricular apex electrogram.
Narrow Complex Tachycardia on the SVT, and ventricular overdrive pacing during SVT did not preexcite or postexcite the first fused beat, a concealed nodofascicular or nodoventricular reentrant tachycardia is less likely. VA linking argues against atrial tachycardia. An extranodal accessory pathway is excluded by the short VA interval (<70 milliseconds). AOD during SVT led to an AHHA response, which could be caused by JT or AVNRT termination with AOD and reinduction with a 2:1 response to atrial pacing.1 Thus, the main differential diagnosis was between JT and AVNRT initiating with double fire. AVNRT involves a reentrant circuit within the AV node, whereas the mechanism of JT in adults is enhanced automaticity or triggered activity. As shown in Fig. 2, progressively tighter extrastimuli (360 milliseconds in [A] to 320 milliseconds in [C]) lead to longer A2H20 and H2H20 that favors a reentrant mechanism (AVNRT). A focus with triggered activity (JT) would have yielded a shorter A2H20 and H2H20 with tighter extrastimuli. A late PAC induced during His bundle refractoriness delayed the next His and A. These findings exclude focal JT and favor AVNRT as the diagnosis.2,3 Following determination of the SVT mechanism, a deflectable-tip mapping/ablation catheter was maneuvered into position along the medial tricuspid annulus at the traditional slow pathway region, to about one-third of the way between the coronary sinus os and the His recording position; this latter distance comprised about 5 mm fluoroscopically. The patient had a small circuit with a narrow distance from the coronary sinus to the His catheter. At this location, the local
electrogram showed a configuration consistent with an AV nodal slow-pathway potential. The bipolar signal in sinus rhythm had a small atrial component ending in a small upward deflection, and a larger ventricular component. Catheter ablation at this site led to junctional beats and made SVT noninducible. The patient has been symptom free for 18 months. This article presents a diagnostic dilemma in that AVNRT and JT were differentiated based on tachycardia initiation with atrial extrastimulus as well as on the response to progressive decremental atrial extrastimuli. The progressive increase in A2H20 and H2H20 in response to atrial extrastimuli favors reentry as the mechanism of the tachycardia, which is a novel mechanistic differentiation of AVNRT from focal JT.
REFERENCES 1. Fan R, Tardos JG, Almasry I, et al. Novel use of atrial overdrive pacing to rapidly differentiate junctional tachycardia from atrioventricular nodal reentrant tachycardia. Heart Rhythm 2011;8:840–4. 2. Viswanatham MN, Scheinman MM, Badhwar N. A new diagnostic maneuver to differentiate atrioventricular nodal reentrant tachycardia from junctional tachycardia: a difficult distinction. Heart Rhythm 2007;4(5):S288. 3. Padanilam BJ, Manfredi JA, Steinberg LA, et al. Differentiating junctional tachycardia and atrioventricular node re-entry tachycardia based on response to atrial extrastimulus pacing. J Am Coll Cardiol 2008; 52(21):1711–7.
3