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Incessant Palpitations and Narrow Complex Tachycardia
I n cessant Palpita t io n s and N arro w C omp lex Tac h yc ardia Frederick T. Han, MD, FHRS KEYWORDS Supraventricular tachycardia AV dissociation Junctional tachycardia
KEY POINTS
CLINICAL PRESENTATION A 48-year-old woman presented for evaluation and management of daily palpitations, lasting for hours. The palpitations started when the patient was in her 20s, but gradually progressed, such that in the months before presentation the palpitations occurred for up to 8 hours a day on a daily basis. The palpitations occurred irrespective of whether the patient was at rest or exercising. Physical examination, laboratory studies, and echocardiogram were normal. Ambulatory monitoring identified multiple episodes of palpitations correlating with a narrow complex tachycardia occurring throughout the day (Fig. 1). The patient was subsequently referred for electrophysiology study and catheter ablation.
catheter was placed in the coronary sinus. Normal atrial-His and His-ventricular intervals were recorded in sinus rhythm. Ventricular-atrial conduction was present with ventricular pacing; there was a concentric retrograde atrial activation pattern. A sustained A on V narrow QRS complex tachycardia at a cycle length of 386 to 573 milliseconds was induced with ventricular overdrive pacing (VOD), single ventricular extrastimulus testing, and atrial overdrive pacing from the coronary sinus on and off isoproterenol infusion up to 10 mg/min (Fig. 2). Significant cycle length variation was observed with variations in isoproterenol dosing. Spontaneous variations in the His-His interval preceded changes in the atrial-atrial and ventricular-ventricular intervals during tachycardia (Fig. 3).
ELECTROPHYSIOLOGY STUDY Tachycardia Induction
QUESTION
Quadripolar electrode catheters were positioned in the high right atrium, right ventricular apex, and the His bundle region. A decapolar electrode
What is the differential diagnosis for a narrow QRS complex tachycardia? How can the tachycardia mechanism be established?
Section of Cardiac Electrophysiology, Division of Cardiovascular Medicine, University of Utah Health Sciences Center, 30 North 1900 East, Room 4A-100 SOM, Salt Lake City, UT 84132, USA E-mail address: [email protected] Card Electrophysiol Clin 8 (2016) 61–65 http://dx.doi.org/10.1016/j.ccep.2015.10.005 1877-9182/16/$ – see front matter Ó 2016 Elsevier Inc. All rights reserved.
cardiacEP.theclinics.com
Junctional tachycardia (JT) is rare cause of supraventricular tachycardia. The intracardiac activation sequence is similar to atrioventricular nodal reentrant tachycardia (AVNRT). Premature atrial contractions inserted during tachycardia can help distinguish JT from AVNRT. As noted in this case, slow pathway ablation for JT may not always be effective for termination of JT. Activation mapping during JT identified a low-amplitude potential in the region of the coronary sinus ostium and the inferior margin of the triangle of Koch that marked the successful ablation site for JT.
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Fig. 1. (A) Tachycardia initiation on ambulatory monitor. (B) Tachycardia with atrioventricular dissociation.
MANEUVERS DURING TACHYCARDIA The differential diagnosis of a narrow QRS complex tachycardia with a ventricular-atrial (VA) interval of 0 milliseconds includes atrioventricular nodal reentrant tachycardia (AVNRT), junctional tachycardia (JT), and circus movement tachycardia using a concealed nodofascicular (NF) accessory pathway.1 VOD during tachycardia entrained the tachycardia and produced a VAHV (Ventricle-Atrial-HisVentricle) response, ruling out atrial tachycardia. His refractory premature ventricular contractions during the tachycardia did not affect the subsequent A within the confines of wobble noted in tachycardia.2 This finding argues against concealed NF accessory pathway–mediated tachycardia. Single early programmed atrial extrastimuli advanced the subsequent QRS via conduction down the fast atrioventricular nodal pathway with continuation of tachycardia (Fig. 4). Late premature atrial contractions (PACs) did not
delay or terminate the tachycardia via the slow pathway.3,4 With AVNRT, late premature atrial contractions are expected to advance the tachycardia via conduction down the slow pathway; early premature atrial contractions that conduct down the fast pathway should terminate tachycardia.
MAPPING AND ABLATION A 4-mm quadripolar radiofrequency ablation catheter was used for mapping and ablation. All lesions were delivered in the temperature-controlled mode at 50 W with a 60 C temperature limit for up to 60 seconds. For ablation of the JT, we decided to proceed with a stepwise approach with inducibility testing after each series of ablations. First, we targeted the slow pathway during sinus rhythm. Two radiofrequency lesions were in the slow pathway region with junctional beats observed during ablation. The JT remained inducible (the 2 red lesions in Fig. 5).
Incessant Tachycardia
Fig. 2. (A) Tachycardia initiation with ventricular overdrive pacing. Ventricular overdrive pacing at cycle length of 400 milliseconds induced a narrow QRS complex tachycardia with a VAHV initiation. (B) Tachycardia initiation with atrial overdrive pacing. Atrial overdrive pacing the proximal coronary sinus (CS 9,10) at 550 milliseconds induced a narrow QRS complex tachycardia with a AHHA (atrial-His-His-atrial) initiation pattern.
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Fig. 3. Spontaneous variation in tachycardia cycle length. Spontaneous variations in the tachycardia cycle length were noted with variations in the His-His interval preceding changes in the atrial-atrial and ventricular-ventricular intervals.
Fig. 4. Spontaneous right atrial premature atrial contraction during tachycardia. A spontaneous late right atrial premature atrial contraction advances the next QRS via conduction down the fast atrioventricular nodal pathway with continuation of tachycardia that rules out AVNRT.
Incessant Tachycardia Fig. 5. CARTO activation map of JT in left anterior oblique cranial view. Activation mapping of JT after 2 slow pathway ablations and 3 ablations on the roof of the proximal coronary sinus failed to terminate the JT. The lesion at the successful ablation site identified a low-amplitude potential that preceded the His potential during tachycardia. Ablation at this site rendered the tachycardia noninducible.
Next, during tachycardia we mapped the earliest atrial activation and delivered 3 lesions at the roof of the proximal coronary sinus.5 The tachycardia remained inducible at this point. During tachycardia, we performed mapping to identify a prepotential during the tachycardia. As noted in Fig. 5, we identified a low-amplitude potential at the roof of the coronary sinus ostium that preceded the His potential during tachycardia. A single radiofrequency lesion delivered at this site terminated the tachycardia and rendered it noninducible.
SUMMARY JT is rare cause of supraventricular tachycardia. The intracardiac activation sequence is similar to AVNRT. Premature atrial contractions inserted during tachycardia can help distinguish JT from AVNRT. As noted in this case, slow pathway ablation for JT may not always be effective for termination of JT. Activation mapping during JT identified a low-amplitude potential in the region of the coronary sinus ostium and the inferior margin of the triangle of Koch that marked the successful ablation site for JT.
REFERENCES 1. Hamdan MH, Page RL, Scheinman MM. Diagnostic approach to narrow complex tachycardia with VA block. Pacing Clin Electrophysiol 1997;20:2984–8. 2. Knight BP, Ebinger M, Oral H, et al. Diagnostic value of tachycardia features and pacing maneuvers during paroxysmal supraventricular tachycardia. J Am Coll Cardiol 2000;36:574–82. 3. Viswanathan MN, Scheinman MM, Badhwar N. A new diagnostic maneuver to differentiate atrioventricular nodal reentrant tachycardia from junctional tachycardia: a difficult distinction [abstract]. Heart Rhythm 2007;4(5):S288. 4. 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; 52:1711–7. 5. Hamdan MH, Badhwar N, Scheinman MM. Role of invasive electrophysiologic testing in the evaluation and management of adult patients with focal junctional tachycardia. Card Electrophysiol Rev 2002; 6(4):431–5.
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KEY POINTS
CLINICAL PRESENTATION A 48-year-old woman presented for evaluation and management of daily palpitations, lasting for hours. The palpitations started when the patient was in her 20s, but gradually progressed, such that in the months before presentation the palpitations occurred for up to 8 hours a day on a daily basis. The palpitations occurred irrespective of whether the patient was at rest or exercising. Physical examination, laboratory studies, and echocardiogram were normal. Ambulatory monitoring identified multiple episodes of palpitations correlating with a narrow complex tachycardia occurring throughout the day (Fig. 1). The patient was subsequently referred for electrophysiology study and catheter ablation.
catheter was placed in the coronary sinus. Normal atrial-His and His-ventricular intervals were recorded in sinus rhythm. Ventricular-atrial conduction was present with ventricular pacing; there was a concentric retrograde atrial activation pattern. A sustained A on V narrow QRS complex tachycardia at a cycle length of 386 to 573 milliseconds was induced with ventricular overdrive pacing (VOD), single ventricular extrastimulus testing, and atrial overdrive pacing from the coronary sinus on and off isoproterenol infusion up to 10 mg/min (Fig. 2). Significant cycle length variation was observed with variations in isoproterenol dosing. Spontaneous variations in the His-His interval preceded changes in the atrial-atrial and ventricular-ventricular intervals during tachycardia (Fig. 3).
ELECTROPHYSIOLOGY STUDY Tachycardia Induction
QUESTION
Quadripolar electrode catheters were positioned in the high right atrium, right ventricular apex, and the His bundle region. A decapolar electrode
What is the differential diagnosis for a narrow QRS complex tachycardia? How can the tachycardia mechanism be established?
Section of Cardiac Electrophysiology, Division of Cardiovascular Medicine, University of Utah Health Sciences Center, 30 North 1900 East, Room 4A-100 SOM, Salt Lake City, UT 84132, USA E-mail address: [email protected] Card Electrophysiol Clin 8 (2016) 61–65 http://dx.doi.org/10.1016/j.ccep.2015.10.005 1877-9182/16/$ – see front matter Ó 2016 Elsevier Inc. All rights reserved.
cardiacEP.theclinics.com
Junctional tachycardia (JT) is rare cause of supraventricular tachycardia. The intracardiac activation sequence is similar to atrioventricular nodal reentrant tachycardia (AVNRT). Premature atrial contractions inserted during tachycardia can help distinguish JT from AVNRT. As noted in this case, slow pathway ablation for JT may not always be effective for termination of JT. Activation mapping during JT identified a low-amplitude potential in the region of the coronary sinus ostium and the inferior margin of the triangle of Koch that marked the successful ablation site for JT.
62
Han
Fig. 1. (A) Tachycardia initiation on ambulatory monitor. (B) Tachycardia with atrioventricular dissociation.
MANEUVERS DURING TACHYCARDIA The differential diagnosis of a narrow QRS complex tachycardia with a ventricular-atrial (VA) interval of 0 milliseconds includes atrioventricular nodal reentrant tachycardia (AVNRT), junctional tachycardia (JT), and circus movement tachycardia using a concealed nodofascicular (NF) accessory pathway.1 VOD during tachycardia entrained the tachycardia and produced a VAHV (Ventricle-Atrial-HisVentricle) response, ruling out atrial tachycardia. His refractory premature ventricular contractions during the tachycardia did not affect the subsequent A within the confines of wobble noted in tachycardia.2 This finding argues against concealed NF accessory pathway–mediated tachycardia. Single early programmed atrial extrastimuli advanced the subsequent QRS via conduction down the fast atrioventricular nodal pathway with continuation of tachycardia (Fig. 4). Late premature atrial contractions (PACs) did not
delay or terminate the tachycardia via the slow pathway.3,4 With AVNRT, late premature atrial contractions are expected to advance the tachycardia via conduction down the slow pathway; early premature atrial contractions that conduct down the fast pathway should terminate tachycardia.
MAPPING AND ABLATION A 4-mm quadripolar radiofrequency ablation catheter was used for mapping and ablation. All lesions were delivered in the temperature-controlled mode at 50 W with a 60 C temperature limit for up to 60 seconds. For ablation of the JT, we decided to proceed with a stepwise approach with inducibility testing after each series of ablations. First, we targeted the slow pathway during sinus rhythm. Two radiofrequency lesions were in the slow pathway region with junctional beats observed during ablation. The JT remained inducible (the 2 red lesions in Fig. 5).
Incessant Tachycardia
Fig. 2. (A) Tachycardia initiation with ventricular overdrive pacing. Ventricular overdrive pacing at cycle length of 400 milliseconds induced a narrow QRS complex tachycardia with a VAHV initiation. (B) Tachycardia initiation with atrial overdrive pacing. Atrial overdrive pacing the proximal coronary sinus (CS 9,10) at 550 milliseconds induced a narrow QRS complex tachycardia with a AHHA (atrial-His-His-atrial) initiation pattern.
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Fig. 3. Spontaneous variation in tachycardia cycle length. Spontaneous variations in the tachycardia cycle length were noted with variations in the His-His interval preceding changes in the atrial-atrial and ventricular-ventricular intervals.
Fig. 4. Spontaneous right atrial premature atrial contraction during tachycardia. A spontaneous late right atrial premature atrial contraction advances the next QRS via conduction down the fast atrioventricular nodal pathway with continuation of tachycardia that rules out AVNRT.
Incessant Tachycardia Fig. 5. CARTO activation map of JT in left anterior oblique cranial view. Activation mapping of JT after 2 slow pathway ablations and 3 ablations on the roof of the proximal coronary sinus failed to terminate the JT. The lesion at the successful ablation site identified a low-amplitude potential that preceded the His potential during tachycardia. Ablation at this site rendered the tachycardia noninducible.
Next, during tachycardia we mapped the earliest atrial activation and delivered 3 lesions at the roof of the proximal coronary sinus.5 The tachycardia remained inducible at this point. During tachycardia, we performed mapping to identify a prepotential during the tachycardia. As noted in Fig. 5, we identified a low-amplitude potential at the roof of the coronary sinus ostium that preceded the His potential during tachycardia. A single radiofrequency lesion delivered at this site terminated the tachycardia and rendered it noninducible.
SUMMARY JT is rare cause of supraventricular tachycardia. The intracardiac activation sequence is similar to AVNRT. Premature atrial contractions inserted during tachycardia can help distinguish JT from AVNRT. As noted in this case, slow pathway ablation for JT may not always be effective for termination of JT. Activation mapping during JT identified a low-amplitude potential in the region of the coronary sinus ostium and the inferior margin of the triangle of Koch that marked the successful ablation site for JT.
REFERENCES 1. Hamdan MH, Page RL, Scheinman MM. Diagnostic approach to narrow complex tachycardia with VA block. Pacing Clin Electrophysiol 1997;20:2984–8. 2. Knight BP, Ebinger M, Oral H, et al. Diagnostic value of tachycardia features and pacing maneuvers during paroxysmal supraventricular tachycardia. J Am Coll Cardiol 2000;36:574–82. 3. Viswanathan MN, Scheinman MM, Badhwar N. A new diagnostic maneuver to differentiate atrioventricular nodal reentrant tachycardia from junctional tachycardia: a difficult distinction [abstract]. Heart Rhythm 2007;4(5):S288. 4. 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; 52:1711–7. 5. Hamdan MH, Badhwar N, Scheinman MM. Role of invasive electrophysiologic testing in the evaluation and management of adult patients with focal junctional tachycardia. Card Electrophysiol Rev 2002; 6(4):431–5.
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