Dual Antegrade Response Tachycardia Induced Cardiomyopathy DEEPAK GABA, BEHZAD B. PAVRI, ARNOLD J. GREENSPON, and REGINALD T. HO From the Department of Medicine, Division of Cardiovascular Medicine, Thomas Jefferson University Hospital, Philadelphia, Pennsylvania
GABA, D., ET AL.: Dual Antegrade Response Tachycardia Induced Cardiomyopathy. We report a rare case of tachycardia induced cardiomyopathy resulting from nearly incessant dual antegrade response tachycardia. Criteria necessary for sustaining dual antegrade responses are discussed, including: (1) sufficient antegrade dissociation of the AV node; (2) absence of retrograde conduction over each AV nodal pathway following antegrade conduction over its counterpart; (3) difference between fast and slow pathway conduction times exceeding His-Purkinje refractoriness; and (4) critical timing of sinus impulses relative to preceding AV nodal conduction. Both the arrhythmia and cardiomyopathy were successfully treated by slow pathway ablation. (PACE 2004; 27:533–536) dual antegrade response tachycardia, tachycardia induced cardiomyopathy Introduction A dual antegrade response (DAR) where a single atrial input generates two ventricular complexes, can result from simultaneous conduction over the fast (FP) and slow (SP) pathways of the AV node, and can be an unusual cause of tachycardia, which is twice the sinus rate.1 Sufficient tachycardia to induce cardiomyopathy is extremely rare.2 Case Report A 39-year-old man presented with long standing palpitations. Echocardiography revealed an ejection fraction (EF) of 20%. Coronary angiography was normal. His 12-lead electrocardiogram (ECG) is shown in Figure 1. Electrophysiological Study The patient was brought to the electrophysiological laboratory in the postabsorptive, drug- free state where three quadripolar catheters were inserted under local anesthesia into the right femoral vein and positioned along the high right atrium (HRA), His bundle region, and right ventricular apex (RVA). Burst pacing was delivered from the HRA and RVA. Atropine (1 mg IV) was administered. A 4-mm tip Blazer II ablation catheter (EP Technologies; San Jose, CA, USA) was then positioned along the posteroseptal right atrium where delivery of radiofrequency energy to the SP of the AV node resulted in immediate disappearance of tachycardia.
Address for reprints: Reginald T. Ho, M.D., 925 Chestnut Street, Mezzanine Level, Philadelphia, PA 19107. Fax: (215) 923-2539; e-mail:
[email protected] Received May 23, 2003; accepted July 15, 2003.
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Results ECG The 12-lead ECG demonstrates a narrow complex tachycardia with sinus P waves totaling half the number of QRS complexes. All but one P wave (arrow) is followed by two PR intervals (160 ms and 460 ms) and QRS complexes suggesting dual conduction over a longitudinally dissociated AV node. Electrophysiological Study Baseline
Spontaneous dual antegrade response tachycardia (DART) was observed during sinus cycle lengths (SCL) 850 ms to 1050 ms. Atrial Stimulation
Pacing cycle lengths (PCL, 900 ms to 700 ms) resulted in DAR (Fig. 2A,B). The AH interval of the fast (AHFP ) and slow (AHSP ) pathways measured 79 ms and 385 ms, respectively (AHSP − AHFP = 306 ms). The interval from the end of SP conduction to subsequent atrial activation (HSP A interval) was long: 520 ms and 323 ms at PCL 900 ms and 700 ms, respectively. HV prolongation and alternating bundle branch block (BBB) were observed at PCL 900 ms. Shorter HV intervals and less aberration occurred at PCL 700 ms. PCL 600 ms resulted in sustained SP conduction (HSP A interval = 196ms, Fig. 2C). PCL 400 ms resulted in sustained FP conduction. The FP Wenckebach cycle length measured 390 ms. Atropine (1 mg)
At a baseline SCL 860 ms, DAR was accompanied again by alternating BBB (Fig. 3A). The AHFP and SP measured 69 ms and 370 ms, respectively (AHSP − AHFP = 301 ms). Atropine shortened the SCL over several minutes. SCL 580 ms resulted in DAR but aberration was less prominent (Fig. 3B).
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Figure 1. 12-lead electrocardiogram of dual antegrade response tachycardia.
DAR followed long HSP A intervals (497 ms and 245 ms at SCL 860 ms and 580 ms, respectively). SCL 460 ms resulted in sustained SP conduction (HSP A interval = 106 ms) followed by sustained FP conduction when the SCL reached 360 ms (Fig. 3C, D). Ventricular Stimulation
VA conduction was absent at baseline and following atropine administration. Discussion Although the determinants for isolated DAR have been described, the key factors necessary to sustain DART and induce cardiomyopathy are less well established.2−6 The rarity of sustained DART stems from its requirement for the simultaneous coexistence of multiple important factors, including: (1) sufficient dissociation of the AV node (AHSP -AHFP interval); (2) absence of retrograde conduction over each AV nodal pathway following antegrade conduction over its counterpart; 534
(3) HSP -HFP interval > His Purkinje effective refractory period (ERP); and (4) a critical HA interval.1 Sufficient disparity between SP and FP conduction times (AHSP -AHFP interval) allow their simultaneous conduction and then sequential activation of the His-Purkinje system (HPS) following each sinus beat. Reduction of this disparity prevents DAR. AHFP intervals, which are too long, result in late retrograde penetration of the SP rendering it refractory upon arrival of its own antegrade impulse. AHSP intervals, which are too short, provide insufficient delay to allow recovery of distal tissue rendered refractory by concealment from the FP. Conversely, enhanced FP conduction and long SP conduction times facilitate DAR.3−6 Previous cases of DAR reported AHSP > 400 ms; but perhaps more importantly, the AHSP –AHFP interval exceeded 300 ms.1,2,4−8 In the present case, the AHSP measured 370 ms and 385 ms during sinus rhythm and atrial pacing, respectively; but the AHSP –AHFP interval exceeded 300 ms because of relatively rapid FP conduction.
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DUAL ANTEGRADE RESPONSE TACHYCARDIA INDUCED CARDIOMYOPATHY
Figure 2. (A-D) Various manifestations of dual AV node physiology at different atrial PCL’s. (A) PCL = 900 ms: DART with alternating BBB. (B) PCL = 700 ms: DART with less aberration. (C) PCL = 600 ms: sustained SP conduction. (D) PCL = 400 ms: sustained FP conduction. See text for details. PCL = Pacing cycle length; His = His bundle; H FP = His bundle electrogram after FP conduction; H SP = His bundle electrogram after SP conduction.
Figure 3. (A-D) Various manifestations of dual AV node physiology at different SCL’s after atropine administration. (A) Baseline SCL = 860 ms: DART with alternating BBB. (B) SCL = 580 ms: DART with less aberration. (C) SCL = 460 ms: sustained SP conduction. (D) SCL = 360 ms: sustained FP conduction. See text for details. Arrows denote P waves. His = His bundle; H FP = His bundle electrogram after FP conduction; H SP = His bundle electrogram after SP conduction.
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Antegrade conduction over either pathway must be followed by retrograde block in the counterpart pathway in order to prevent retrograde atrial activation from interrupting sinus driven tachycardia.5,6 Retrograde block in the FP after SP conduction may be due to functional refractoriness following conduction of its own impulse. Intact retrograde FP conduction would result in either AV nodal echoes or AVNRT.2,4 Retrograde block in the SP may be preceded by penetration from the FP; and is suggested by longer AHSP during DAR than during exclusive SP conduction.2 VA conduction was absent in the present case. The HSP -HFP interval resulting from dual AV nodal transmission must exceed the ERP of the HPS.2 HSP -HFP intervals shorter than the RRP or ERP result in intra- and infrahisian conduction delay or block, respectively. Slow SCL and PCL exposes the HPS to longer diastolic intervals, increases subsequent refractoriness, and facilitates aberration. In the present case, a unique pattern of alternating BBB occurred when the HSP -HFP measured 301 and 306 ms during sinus and atrial pacing, respectively. Alternating BBB results from concealed, transeptal, retrograde conduction and penetration from the conducting bundle into the blocked bundle. Late retrograde activation of the blocked bundle shortens its subsequent diastolic interval, reduces its refractoriness, and allows sub-
sequent activation following SP conduction. Conversely, exposure of the conducting bundle to a longer diastolic interval increases its refractoriness and favors subsequent block. The timing of each sinus impulse relative to preceding AV nodal conduction (HA interval) is critical to sustain DART. P waves following short HSP A intervals encounter a partially or fully refractory FP rendered inexcitable by concealment from the SP. Prolongation of the AHFP interval because of partial refractoriness, results in late penetration by the FP into the SP, reduction of the AHSP -AHFP interval, and loss of DAR. An example of this phenomenon is the fourth P wave on the ECG which follows the shortest RP interval on the tracing and conducts slowly only over the FP (Fig. 1, arrow). P waves encountering a fully refractory FP conduct only over the SP. 9 Earlier timed P waves (HSP A intervals measuring 100 ms) can block in either the upper common pathway, or simultaneously in both the FP and SP, resulting in 2:1 AV block with DAR following alternate P waves.2 P waves occurring too quickly following FP conduction, as a result of rapid sinus or atrial pacing rates, preempt SP conduction and conduct only over the FP. In this patient, nearly incessant DART induced cardiomyopathy. Successful ablation of the SP resulted in immediate disappearance of tachycardia. At 2 month follow-up, he was asymptomatic and his EF had improved to 45%.
References 1. Csapo G. Paroxysmal nonreentrant tachycardia due to simultaneous conduction in dual atrio-ventricular pathways. Am J Cardiol 1979; 43:1033–1045. 2. Anselme F, Frederiks J, Boyle N, et al. An unusual cause of tachycardia-induced myopathy. PACE 1996; 19:115–119. 3. Shimizu A, Fukatani M, Centurion O, et al. Double response of the ventricle during transient entrainment in a common atrioventricular nodal reentrant tachycardia. PACE 1993; 16:39–45. 4. Gomes J, Kang P, Kelen G, et al. Simultaneous anterograde fast-slow atrioventricular nodal pathway conduction after procainamide. Am J Cardiol 1980; 46:677–684. 5. Lin F, Yeh S, Wu D. Determinants of simultaneous fast and slow pathway conduction in patients with dual atrioventricular nodal pathways. Am Heart J 1985; 109:963–970.
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Sakurada H, Sakamoto M, Hiyoshi Y, et al. Double ventricular response to a single atrial depolarization in a patient with dual AV nodal pathways. PACE 1992; 15:28–33. Sutton F, Lee Y. Supraventricular nonreentrant tachycardia due to simultaneous conduction through dual atrioventricular nodal pathways. Am J Cardiol 1983; 51:897–900. Nakao K, Hayano M, Iliev I, et al. Double ventricular response via dual atrioventricular nodal pathways resulting with nonreentrant supraventricular tachycardia and successfully treated with radiofrequency catheter ablation. J Electrocardiol 2001; 34:59– 63. Wu D, Denes P, Dhingra R, et al. Determinants of fast- and slowpathway conduction in patients with dual atrioventricular nodal pathways. Circ Res 1975; 36:782–790.
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