Reprinted with permission from JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Volume 12, No. 1, January 2001 Copyright ©2001 by Futura Publishing Company, Inc., Armonk, NY 10504-0418
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Concealed Accessory Pathway with Long Conduction Times and Incremental Properties: A Case Report ´ RCIO GERKEN, M.D., EDUARDO BACK STERNICK, M.D., LUIS MA and EPOTAMENIDES GOOD GOD, M.D. From the Arrhythmia Unit, Department of Cardiology, Hospital Vera Cruz, Belo Horizonte, Minas Gerais, Brazil
Concealed AP with Slow and Incremental Conduction. We report a peculiar form of
permanent junctional reciprocating tachycardia that occurs only during daytime and physical activity. ECG obtained during tachycardia showed an unusual progressive shortening of the ventriculoatrial (VA) interval that was maximal at the rst complex and shortest at the last one before block occurred, always at the accessory pathway level. This phenomenon has not been previously described and appears to be a reverse type of Wenckebach block. It was observed during salvos of spontaneous tachycardia and could be reproduced by right ventricular pacing. The accessory pathway was ablated successfully at the right posteroseptal region, close to the coronary sinus ostium. After ablation, there was no VA conduction, and tachycardia did not recur during a 9-month follow-up period. (J Cardiovasc Electrophysiol, Vol. 12, pp. 103-107, January 2001) accessory pathway, permanent junctional reciprocating tachycardia, slow and incremental conduction
Introduction Accessory pathways exhibiting slow conduction times and decremental properties have been the subject of many studies on pathophysiology, anatomy, and electrophysiology, as well as the relationship with the permanent tachycardia that is its clinical expression.1 The slow and decremental conduction initially were thought to be due to an accessory AV node-like structure.2 However, pathologic examination of one such pathway disclosed an accessory AV connection with a tortuous path and no characteristics of AV nodal tissue.3 Those pathways typically are located in the vicinity of the coronary sinus ostium, but other sites have been reported.4 It also is well known that antiarrhythmic drugs are not effective in treating permanent junctional reciprocating tachycardia (PJRT), and tachycardiomyopathy may occur in some patients.5 The aim of this report is to describe an accessory pathway with long conduction times and incremental conduction, an observation that has not yet been reported. Case Report A 21-year-old man was admitted to the Arrhythmia Unit of the Department of Cardiology of Hospital Vera Cruz for invasive electrophysiologic study. He had a history of pal-
Address for correspondence: Eduardo B. Sternick, M.D., Rua Correias 281/301, 30315340, Belo Horizonte, Minas Gerais, Brazil. Fax: 55-3131-32870103; E-mail:
[email protected] Manuscript received 24 April 2000; Accepted for publication 20 September 2000.
pitations since the age of 6 years. The symptom was related to exercise (he used to play soccer) and emotional stress; it had never occurred during rest. Physical examination revealed no abnormal ndings. The 12-lead ECG obtained during sinus rhythm showed rst-degree AV block. Transthoracic echocardiogram was normal. Holter monitoring disclosed frequent nonsustained salvos of narrow-complex tachycardia with long RP* intervals that lasted from 3 to 20 beats and always ended with missed P waves. Tachycardia occurred only during the daytime, and episodes started without premature beats. Careful assessment of RP* intervals showed a “reverse Wenckebach” phenomenon, i.e., RP* intervals were maximum at the beginning of the salvos and gradually decreased to block (Fig. 1). He was taking no cardioactive drugs. He underwent electrophysiologic study while in the fasting state and was given mild sedation with intravenous diazepam. Electrophysiologic Study Six-French quadripolar catheters (DAIG, Minnetonka, MN, USA) were positioned at the right lateral right atrium, coronary sinus, and right ventricular apex, and a 4-mm tip de ectable 7-French EPT ablation catheter (EP Technologies, Boston Scienti c Corp., Sunnyvale, CA, USA) was rst positioned over the His bundle. The stimulation protocol included up to three extrastimuli during sinus rhythm, and atrial and ventricular pacing at cycle lengths of 500 and 430 ms. Results Basic intervals were as follows: RR 5 900 to 1,100 msec, PA 5 20 msec, AH 5 180 msec, HV 5 40 msec, V 5 80 msec, Wenckebach point 5 550 msec. Effective refractory period (ERP) of the right atrium 5 210 msec, ERP of the AV node 5 370 msec, ERP of the right ventricle 5 230 msec, and corrected sinus node recovery time (CSRT) 5
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Figure 1. Narrow complex tachycardia showing 1:1 VA relationship and long VA conduction time that gradually shortens until block. Sinus rhythm with rst-degree AV block.
350 msec. There was no ventriculoatrial (VA) conduction at the very beginning of the procedure. However, after longer periods of right ventricular pacing at a cycle length of 600 msec, VA conduction was present with earliest activation time at the coronary sinus ostium. The AV conduction curve was not discontinuous. Retrograde conduction showed no typical Wenckebach periodicity, but rather a “reverse” Wenckebach with a gradually shorter VA interval until block occurred (Fig. 2). After low-dose intravenous isoproterenol infusion was started, tachycardia could be induced by ventricular pacing. Cycle length ranged from 440 to 390 msec (Fig. 3). At this point, tachycardia was always non-sustained and terminated with VA block after 3 to 12 beats. The longest VA conduction time was 180 msec and the shortest (before termination) was 100 msec. While increasing isoproterenol dripping, tachycardia became incessant, spontaneously reinitiating after some sinus beats, and VA conduction time became shorter, ranging from 85 to 120 msec at the coronary sinus ostium (Fig. 4). Differen-
tial diagnosis of the tachycardia was an important part of the procedure, because many clinical and ECG aspects did not favor the diagnosis of PJRT. First-degree AV nodal block could be due to slow pathway conduction, and atypical AV nodal reentry had to be ruled out. AH interval was still prolonged after isoproterenol. In our experience, the absence of VA conduction at baseline ventricular pacing is not a common feature of accessory pathways, and that was consistent with AV nodal reentry as well. The RP*/P*R relationship during tachycardia did not suggest PJRT once RP* was shorter than P*R. Nonetheless, the AV node anterograde conduction curve was not discontinuous. After intravenous isoproterenol, ventricular premature beats delivered at the time of His-bundle refractoriness could advance atrial activation by 20 msec, with the same atrial depolarization sequence as that seen during tachycardia. Catheter ablation was accomplished with radiofrequency current applied at the coronary sinus ostium (three pulses). After ablation, there was no VA conduction. The patient
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Figure 2. Right ventricular pacing at a cycle length of 500 msec with long VA conduction time ( rst VA time 5 310 msec) showing “reverse” Wenckebach with shortening of the VA interval (earliest site at coronary sinus ostium) until block occurs at the seventh beat.
has remained arrhythmia-free during a 9-month follow-up period.
Discussion It is well known that, in the setting of PJRT, the accessory pathway shows a particular behavior charac-
terized by slow conducting times and decremental properties. The most likely explanation is slow conduction in a tortuous accessory pathway and anisotropic conduction in the bypass tract and its connection to atrial and ventricular myocardium.6 In this unique case, we did not observe decremental conduction, but rather incremental
Figure 3. Induction of tachycardia by ventricular pacing at a cycle length of 600 msec. Asterisk marks a fusion atrial beat (sinus 1 accessory pathway conduction). The “reverse” Wenckebach also can be seen here. VA conduction time began with 160 msec and shortened until block occurred in the accessory pathway.
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Figure 4. Tachycardia became faster and incessant, and the VA interval progressively shortened as isoproterenol dosing was increased.
conduction, which was expressed as a reverse type of Wenckebach periodicity of retrograde conduction over the accessory pathway either during tachycardia or ventricular pacing. Another striking feature of this pathway was the absence of VA conduction at baseline (rest and
sedated state). This feature was reported by Chien et al.,7 who pointed out that the conduction properties of this pathway are very sensitive to changes in autonomic tone. Their observation matched ours, as we observed that, at baseline, a dominant vagal drive modulated both AV and
Figure 5. (A) Asymmetric nonuniformity that might cause unidirectional block. Conduction from left to right blocks at the region where there is an abrupt increase in ber diameter (membrane potentials 1 and 2). The transition from small to large cable at the opposite end is gradual. An impulse conducting from right to left can still depolarize the membrane to threshold despite a gradual increase in membrane area (action potentials 3/4). (B) Con guration of a myocardial ber where speeding up of conduction is likely to occur as the impulse travels through it from its larger to smaller portion (action potentials 5 and 6). (C-1) Asynchronous arrival of wavefronts in “a” and “b” resulting in lack of summation 5 long conduction time. (C-2) Not quite simultaneous arrival in “a” and “b” leading to partial summation 5 shorter conduction time. (C-3) Simultaneous arrival of wavefronts 5 complete summation and shortest conduction time.
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VA conduction; infusion of isoproterenol restored VA conduction; and tachycardia could be induced. Increasing isoproterenol dosage led to sustained tachycardia, and VA conduction time was shortened from a maximum of 160 msec to 85 msec (at the site of successful ablation). Reverse Wenckebach was still present during maximal adrenergic stress, although less pronounced. An accessory pathway with slow and incremental conduction as a phenomenon has not yet been reported, but Wit and Janse,8 who discussed geometric factors causing unidirectional block, predicted speeding up of conduction velocity in a myocardial ber. According to their view, the conduction velocity of an impulse passing abruptly from a ber of small diameter to one of larger diameter transiently slows because there is more membrane for the current to depolarize to threshold if conduction of the impulse is to continue. In the opposite direction, it can be predicted that “conduction velocity will speed transiently as the impulse moves from a larger to a smaller cable because the small sink for axial current results in more rapid depolarization of the membrane threshold.” We can speculate that a peculiar insertion of the accessory pathway into the right atrium consistent with the larger-to-smaller cable con guration (Fig. 5, panels A and B) might have caused incremental conduction. An alternative and more plausible explanation based on a different structure of the accessory bundle in which two bundles merge (Fig. 5, panel C), conduction velocity would be faster, depending on synchronous arrival of wavefronts “a” and “b.” Reentrant arrhythmias require slowing of impulse conduction and/or unidirectional block and are dependent on factors such as anisotropy, and uncoupling of bers as a result of either separation or interposition of a poor conducting medium (connective tissue, ischemic cells).
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What is exciting about this case is precisely the phenomenon of transient speeding of the conduction velocity, which is highly unexpected in a stable reentrant circuit and has never before been reported in an accessory pathway. The presence of prolonged AV nodal conduction, even during adrenergic stress, might have played a role in supporting reentry in the circuit. References 1. Gallagher JJ, Pritchett ELC, Sealy WC, Kasell J, Wallace G: The preexcitation syndromes. Prog Cardiovasc Dis 1978;20:285-327. 2. Coumel P, Cabrol C, Fabiato A, Gourgon R, Salma R: Tachycardie permanente par rythme reciproque. Arch Mal Coeur 1967;60: 1830-1864. 3. Critelli G, Gallagher JJ, Monda V, Coltorti F, Scherillo M, Rossi L: Anatomic and electrophysiologic substrate of the permanent junctional reciprocating tachycardia. J Am Coll Cardiol 1984;4: 601-610. 4. Okumura K, Henthorn RW, Epstein AE, Plumb VJ, Waldo A: “Incessant” atrioventricular (AV) reciprocating tachycardia utilizing left lateral AV bypass pathway with a long retrograde conduction time. PACE 1986;9:332-342. 5. Packer DL, Bardy CH, Worley SJ, Smith MS, Cobb FR, Coleman E, Gallagher JJ, German LD: Tachycardia induced cardiomyopathy: A reversible form of left ventricular dysfunction. Am J Cardiol 1986;57:563-570. 6. Spach MS, Miller WT III, Geselowitz BB, Barr RC, Kootsey JM, Johnson EA: The discontinuous nature of propagation in normal canine cardiac muscle. Evidence for recurrent discontinuities on intracellular resistance that affect the membrane currents. Circ Res 1981;48:39-54. 7. Chien WW, Cohen TJ, Lee MA, Lesh MD, Grif n JC, Schiller NB, Scheinman MM: Electrophysiological ndings and long-term follow-up of patients with the permanent form of junctional reciprocating tachycardia treated by catheter ablation. Circulation 1992; 85:1329-1336. 8. Wit AL, Janse MJ: The Ventricular Arrhythmias of Ischemia and Infarction: Electrophysiological Mechanisms. Futura Publishing Co., Armonk, NY, 1993, pp. 92-94.
