Adenosine-Dependent Concealed Accessory Pathway

CASE REPORT Adenosine-Dependent Concealed Accessory Pathway DIANA TINT, M.D., PH.D., CSABA KUN, M.D., ILDIKO BEKE, M.D., and ZOLTAN CSANADI, M.D., PH.D. From the Institute of Cardiology, University of Debrecen, Debrecen, Hungary Adenosine is routinely used during ventricular pacing to exclude the persistence of retrograde accessory pathways conduction after radiofrequency (RF) ablation procedures by blocking conduction over the atrioventricular node. This is the first report of an adenosine-dependent concealed accessory pathway demonstrating transient conduction only after adenosine administration. Our findings may have potential clinical implications in reducing recurrence after accessory pathway ablation. Furthermore, it may add relevant information regarding the ability of adenosine to elicit dormant conduction after RF ablation, a phenomenon that has acquired considerable interest in the era of pulmonary vein isolation. (PACE 2011; 1–3) ablation, accessory pathway, decremental conduction Introduction Adenosine is known to produce a transient conduction block over the atrioventricular (AV) node and also over some atypical AV accessory pathways (APs) that exhibit decremental conduction properties, which account for less than 10% of the APs. Conduction in the vast majority of APs is not depressed, however, and adenosine is routinely used during ventricular pacing to exclude the persistence of retrograde AP conduction after radiofrequency (RF) ablation.1 Indeed, adenosine improves the conduction by the shortening effective refractory period (ERP) and functional refractory period (FRP) of typical APs. An AP demonstrating retrograde conduction only after adenosine administration (adenosinedependent AP) may be a new observation.2 Case Report A 27-year-old man was admitted for a repeat electrophysiology study because of paroxysmal palpitations and documented narrow QRS complex tachycardia. Two APs on the left side and one on the right had been ablated 6 months earlier, with no AP conduction and inducible tachycardia at conclusion. At the present admission, his electrocardiogram (ECG) showed a sinus rhythm at 80 beats/min, a PR interval of 180 msec, and narrow QRS (80 msec) complexes with no overt preexcitation. A standard electrophysiology (EP) Address for reprints: Zoltan Csanadi, M.D., Ph.D., 22 Moricz Zs. krt. Debrecen, Hungary H-4032. Fax: 36-52-255280; e-mail: [email protected] Received October 18, 2010; revised December 1, 2010; accepted December 23, 2011. doi: 10.1111/j.1540-8159.2011.03063.x study was performed with multipolar catheters positioned in the right ventricle (RV), the coronary sinus (CS), and the His bundle. No anterograde AP conduction was revealed. Orthodromic AV reentrant tachycardia (AVRT) with a cycle length of 350 msec utilizing a left lateral AP was reproducibly induced with ventricular and CS extrastimuli. The earliest atrial activation during AVRT was found at CS electrodes 5–6 with a local ventriculoatrial (VA) time of 75 msec. The transseptal approach was used and after two RF applications (25 W, 60◦ C, 60 s) at the site of the earliest atrial electrogram (Fig. 1), the retrograde activation in the CS electrodes became centric and the retrograde conduction decremental during RV pacing. No arrhythmia was inducible after the ablation. To demonstrate the absence of any retrograde AP conduction, a rapid intravenous bolus of adenosine (6 mg) was administered during continuous RV stimulation at 400 msec. Unexpectedly, this resulted in reappearance of the eccentric retrograde activation pattern, with the earliest atrial electrogram and the shortest local VA time at CS poles 5–6 and 3–4 (Fig. 2). This was a reproducible phenomenon lasting for approximately 10–15 s after each adenosine bolus. Although sustained arrhythmia was not inducible and the clinical significance of these phenomena was unknown, further RF pulses were deployed on an anatomical basis from CS poles 5–6 to 3–4 until no indication of any AP conduction and transient VA block was revealed with adenosine. The patient was free of any arrhythmia at the 6month follow-up. Discussion Adenosine has been routinely used for the differentiation of conduction over the AV node versus an accessory AV connection on the basis  C 2011 Wiley Periodicals, Inc. C 2011, The Authors. Journal compilation  PACE 2011 1 TINT, ET AL. reported two cases in which preexcitation after RF ablation was transiently unmasked by adenosine. They postulated two possible mechanisms by which adenosine elicited AP conduction: (1) AP conduction rendered slower by injury from the RF energy became manifest after slowing or blocking of the AV node; (2) retrograde penetration to AP was transiently abolished by blocking anterograde conduction over the AV node. Kabell et al. investigated the change in retrograde ERP of APs in response to adenosine in 17 patients and found a shortening of at least 30 msec in 11 patients after a 6-mg, and in another four patients after a 12mg, rapid intravenous bolus. This shortening in ERP was not prevented in any of the three patients who underwent repeat testing under β blockade. It was concluded that, although reflex activation of the sympathetic nervous system with a rapid increase in catecholamine levels may potentially contribute to a decrease in refractoriness, this may also result from a direct effect of adenosine, similarly as observed in working atrial myocytes.2 Our case is unique in that the AP conduction was most likely dependent on adenosine and was unmasked independently of any alteration in AV node conduction potentially resulting from the drug. Whether this phenomenon could have been demonstrated after the previous procedure is unknown, as adenosine was not administered at that time. There are two possiblities concerning the site of transient retrograde conduction: (1) there was a second AP located somewhat more laterally to the one ablated first. This explanation is supported by the evidence that adenosine can improve AP conduction. (2) The reappearence of Figure 1. Site of ablations of the APs. The position of the ablation catheter (Abl) is shown at the site of the first two ablations that apparently eliminated AP conduction. The red dots indicate the area of further ablations after the adenosine test. of its different electrophysiological effects on these structures. Further, the use of adenosine to elicit APs that were viable but conducted more slowly due to modification by RF applications was advocated early in the ablation era, with a view to reducing late recurrences after apparently successful catheter ablations. Engelstein et al.3 Figure 2. Administration of adenosine 6 mg intravenously after the first two ablations. During continuous RV pacing, abrupt changes in the activation sequence and VA times can be observed. 2 2011 PACE ADENOSINE-DEPENDENT ACCESSORY PATHWAY in the PV cells that were depolarized and rendered nonexcitable by RF current. The RMP after RF application but before adenosine exposure was significantly more negative in dormant veins than is those with a definite conduction block.5,6 In our patient, the long-term clinical significance of this adenosine-dependent AP conduction was not clear, but we felt that total elimination was the safer procedure, especially during a repeat ablation. Although RF ablation of APs has become a very successful mode of treatment, offering a more than 90% cure in experienced hands, recurrences after an apparently successful procedure do still occur. Whether the routine use of adenosine after AP ablations could eliminate or significantly reduce these long-term failures requires further evaluation. AP conduction only after adenosine administration was related to RF injury of the originally targeted AP. The use of adenosine to elicit dormant conduction due to RF applications has become a common practice in the era of pulmonary vein isolation (PVI). In some reports, the rate of reconnection after an apparently successful PVI is over 30%, suggesting the long-term instability of lesions created by RF energy.4 The mechanism of this acquired adenosine dependency was recently studied in canine left atrium-PV preparations. Before ablation, adenosine shortened the action potential duration in both the atrial working myocardium and PV sleeves, though significant hyperpolarization of the resting membrane potential (RMP) was observed exclusively in PVs. After ablation, adenosine also hyperpolarized the RMP References 1. Walker KW, McAnulty JH, Kron J, Silka MJ, Halperin BD. Unmasking accessory pathway conduction with adenosine-induced atrioventricular nodal block after radiofrequency catheter ablation. Chest 1993; 104:1614–1616. 2. Kabell G, Corbisiero R, Miller GD, Fitzgerald TF, Cook JR, Kirchhoffer JB. Effects of adenosine on retrograde refractoriness of accessory atrioventricular connections. Am J Cardiol 1998; 82:680–683. 3. Engelstein ED, Wilber D, Wadas M, Stein KM, Lippman N, Lerman BB. Limitations of adenosine in assessing the efficacy of radiofrequency catheter ablation of accessory pathways. Am J Cardiol 1994; 73:774–779. PACE 4. Trittoa M, De Ponti R, Salerno-Uriarteb JA, Spadacinia G, Marazzib R, Morettia P, Lanzotti M. Adenosine restores atrio-venous conduction after apparently successful ostial isolation of the pulmonary veins. Eur Heart J 2004; 25:2155–2163. 5. Ehrlich JR, Cha T-J, Zhang L, Chartier D, Melnyk P. Cellular electrophysiology of canine pulmonary vein cardiomyocytes: Action potential and ionic current properties. J Physiol 2003; 551:801– 813. 6. Datino T, Macle L, Qi X, Maguy A, Comtois P, Chartier D, Guerra PG, et al. Mechanisms by which adenosine restores conduction in dormant canine pulmonary veins. Circulation 2010; 121:963–972. 2011 3