Adenosine-Sensitive Focal Reentrant Atrial Tachycardia Originating From the Mitral Annulus Aorta Junction

Size: px

Start display at page:

Download "Adenosine-Sensitive Focal Reentrant Atrial Tachycardia Originating From the Mitral Annulus Aorta Junction"

Homer Wilson
5 years ago
Views:

1 Case Report Adenosine-Sensitive Focal Reentrant Atrial Tachycardia Originating From the Mitral Annulus Aorta Junction tsuro Morishima MD, Takahito Sone MD, Hideyuki Tsuboi MD, Hiroaki Mukawa MD, Michitaka Uesugi MD Department of Cardiology, Ogaki Municipal Hospital Adenosine-sensitive reentrant atrial tachycardia (AT) has been recognized to originate from the confined area of either the right or left atiroventricular nodal regions. We describe a case with adenosine-sensitive focal AT which was successfully ablated at the uncommon focus located at the mitral annulus-aorta junction. The mode of AT initiation during the atrial extrastimulus suggested as the mechanism tachycardia reentry; AT was terminated by a bolus of 2 mg of adenosine 5 0 -triphosphate. These electrophysiological features are sibly associated with a substrate involved in the mitral annulus-aorta junction with node-like properties that is responsive to adenosine. (J Arrhythmia 2008; 24: ) Key words: Atrial tachycardia, Catheter ablation, Mitral annulus-aorta junction, Adenosine, Reentry ntroduction The mitral annulus-aorta (MA-Ao) junction, where the left atrium is continuous through the subaortic curtain with the musculature of the anterior mitral leaflet, 1) has recently been recognized as a unique source of atrial tachycardia (AT). 2,3) AT is rare, and its characteristics are yet to be elucidated. Case Report A 63-year-old female was referred for catheter ablation to treat supraventricular tachycardia. She had a 13-year history of paroxysmal palpitation with dizziness. The heart was structurally normal. A 12- lead electrocardiogram (ECG) revealed sinus rhythm with right bundle branch block (Figure 1A). ECG during tachycardia demonstrated a long R-P 0 tachycardia with two-to-one or one-to-one atrioventricular (AV) conduction (Figure 1B). The P-wave morphology during the tachycardia was electric in leads, avr, V5, and V6, itive in leads,, and avf, negative in lead avl, and biphasic with negative followed by itive in leads V1-V4. An electrophysiologic study was performed. The patient was on no antiarrhythmic drugs for 2 weeks prior to the procedure. Electrode catheters were itioned in the high right atrial (HRA) septum, His bundle region (HS), coronary sinus (CS), and right ventricular apex (RVA). The most proximal electrode of the CS catheter was itioned at the CS ostium. At baseline, the patient exhibited normal AH (110 ms) and HV (43 ms) intervals with a sinus cycle length of 610 ms (Figure 2A). Retrograde AV nodal conduction was present with the earliest activation recorded at the His bundle region during the RVA Received 12, September, 2008: accepted 7, November, Address for correspondence: tsuro Morishima MD, Department of Cardiology, Ogaki Municipal Hospital, 4-86 Minaminokawa-cho, Ogaki, , Japan. Phone: Fax: morishima-i@muc.biglobe.ne.jp 209

2 J Arrhythmia Vol 24 No av R av L A) Sinus Rhythm B) Atrial Tachycardia 500ms P-wave Morphology neg Figure 1 Twelve-lead electrocardiograms during sinus rhythm (A) and atrial tachycardia (AT) (B). The P-wave morphology during the AT is shown. The P-wave morphology is consistent with a superior mitral annular focus (biphasic pattern with negative followed by itive in precordial leads). Pos: itive, neg: negative, : electric V 2 V 3 V 4 V 5 V 6 pacing (Figure 2B). The tachycardia (cycle length 345 ms) was reproducibly induced by an atrial extrastimulus (S1S1 550 ms, S1S2: ms) from HRA and was terminated by a single atrial stimulus. There was a significant negative correlation between the coupling interval of the extrastimulus (S1S2) and the interval between the extrastimulus and the first beat of the tachycardia (S2Ae) (S2Ae ¼ 0:45 S1S2 þ 558, R 2 ¼ 0:99, P ¼ 0:007) (Figure 3). An intravenous administration of 2 mg of adenosine 5 0 -triphosphate prolonged the tachycardia cycle length and terminated the tachycardia reproducibly without causing AV block. Ventricular overdrive pacing during the tachycardia demonstrated AV dissociation without tachycardia entrainment; an A-A-V response was observed after discontinuation of the pacing (Figure 2C). The atrial activation sequence during the tachycardia was different from sinus rhythm and retrograde VA conduction; the atrial potential was earliest at the His bundle region where the potential was 4 ms behind the onset of the P wave, followed by the potential at the proximal HRA septum. Accordingly, the tachycardia was diagnosed as an adenosine-sensitive reentrant AT. The CS catheter was advanced distally because it was sible that earlier activity would be present on the left atrial side. The earliest atrial activation was then recorded at the most distal pair of electrodes of CS, and the potential preceded P wave onset by 10 ms, which was suggestive of a left atrial focus. Subsequently, transseptal puncture was done, and the endocardial activation mapping of the left atrium was performed by a 4-mm-tip ablation catheter. Finally, the earliest atrial activation was obtained at the 11 o clock ition of the mitral annulus in the left anterior oblique projection, the bipolar electrogram preceded the onset of the P wave by 40 ms, and a uni-polar electrogram exhibited a QS pattern (Figure 4A). The activation from this site radiated in all directions as shown by the electrograms at CS, the HRA septum and HS, and the range of activation times including the other part of the atrium was less than the tachycardia cycle length. These findings were consistent with focal AT. At this location the motion of the catheter was synchronized to the motion of the CS catheter, indicating that the tip of the catheter was located at the mitral annulus. 2) Left ventriculogram confirmed that the catheter was located at the MA-Ao junction (Figure 4B). A single radiofrequency current application at this site terminated the AT within 2 seconds without transient acceleration. The AT became no longer inducible. The patient has been free from the recurrent tachycardia without antiarrhythmic drugs for the subsequent 12 months. Discussion The present focal AT has two uncommon aspects. First, the site of origin was located at the MA-Ao junction. Second, the mechanism of the AT was sibly focal reentry, and the AT was adenosinesensitive. 210

3 A B C HRA ds HRA px HS px HS ds CS 1-2 CS 3-4 CS 5-6 CS 7-8 CS 9-10 RVA H Figure 2 ntracardiac electrograms during sinus rhythm (A), at ventricular pacing with retrograde AV nodal conduction (B), and at the cessation of ventricular overdrive pacing during the tachycardia (C). The atrial activation sequence during the tachycardia was different from that at sinus rhythm and the retrograde VA conduction. The atrial potential was earliest at the His bundle region (arrows), where the potential was 4 ms behind the onset of the P wave, followed by the potential at the proximal HRA septum. Ventricular overdrive pacing during the tachycardia demonstrated AV dissociation without tachycardia entrainment; the tachycardia showed an A-A-V response upon cessation of ventricular pacing. HRA ds: high right atrium distal, HRA px: high right atrium proximal, HS px: His-bundle proximal, HS ds: His-bundle distal, CS: coronary sinus, RVA: right ventricular apex, H: His-bundle potential 410 S2Ae = x S1S R 2 = 0.99 P = S2Ae (ms) S1S2 (ms) Figure 3 Linear regression analysis of the relation between the coupling interval of the extrastimulus (S1S2) and the interval between the extrastimulus and the first beat of the tachycardia (S2Ae). A significant inverse correlation was observed (R 2 : 0.99, P: 0.007). At the MA-Ao junction, a subaortic curtain supports three structural components: the left coronary cusp, noncoronary cusp, and the anterior leaflet of the mitral valve. 1) The arrhythmogenicity of this site has been explained as follows. The leaflet musculature at this site has been shown to have action potential with AV nodal-type characteristics. 4,5) These properties may be explained by calcium-dependent cells, which are responsive to adenosine and similar to AV nodal cells. 6) Furthermore, embryological study suggested that remnants of the developing conduction system may be the substrate of the tachycardia. 3) These findings suggest that the MA-Ao junction may cause both reentry 4) and triggered activity. 5) Clinically, the mechanism of the AT originating at the MA-Ao 211

J Arrhythmia Vol 24 No 4 2008 HRA ds HRA px A B HS px HS ds ABL uni ABl ds H H H H - 40 ABL px CS 1-2 CS 5-6 CS 9-10 RVA Figure 4 (A) ntracardiac electrograms at the successful ablation site of the

4 J Arrhythmia Vol 24 No HRA ds HRA px A B HS px HS ds ABL uni ABl ds H H H H - 40 ABL px CS 1-2 CS 5-6 CS 9-10 RVA Figure 4 (A) ntracardiac electrograms at the successful ablation site of the mitral annulus aorta junction. The local bipolar electrogram preceded the onset of the P wave by 40 ms (arrow) and a uni-polar electrogram exhibited a QS pattern. (B) The site of successful ablation delineated by left ventriculogram. The ablation catheter was located at the mitral annulus-aorta junction. The CS catheter was distally itioned. ABL uni: unipolar electrogram of distal electrode of the ablation catheter, ABL ds: ablation catheter, distal, ABL px: ablation catheter, proximal, L: left coronary cusp, N: noncoronary cusp, R: right coronary cusp, RAO: right anterior oblique projection, LAO: left anterior oblique projection. The other abbreviations are as in Figure 2. junction may not be uniform. Gonzalez et al. combined the data of 10 cases to determine the triggered activity based on the mode of initiation. 3) However, Kistler, et al. concluded that the mechanism is unclear. 2) The present focal AT is unique in the way that reentry was suggested based on the mode of initiation. From the above arrhythmogenic properties of the MA-Ao junction, certain characteristics of the focal reentrant AT emerge. n 1997, esaka et al. proed a clinical entity of adenosine-sensitive reentrant AT due to focal reentry involving the AV node and/or AV nodal transitional tissues without any involvement of the AV nodal pathway originating in the vicinity of the apex of Koch s triangle. 7) The AT can be ablated at the earliest atrial activation site in the right superoseptal area. Recently, a left variant form of the adenosine-sensitive reentrant ATs was reported; the circuit of the AT may involve the leftward AV nodal transitional tissue, and the ATs are amenable for ablation from the noncoronary aortic sinus 8,9) or the left coronary aortic sinus. 10) The AT in the present case shares some characteristics of this entity: the AT was sensitive to a small dose of adenosine (2 mg), and the mechanism was focal reentry. Apparently, the site of origin of the present AT differs from those of the others, which were located within the confined area of either the right or left para-hisian regions. 7 10) However, as stated above, the MA-Ao junction involves the remnant of the conduction system with AV nodal properties. 3 6) Thus, the present AT may have arisen from a substrate with similar properties to the para- Hisian type of adenosine-sensitive focal reentrant ATs. Limitation needs to be addressed regarding the mechanism of the AT. An inverse relationship between the coupling interval of the artial extrastimulus and the first beat of the tachycardia is suggestive, but not a specific criterion for reentry. Entrainment of the tachycardia would have shown convincing evidence. 11) n conclusion, the adenosine-sensitive focal-reentrant AT may originate from the MA-Ao junction. The AT may share a substrate with node-like properties that is responsive to adenosine with the previously recognized para-hisian type of adenosine-sensitive focal reentrant AT. 212

5 References 1) Dean JW, Ho SY, Rowland E, Mann J, Anderson RH: Clinical anatomy of the atrioventricular junctions. J Am Coll Cardiol 1994; 24: ) Kistler PM, Sanders P, Hussin A, Morton JB, Vohra JK, Sparks PB, Kalman JM: Focal atrial tachycardia arising from the mitral annulus: electrocardiographic and electrophysiologic characterization. J Am Coll Cardiol 2003; 41: ) Gonzalez MD, Contreras LJ, Jongbloed MR, Rivera J, Donahue TP, Curtis AB, Bailey MS, et al: Left atrial tachycardia originating from the mitral annulus-aorta junction. Circulation 2004; 110: ) Wit AL, Fenoglio JJ Jr, Wagner BM, Bassett AL: Electrophysiological properties of cardiac muscle in the anterior mitral valve leaflet and the adjacent atrium in the dog. Possible implications for the genesis of atrial dysrhythmias. Circ Res 1973; 32: ) Wit AL, Cranefield PF: Triggered activity in cardiac muscle fibers of the simian mitral valve. Circ Res 1976; 38: ) McGuire MA, de Bakker JM, Vermeulen JT, Moorman AF, Loh P, Thibault B, Vermeulen JL, et al: Atrioventricular junctional tissue. Discrepancy between histological and electrophysiological characteristics. Circulation 1996; 94: ) esaka Y, Takahashi A, Goya M, Soejima Y, Okamoto Y, Fujiwara H, Aonuma K, et al: Adenosine-sensitive atrial reentrant tachycardia originating from the atrioventricular nodal transitional area. J Cardiovasc Electrophysiol 1997; 8: ) Tada H, Naito S, Miyazaki A, Oshima S, Nogami A, Taniguchi K: Successful catheter ablation of atrial tachycardia originating near the atrioventricular node from the noncoronary sinus of Valsalva. Pacing Clin Electrophysiol 2004; 27: ) Ouyang F, Ma J, Ho SY, Bänsch D, Schmidt B, Ernst S, Kuck KH, et al: Focal atrial tachycardia originating from the non-coronary aortic sinus: electrophysiological characteristics and catheter ablation. J Am Coll Cardiol 2006; 48: ) Otomo K, Nagata Y, Uno K, esaka Y: Left-variant adenosine-sensitive atrial reentrant tachycardia ablated from the left coronary aortic sinus. Pacing Clin Electrophysiol 2008; 31: ) Hsieh MH, Chen SA: Catheter ablation of focal atrial tachycardia. n: Zipes DP and Haïssaguerre M, editor. Catheter ablation of arrhythmias, second edition. Armonk, NY. Futura Publishing Company, nc., 2002;

Ankara, Turkey 2 Department of Cardiology, Division of Arrhythmia and Electrophysiology, Yuksek Ihtisas

Ankara, Turkey 2 Department of Cardiology, Division of Arrhythmia and Electrophysiology, Yuksek Ihtisas 258 Case Report Electroanatomic Mapping-Guided Radiofrequency Ablation of Adenosine Sensitive Incessant Focal Atrial Tachycardia Originating from the Non-Coronary Aortic Cusp in a Child Serhat Koca, MD