Europace Advance Access originally published online on March 9, 2007
Europace 2007 9(4):216-219; doi:10.1093/europace/eum026
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
ABLATION
Successful catheter ablation of focal atrial tachycardia from the non-coronary aortic cusp
Department of Internal Medicine, Division of Cardiology, University of Oulu, PO Box 5000, FIN-90014, Finland
Manuscript submitted 18 November 2006. Accepted after revision 31 January 2007.
* Corresponding author. Tel: +358 8 315 3550; fax: +358 3152127. E-mail address: pekka.raatikainen{at}oulu.fi
 |
Abstract |
|---|
 Top Abstract IntroductionCase reportDiscussionAcknowledgementsReferences |
|---|
We describe a patient with frequent episodes of unusual paroxysmal supraventricular tachycardia. During the electrophysiological examination, the tachycardia was easily induced and terminated by atrial pacing. The earliest activation during right atrial activation mapping was located near the atrioventricular node and the His bundle. However, detailed mapping of the aortic root demonstrated that the local activation in the non-coronary aortic cusp preceded the activation at the His bundle region. Radiofrequency catheter ablation at this site terminated the tachycardia with no complications.
Key Words: Atrial tachycardia, Aortic cusp, Catheter ablation
|
Introduction |
|---|
|
TopAbstractIntroductionCase reportDiscussionAcknowledgementsReferences |
|---|
Focal atrial tachycardias (AT) in the right atrium (RA) tend to cluster around the crista terminalis, coronary sinus (CS) region, tricuspid annulus, and parahisian region.1
,2 In most cases, the AT focus can be identified by careful activation mapping, and completely eliminated by radiofrequency (RF) catheter ablation.1,2 However, RF ablation near the His bundle (HB) carries a risk of inadvertent damage to the atrioventricular (AV) conduction system.3 Here we describe a patient with an AT originating in the vicinity of the AV node, which was successfully treated by RF ablation from the non-coronary aortic cusp. |
Case report |
|---|
|
TopAbstractIntroductionCase reportDiscussionAcknowledgementsReferences |
|---|
A 44-year-old woman was admitted to our hospital for evaluation of frequent palpitations. She had been diagnosed previously with hypertension, asthma, and Grave
disease. The duration of the arrhythmia symptoms was almost 10 years. She had no other cardiac symptoms and the results of clinical evaluation and echocardiographic examination were normal. The tachycardia presented generally during exercise with abrupt onset and offset. The tachycardia was refractory to beta-blocking medication and verapamil. The 12-lead ECG at the time of admission was normal. An ECG recorded during the symptoms showed a narrow-complex tachycardia with alternating R-P interval and atrial cycle length of 390 ms (Figure 1A). Occasionally, AV block was observed during the tachycardia. P-wave morphology on the surface ECG was analysed during the periods of transient AV block. The P-waves were positive in lead I and aVL and negative or indifferent in the inferior leads II, III, and aVF. In the precordial leads V1 and V2, P-waves were biphasic (Figure 1A).
|
Antiarrhythmic medication was withdrawn 3 days before the electrophysiological examination. Multielectrode catheters were introduced percutaneously into the femoral veins and positioned into high RA (hRA), His bundle region (HBE), CS, and right ventricular apex (RVa) under fluoroscopic guidance. Sustained clinical tachycardia with a cycle length of 390 ms was induced reproducibly by a single atrial extrastimulus as well as by incremental atrial pacing. The earliest activation during the tachycardia was recorded in the proximal His electrode (Figure 1B). At this site, the local activation preceded the P-wave onset by 25 ms. The diagnosis of focal AT was confirmed using commonly accepted diagnostic criteria.1
,2 For example, transient AV block was observed occasionally during the arrhythmia, and ventricular pacing during the tachycardia had no effect on atrial activation. The tachycardia was easily terminated by burst atrial pacing.
A 7 F quadripolar 4-mm tip catheter (C.R. Bard Inc., Murray Hill, NJ, USA) was used for activation mapping and ablation. Detailed mapping within the RA demonstrated earliest activation near the AV node and the HB electrodes. Given the high risk of AV block, we decided not to apply RF energy at this site, although the local activation preceded the onset of the P-wave in the surface ECG. Instead, encouraged by the case report of Tada et al.,4 we elected to map also the aortic root before delivering RF energy. The aortic root was mapped retrogradely with the same catheter as the RA. The earliest local activation during the AT was found within aortic sinus of Valsalva slightly superior to the HB catheter. Aortic root angiography demonstrated that the ablation catheter was located on the non-coronary cusp (Figure 2). The local activation in the non-coronary aortic cusp was 15 ms earlier than the earliest action in the RA and preceded the onset of the P-wave in the surface ECG by 40 ms (Figure 3A). No His potential was visible. RF ablation for 60 s (maximum power 30 W and maximum temperature 55°C) at this site abruptly terminated the AT within 2.7 s (Figure 3B). No junctional beats were observed during the ablation. After the ablation no sustained tachycardia was inducible, but an additional ablation was applied because of short runs of non-sustained AT. After the ‘safety burn’ no arrhythmia was inducible. No complications were observed. The patient was discharged next day with no medication except for oral aspirin for 4 weeks. She has had no recurrence of arrhythmias during follow-up of 7 months.
|
|
|
Discussion |
|---|
|
TopAbstractIntroductionCase reportDiscussionAcknowledgementsReferences |
|---|
We have described successful catheter ablation of focal AT originating from an unusual site in the non-coronary aortic cusp. The tachycardia was characterized by easy induction and termination by programmed atrial stimulation. Ventricular pacing had no effect on atrial activation during the tachycardia. The P-waves were positive in lead I and aVL and negative or isoelectric in the inferior leads II, III, and aVF. In the precordial leads V1 and V2, P-waves were biphasic.
Focal AT originates typically from the crista terminalis, the tricuspid or mitral annulus, pulmonary veins or septal region.1,2,5 Most ATs are amenable to curative RF ablation. However, RF ablation of an AT originating from the apical region of the triangle of Koch carries a risk of inadvertent damage to the AV nodal conduction system. It has been shown that in the vicinity of the AV node a focal AT may originate from either side of the interatrial septum.3 Therefore, in many cases careful mapping of both the right and left side of the interatrial septum is crucial to decrease the risk of post-ablation AV block.3 Another structure and a potential source of arrhythmias, which is located close to the HBE, is the aortic root. In a normal heart, the aortic root is adjacent to epicardial atrial myocardium and occupies a central location within the tricuspid and mitral annulus (Figure 4). Recently, this region has been shown to give rise to various tachyarrhytmias.4,6–8
|
In the present case, the origin of the focal AT was located in the non-coronary aortic cusp. Despite the immediate vicinity of the His bundle, no His potentials were observed at the successful ablation site in the non-coronary aortic cusp. The atrial signal at ablation site was
15 ms earlier than that recorded at the His region. The tachycardia terminated rapidly, and no junctional beats were observed during the ablation. These observations are in agreement with previous observations and suggest that the arrhythmogenic focus may have been located epicardially in the atrial wall.8 Neither here nor in the previous cases4,8 did the ablation of AT from the non-coronary aortic cusp cause any deleterious effects on the aortic wall or coronary arteries. Likewise, no complications were observed during the follow-up.
In lieu of the present and previous findings,4,8 the clinical and electrophysiological characteristics suggesting non-coronary aortic cusp origin of AT include: (i) abrupt onset and offset of the tachycardia, (ii) easy induction and termination by atrial stimulation, and (iii) earliest activation in the RA near the His bundle. Furthermore, the tachycardia can be terminated by adenosine.4,8 Surface ECG is only of limited help, as the P-wave morphology during the tachycardia is similar to that seen during focal AT originating from the interatrial septum or parahisian region.9 Before ablation in the aortic root, it is essential to demonstrate that the local activation in the non-coronary aortic cusp precedes that recorded at the His region. In addition, pre-ablation aortic root angiography and continuous visualization of the ablation catheter during RF delivery should be used to minimize the risk of injuring the coronary arteries and other important structures.
In conclusion, our findings strongly support the concept that in a case of a ‘parahisian’ AT it may be necessary to map not only both sides of the interatrial septum but also the aortic root. Although the non-coronary aortic cusp seems to be an uncommon source of AT,8 in selected cases such as this, the potentially harmful effect of RF delivery in the vicinity of the His bundle on the AV nodal conduction can be avoided by mapping the aortic root. Given the efficacy and safety of ablation of focal AT from the non-coronary cusp, this approach may be considered primary ablation strategy and not limited to those cases with previous ablation failure.
|
Acknowledgements |
|---|
|
TopAbstractIntroductionCase reportDiscussionAcknowledgementsReferences |
|---|
We thank the Finnish Foundation for Cardiovascular Research for financial support.
|
References |
|---|
|
TopAbstractIntroductionCase reportDiscussionAcknowledgementsReferences |
|---|
[1] Hsieh MH and Chen SA.Catheter ablation of focal atrial tachycardia. In. In Zipes DP and Haissaguerre M (Eds.). Catheter Ablation of Arrhythmias 2002; 2nd ed. New York Futura Publishing Company, Inc pp. 185–203.
[2] Roberts-Thomson KC, Kistler PM, Kalman JM. Atrial tachycardia: mechanisms, diagnosis, and management. Curr Probl Cardiol 2005; 30: 529–73.[CrossRef][ISI][Medline]
[3] Frey B, Kreiner G, Gwechenberger M, Gossinger HD. Ablation of atrial tachycardia originating from the vicinity of the atrioventricular node: significance of mapping both sides of the interatrial septum. J Am Coll Cardiol 2001; 38: 394–400.
[4] 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: 1440–3.[CrossRef][Medline]
[5] Gonzalez MD, Contreras LJ, Jongbloed MR, et al. Left atrial tachycardia originating from the mitral annulus-aorta junction. Circulation 2004; 110: 3187–92.
[6] Ouyang F, Fotuhi P, Ho SY, et al. Repetitive monomorphic ventricular tachycardia originating from the aortic sinus cusp: electrocardiographic characterization for guiding catheter ablation. J Am Coll Cardiol 2002; 39: 500–8.
[7] Tada H, Naito S, Nogami A, Taniguchi K. Successful catheter ablation of an anteroseptal accessory pathway from the noncoronary sinus of Valsalva. J Cardiovasc Electrophysiol 2003; 14: 544–6.[CrossRef][ISI][Medline]
[8] Ouyang F, Ma J, Ho SY, et al. Focal atrial tachycardia originating from the non-coronary aortic sinus: electrophysiological characteristics and catheter ablation. J Am Coll Cardiol 2006; 48: 122–31.
[9] Kistler PM, Roberts-Thomson KC, Haqqani HM, et al. P-wave morphology in focal atrial tachycardia: development of an algorithm to predict the anatomic site of origin. J Am Coll Cardiol 2006; 48: 1010–17.
CiteULike 
Connotea 
Del.icio.us What's this?
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||