Uncommon Atrial Flutter Originating in the Left Atrioventricular Groove

Transcription

1 Jpn Circ J 1999; 63: Uncommon Atrial Flutter Originating in the Left Atrioventricular Groove Emergence After Successful Catheter Ablation for a Left Concealed Accessory Pathway Yoshinori Kobayashi, MD; Meiso Hayashi, MD; Yasushi Miyauchi, MD; Naomi Kawaguchi, MD; Hiromichi Ogura, MD; Hirokazu Saitoh, MD; Takeshi Ino, MD; Hirotsugu Atarashi, MD; Hiroshi Kishida, MD; Hirokazu Hayakawa, MD This report describes a 49-year-old male with concealed Wolff-Parkinson-White syndrome in whom a true uncommon atrial flutter suddenly emerged 2 weeks after successful catheter ablation of a left-sided accessory pathway. The earliest atrial activation during the atrial flutter was recorded at the posterolateral mitral annulus 2 cm proximal to the previous successful ablation site for the accessory pathway. Two applications of radiofrequency (RF) current directed at the supravalvular mitral annulus could not terminate the atrial flutter. A subsequent delivery of RF current directed at the subvalvular annulus, where a local fragmented potential preceded the earliest atrial activation, eliminated the atrial flutter. (Jpn Circ J 1999; 63: ) Key Words: Atrioventricular accessory pathway; Local fragmented potential; Radiofrequency catheter ablation; Uncommon atrial flutter; Wolff-Parkinson-White syndrome True uncommon atrial flutter, generally defined as a broad category of atrial flutter other than the common and so-called reversed common flutter, 1 is relatively prevalent in patients who have undergone surgery involving significant alteration of the atrium. 2,3 In these patients, the flutter is usually due to reentry propagating around an extensive atrial incision, and interruption of this reentry has been achieved by modification of the zone of slow conduction critical for the perpetuation of the arrhythmias. 2 However, the mechanism of true uncommon atrial flutter in patients without structural heart disease has not been well elucidated because this is a relatively rare arrhythmia in clinical practice and includes a variety of mechanisms that often require an individualized approach. We report a unique patient with a left-sided concealed accessory pathway (AP) in whom a true form of uncommon atrial flutter suddenly appeared 2 weeks after successful catheter ablation of the accessory pathway. A mapping study revealed that this arrhythmia originated from the posterolateral mitral annulus, and the flutter was successfully ablated by a radiofrequency (RF) energy delivery directed at the subvalvular mitral annulus. At the successful ablation site for the atrial flutter, a local electrogram exhibited a small fragmented potential preceding the onset of the F wave by 30ms. (Received December 3, 1998; revised manuscript received January 18, 1999; accepted January 27, 1999) First Department of Internal Medicine, Nippon Medical School, Tokyo, Japan Mailing address: Yoshinori Kobayashi, MD, The First Department of Internal Medicine, Nippon Medical School, Sendagi, Bunkyoku, Tokyo 113, Japan Case Report Clinical History A 49-year-old male had experienced palpitations since an abrupt onset in 1988, and the frequency of the symptoms had gradually increased since July of His palpitations usually disappeared either spontaneously or by the Valsalva s maneuver. In August 1996, his symptoms did not subside and lasted for 2 h. He then visited a general physician and a diagnosis of paroxysmal supraventricular tachycardia (PSVT) was made. Subsequently, he was admitted to hopsital for further evaluation and treatment of his tachycardia. There were no abnormal physical or laboratory findings on admission. Electrophysiologic (EP) Study and Catheter Ablation for Accessory Pathway (First Session) The first EP study and ablation procedure were undertaken in September, The patient was brought to the EP laboratory in the fasting and mildly sedated state. After local anaesthesia, 4 multielectrode catheters were positioned at the high right atrium (HRA), His bundle area, the right ventricular apex (RVA) and coronary sinus (CS). Intracardiac signals were amplified and filtered from 30 to 500Hz, and all signals were recorded on an optical disk by using an EP Lab (Quinton Instrument Co, Bothell, WA, USA). At the baseline study, pacing from the RVA showed consistent retrograde conduction without a decremental property and the earliest atrial activation was obtained from the distal pair of CS electrodes (CS1 2), suggesting the presence of a left-sided concealed AP. The effective refractory period of the AP was 260 ms. Orthodromic atrioventricular reciprocating tachycardia (AVRT) was induced by the single extrastimulus method performed from the CS

2 Atypical Atrial Flutter of Left AV Groove 417 Fig1. (Left) Standard 12-lead ECG on admission, showing a regular narrow QRS tachycardia with a cycle length of 460ms. In lead V1, a positive P wave with a 230-ms cycle length was observed. (Right) Intracardiac recordings during conversion of atrial fibrillation (af), induced by an atrial extrastimulus to uncommon atrial flutter (AFL) (arrow). From top to bottom, there are 3 surface ECG leads (I, avf, V1) and 9 intracardiac electrograms. HRA, high right atrium; CS1 2, most distal pair of coronary sinus (CS) electrodes; CS3 4, second pair; CS5 6, third pair; CS7 8, fourth pair; CS9 10, most proximal pair; HBEp, proximal His bundle electrogram; HBEd, distal His bundle electrogram; RV, RV outflow tract. Note that the earliest atrial activation was seen at CS1 2 and activation of the right atrium was delayed behind that of the distal CS. with reproducibility. The cycle length of the AVRT was 260ms and the atrial activation sequence was the same as that during RVA pacing. Throughout the study, manifest preexcitation was not documented. Radiofrequency catheter ablation (RF-CA) was performed using a generator with a closed-loop temperature control system (HAT 300s: Osypka, Grenzach-Wyhlen, Germany), and the target temperature was set at 60 C. The AP was successfully ablated by a single delivery of RF current directed at the left anterolateral mitral annulus underneath the valve. After the ablation procedure, conduction via the AP was never documented during RVA pacing even during intravenous administration of isoproterenol (ISP, 0.01 g kg 1 min 1 ). No type of supraventricular tachyarrhythmia was induced by programmed pacing from the HRA or CS, including double extrastimuli. On the 15th post-ablation day while at his home, he suddenly noticed incessant paroxysms of tachycardia and was re-admitted. Fig 1 (left panel) shows the standard 12- lead ECG during the tachycardia, which revealed uncommon atrial flutter with a 2:1 ventricular response. Intravenous administration of adenosine triphosphate (20 mg) did not terminate the tachycardia, although transient atrioventricular block was observed during which the flutter waves were consistently observed (data not shown). A total of 6 antiarrhythmic agents, including disopyramide, aprindine, pilsicainide, flecainide, verapamil and propranolol, were not effective in termination and/or prophylaxis of this arrhythmia. All the class I antiarrhythmic agents significantly lengthened the flutter cycle length, whereas neither propranolol nor verapamil had an effect on it. Prior to the repeat EP study, all antiarrhythmic agents were stopped for at least 3 days. EP Study and Ablation Procedures for Uncommon Atrial Flutter (Second Session) The catheters used for the second session and their positioning were the same as for the first session. At the beginning of the baseline study, it was confirmed during right ventricular pacing that there was no ventriculoatrial conduction through the AP previously ablated. During programmed pacing, atrial fibrillation was unintentionally induced and it spontaneously converted to atrial flutter as shown in Fig 1 (right panel). During the atrial flutter, the earliest atrial activation was seen at the distal pair of the CS electrodes (CS1 2) and the activation of the right atrial sites (HRA and His bundle region) was obviously delayed behind that of CS1 2. The cycle length of the atrial flutter was 210ms. The morphology of the F wave on the 12-lead ECG was almost identical to that of the incessant atrial flutter observed at the time of the second admission. Because the post-pacing interval was almost identical to the flutter cycle length at the distal CS (Fig2, lower panel), but twice the flutter cycle length (455 ms) at the HRA (Fig 2, upper panel), the flutter was considered to originate in the left atrium. The left atrium in the vicinity of the atrioventricular groove was mapped using a large tip catheter introduced retrogradely from the femoral artery. Prior to the mapping procedure, the CS catheter was advanced by approximately 3 cm so that the activation sequence was bracketed throughout the CS electrodes. After advancing the catheter, the earliest atrial activation was seen at the 4th pair of CS electrodes (CS7 8). Fig 4 (right lower panel) shows how the local atrial activity recorded at several points adjacent to the CS7 8 electrodes from both the atrial and ventricular aspects preceded the earliest atrial electrogram of the CS (CS7 8). Mapping for the earliest atrial activation was first performed in the supravalvular left

3 418 KOBAYASHI Y et al. Fig 2. Intracardiac recordings at the cessation of rapid pacing applied from the high right atrium (HRA) (upper) and CS1 2 (lower). The ECGs and intracardiac recordings are the same as in Fig 1. The post-pacing interval was almost equal to the flutter cycle length when pacing was performed from the distal CS (lower), whereas it was twice as long as the flutter cycle length when from the HRA (upper). Fig 3. (Upper) The local electrogram at unsuccessful (supravalvular mitral annulus) and (lower) successful ablation sites (subvalvular mitral annulus). Abl, electrogram at the ablation sites. Note that a small fragmented potential preceded the earliest atrial activation (CS7 8) and the onset of the F wave by 5 and 30 ms, respectively, at the successful ablation site. atrium along the mitral annulus. The earliest activation was obtained in a restricted area between the third (CS5 6) and fourth (CS7 8) pairs of CS electrodes slightly above the annulus. The atrial activation in this area was almost simultaneous to that of CS7 8, as shown in Fig3 (upper panel). It was also noted that the timing of atrial activation was obviously delayed behind the center of the mapped area in the surrounding zone, as shown in Fig 4 (right lower panel). Two applications of RF energy were delivered at the earliest activation site (the point indicated by zero for the Acs A interval in Fig4) and at a slightly more distal adjacent site; however, these applications resulted in failure. Subsequently the mapping catheter was positioned on the subvalvular annulus, the opposite to the site of earliest atrial activation through the annulus. The local electrogram at this site showed a small fragmented potential preceding the earliest atrial activation of the CS (CS7 8) and onset of the F wave on the ECG (avf lead), by 5 and 30ms, respectively (Fig3, lower panel). RF energy applied to this site successfully converted the flutter to sinus rhythm 5.2s after the start of RF current delivery (Fig 4, left panel). The cineframes of the successful ablation site are also shown in Fig 4 (right panels), demonstrating that the tip of the ablation catheter was located at the left posterolateral mitral annulus underneath the valve. The post-ablation induction study failed to induce any atrial tachyarrhythmias even during intravenous administration of ISP (0.01 g kg 1 min 1 ). During the follow-up period of 14 months, the patient has been free of all symptoms. Discussion The major findings in this particular patient are as follows. (1) Incessant uncommon atrial flutter emerged after successful ablation of a left-sided atrioventricular AP. (2) The potential mapping study revealed that the earliest atrial activation during the flutter was seen in the left atrium slightly above the mitral annulus approximately 2 cm more proximal to the previous ablation site for the AP; however, 2 applications of RF energy did not terminate the tachycardia. (3) A subsequent delivery of RF energy directed at the subvalvular mitral annulus (ie, opposite to the site of earliest atrial activation), the atrial flutter was eliminated. (4) The local electrogram from the successful

4 Atypical Atrial Flutter of Left AV Groove 419 Fig 4. Intracardiac recording during successful RF current application (left). At 5.2 s after the onset of RF current delivery, the atrial flutter converted to sinus rhythm. The cine-frames of the successful ablation site (right) demonstrate the position of the ablation catheter tip at the left posterolateral mitral annulus underneath the valve. The numbers on the cine-frame (right lower) indicate the timing of the interval (Acs A interval) of the local atrial potential recorded from the ablation catheter in the vicinity of the mitral annulus in comparison to the earliest atrial activation during the flutter (CS7 8 after advancing the CS catheter). The minus number means activation precedes the earliest atrial activation (CS7 8). (See text for details.) ablation site contained a small fragmented potential preceding the earliest atrial activation during the atrial flutter. With regard to the electrophysiologic mechanism underlying the occurrence and perpetuation of this tachyarrhythmia, macro-reentry can be excluded because the flutter had a small restricted origin, as atrial activation of the surrounding zone was obviously delayed behind the center of the mapped area. From our observation that the flutter could not be either induced or terminated by programmed pacing during the second EP study, it may have occurred due to enhanced automaticity, although micro-reentry can not be excluded as one of possible mechanisms, as the fragmented potential preceding the earliest atrial activation was clearly seen at the successful ablation site. Another important question to be raised is What was the causative electrically excitable structure of the atrial flutter? To date, there have been several case reports of atrial tachyarrhythmias originating in the atrioventricular groove. 4 6 These arrhythmias were assumed to arise either from atrioventricular AP 4 or from Mahaim fibers. 5,6 In each case, the AP potentials were detected in the CS or in the vicinity of the atrioventricular annulus. Moreover, such potentials were shown to be diastolic potentials or pre-p potentials 4,6 during the tachycardia. Because fragmented potentials preceding the F wave were seen only at the mitral annulus of the ventricular aspect during the flutter in the present case, this arrhythmia might have arisen from an AP capable of conduction only to the atrium. It has been demonstrated that AP possess a variety of anatomical and histological characteristics, and are not just a simple strand of muscle fiber. 7 9 Unfortunately, we do not have any evidence for anatomical complexities such as an oblique course or multi-network fibers of the AP in this case, because a standard decapolar catheter (2-8-2 interelectrode spacing) was used for mapping in the first ablation session. However, because the initial ablative therapy augumented the arrhythmogenesis of the flutter origin, it is at least suggested that there might be some electrical interaction between the AP and the flutter origin. To the best of our knowledge, this is the first report of successful catheter ablation of left uncommon atrial flutter with the RF energy directed at the subvalvular mitral annulus. Although 2 prior applications of RF energy directed at the supravalvular annulus may have played a partial role in facilitating the final abolition of the tachycardia, the termination was achieved only by the third RF delivery. Acknowledgments The authors wish to express special gratitude to Eli S. Gang MD and William J Mandel MD of Cedars-Sinai Medical Center, Los Angeles, CA, for reading this manuscript, and to Mr John Martin for his linguistic assistance. References 1. Kalman JM, Olgin JE, Saxn LA, Lee RJ, Scheinman MM, Lesh MD: Electrocardiographic and electrophysiologic characterization of atypical atrial flutter in man: Use of activation and entrainment mapping and implications for catheter ablation. J Cardiovasc Electrophysiol 1997; 8: Triedman JK, Saul JP, Weindling SN, Walsh EP: Radiofrequency ablation of intra-atrial reentrant tachycardia after surgical palliation of congenital heart disease. Circulation 1995; 91: Kanter RJ, Garson A: Atrial arrhythmias during chronic follow-up of surgery for complex congenital heart disease. PACE 1997; 20(Pt II): Jackman WM, Yeung-Lai-Wah JA, Friday K, Khan A, Sakurai M, Lazzara R: Tachycardias originating in accessory pathway networks mimicking atrial flutter and fibrillation (abstract). J Am Coll Cardiol

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