Catheter Ablation of Atrial Fibrillation Originating from Superior Vena Cava

Catheter Ablation of Atrial Fibrillation Originating from Superior Vena Cava

Archives of Medical Research 37 (2006) 415–418 CASE REPORT Catheter Ablation of Atrial Fibrillation Originating from Superior Vena Cava Jingtian Lia...

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Archives of Medical Research 37 (2006) 415–418

CASE REPORT

Catheter Ablation of Atrial Fibrillation Originating from Superior Vena Cava Jingtian Lia and Lexin Wanga,b a

Department of Cardiology, The Affiliated Hospital of Weifang Medical College, Shandong Province, the People’s Republic of China b School of Biomedical Sciences, Charles Sturt University, Wagga Wagga, NSW, Australia Received for publication March 15, 2005; accepted May 23, 2005 (ARCMED-D-05-00103).

Atrial fibrillation originating from rapid firing foci in the superior vena cava is rare. Its electrophysiological features and catheter ablation techniques are described in this report. A decapolar catheter was positioned in the superior vena cava to map the origin of the atrial fibrillation in a 39-year-old female patient who had a 3-year history of symptomatic atrial tachycardia and fibrillation. Intracardiac mapping showed rapid firing foci in the anterior wall of the superior vena cava (SVC), 2.0 cm above the SVC–right atrium junction. During tachycardia, the focal electrogram from SVC was 55 msec earlier than the P waves on body surface ECG. Radiofrequency catheter ablation successfully abolished SVC potentials, resulting in a SVC–atrium conduction block. There was no recurrence of atrial arrhythmia after a 14-month follow-up. Rapid activities from the muscle sleeves in the SVC may cause atrial fibrillation. Such a focal atrial fibrillation can be eliminated by isolating the arrhythmogenic SVC with radiofrequency catheter ablation. Ó 2006 IMSS. Published by Elsevier Inc. Key Words: ECG, Atrial fibrillation, Atrial tachycardia, Superior vena cava, Catheter ablation, Cardiac electrophysiology.

Introduction

Case Report

Recent studies show that atrial tachycardia, especially paroxysmal atrial fibrillation, can be triggered by a rapidly firing focus in the pulmonary veins (1–4). The muscular sleeves surrounding the pulmonary veins are the origin of the arrhythmogenic foci. Radiofrequency catheter ablation can eliminate the triggering foci in the pulmonary veins and prevent atrial fibrillation (1–4). Cardiac muscular sleeves also exist in the junctional area of the superior vena cava (SVC) and the right atrium (5–8). These myocytes often possess electrophysiological properties similar to those of atrial myocytes (9,10). However, atrial arrhythmias originating from SVC are rare. The primary purpose of the article was to report about a patient with atrial fibrillation due to rapidly firing foci from the SVC and to describe the techniques and results of catheter ablation of this rare type of arrhythmia.

A 39-year-old female patient had frequent (fortnightly) attacks before the study with episodes of paroxysmal supraventricular tachycardia for 3 years. Oral propafenone, amiodarone and metoprolol had failed to control or prevent the tachycardia prior to the study. Physical examination, chest X-ray and two-dimensional echocardiography showed a structurally normal heart with a normal left ventricular function. Body surface ECG revealed an irregular atrial tachycardia and atrial fibrillation. After the discontinuation of the anti-arrhythmic drugs for more than five half-lives, an eletrophysiological study was performed. Under local anesthesia, a decapolar catheter was positioned in the coronary sinus via the left subclavian vein. A 6-French quadripolar catheter was placed in the right, middle and low right atrium, respectively, via the right femoral vein. SVC angiography was performed to visualize the junction between SVC and the right atrium (Figure 1). A decapolar mapping catheter (Lasso) was then placed in the SVC to map the arrhythmogenic foci. During sinus rhythm, sharp and fractionated potentials were found in the anterior SVC wall, approximately 2.0 cm

Address reprint requests to: Lexin Wang, M.D., Ph.D., School of Biomedical Sciences, Charles Sturt University, Wagga Wagga, NSW 2678, Australia; E-mail: [email protected]

0188-4409/06 $–see front matter. Copyright Ó 2006 IMSS. Published by Elsevier Inc. doi: 10.1016/j.arcmed.2005.05.019

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Li and Wang/ Archives of Medical Research 37 (2006) 415–418

Figure 1. A fluoroscopic view of the mapping catheter (Lasso) in the superior vena cava approximately 2.0 cm above the right atrium.

above the SVC–right atrial junction. These SVC potentials were also noticeable during programmed pacing in the SVC (Figure 2). Extrastimulation (S1S2) induced a premature atrial complex, which was followed by rapid activities with a variable rate from 310 to 360 bpm (Figure 2). During these rapid SVC activities, there was a 1:1 conduction from the SVC to the atrium, and the earliest focal electrogram

was registered by the 4th Lasso electrode (Figure 2), suggesting that the area where the 4th electrode was located was the origin of the tachycardia. Under sinus rhythm, radiofrequency catheter ablation (4mm tip catheter, Boston Scientific, Natick, MA) was attempted in the area where the earliest SVC potential was recorded. After a total of 17 radiofrequency energy applications (energy output 30 W, 25–30 sec per application), the SVC potentials registered by the 4th Lasso electrode and its adjacent areas (approximately 1.3 cm2) were eliminated. Programmed stimulation in the SVC was unable to induce any atrial tachycardia. Intravenous infusion of isoproterenol induced a short burst of activity in the SVC (Figure 3). However, none of the induced SVC activities were able to break into the right atrium (Figure 3). SVC angiography after the ablation did not show any local abnormality on the venous wall. There were no complications during or immediately after the ablation procedures. The patient was discharged 3 days after the procedure. She was on oral anti-platelet drug aspirin 75 mg/day for 3 months after the hospital discharge but not taking any antiarrhythmic drugs. She remained symptom free after a 14-month follow-up. A standard ECG examination at 6 and 14 months post-ablation showed normal sinus rhythm and a rate of 76 beats/min. Discussion Previous histological studies showed that atrial muscles may extend into the SVC; atrial myocytes can be found

Figure 2. Mapping within the superior vena cava (SVC) showed spiky and fractionated electrograms from the proximal (SVCp) to distal (SVCd) Lasso catheter electrodes during programmed extrastimulation (S1S2) or during stimulation-induced premature atrial complex (PAC) and tachycardia. The earliest SVC potential (SVCP) was found in SVC4, which was 55 msec earlier than the P waves on body surface ECG. There was 1:1 conduction between SVC potentials and the right atrium as shown in the coronary sinus (CS) channels. CSp and CSd: proximal and distal coronary sinus. ABLp and ABLd: proximal and distal ablation catheter electrodes.

Focal Atrial Fibrillation and Superior Vena Cava

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Figure 3. Intravenous infusion of isoproterenol induced a short run of irregular superior vena cava activities (SVCp) at a rate of approximately 342 bpm. The SVCp did not propagate to the right atrium because the atrial rate registered by the coronary sinus electrodes (CSp to CSd) was regular and was at 80 bpm.

in the segment of SVC 2–5 cm above the right atrium (5–8). Myocytes in SVC have distinct action potentials and ionic current profiles that may be responsible for their arrhythmogenic activities (7,8). A recent report on eight patients with SVC-originated paroxysmal atrial fibrillation has demonstrated that SVC potentials can be found in the walls of SVC 24–44 mm above the SVC–atrial junction, with a base at right atrial appendage (11). In the present study, SVC potentials were recorded in an area approximately 2.0 cm above the SVC– right atrial junction. These potentials preceded the high right atrium electrogram and P waves at the onset of the atrial tachycardia; therefore, they represent the ectopic pacemaker activity of myocytes from the muscle sleeves inside or encircling the SVC. The major characteristics of the SVC focus are the variation in their firing rates and the intermittent conduction block to the right atrium (12). A recent study reported that the cycle length of the SVC electrograms may vary from 120 to 175 msec during tachycardia, and a 2:1 exit block to the atria is often observed (11). An area with fractionated potentials and slow condition can be found in the anterior or posterior wall of the SVC (13,14). A recent study in seven patients using three-dimensional mapping of SVC suggest that SVC potentials were mainly found in the anterior wall (15). SVC potentials were either absent from the posterior wall or in very low voltage (15). In the present study, rapidly firing foci with a rate between 310 and 360 bpm were identified on the anterior wall of the SVC. The ablation of focal atrial tachycardia or fibrillation with radiofrequency energy appears to be relatively straightforward. The target site for a successful ablation is usually the site where the earliest onset of

electrocardiogram is found, in comparison with either intra-atrial electrogram or P waves on body surface ECG (16,17). Segmental isolation has also been used to eliminate ectopic foci and all SVC potentials distal to the ectopic foci (15). However, it is difficult to evaluate the superiority of the segmental isolation approach because of the small number of patients in the study (15). In the present case, threedimensional mapping of SVC potential or ectopic foci was not used to guide the ablation procedures. We abolished the ectopic foci and all SVC potentials adjacent to the triggering foci in the anterior wall of the SVC during sinus rhythm. This may explain the relatively higher number of energy applications used in this study than that (five applications on average) reported by Tsai et al. (11), who targeted mainly the ectopic foci in the SVC. After ablation, a short run of rapid SVC potentials was induced by isoproterenol; however, there was no conduction from the SVC to the atrium, indicating that the tachycardia foci in the SVC have been isolated. In conclusion, atrial tachycardia or fibrillation may originate from arrhythmogenic foci inside SVC. In patients who presented with atrial tachycardia and fibrillation, apart from pulmonary vein studies SVC should also be considered to be a potential origin of the arrhythmia.

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