Successful catheter ablation of ventricular tachycardia originating from the idiopathic saccular apical left ventricular aneurysm

Successful catheter ablation of ventricular tachycardia originating from the idiopathic saccular apical left ventricular aneurysm

International Journal of Cardiology 93 (2004) 343 – 346 www.elsevier.com/locate/ijcard Letter to the Editor Successful catheter ablation of ventricu...

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International Journal of Cardiology 93 (2004) 343 – 346 www.elsevier.com/locate/ijcard

Letter to the Editor

Successful catheter ablation of ventricular tachycardia originating from the idiopathic saccular apical left ventricular aneurysm Masahiro Ogawa a,*, Kei Miyoshi b, Natsumi Morito b, Sunao Kodama b, Eiji Yahiro b, Kanta Fujimi b, Takeaki Ohta b, Hiroyuki Mihara b, Yoshio Yamanouchi b, Hidenori Urata b, Tadayuki Hiroki b, Keijiro Saku a a

Department of Cardiology, Fukuoka University School of Medicine, 7-45-1 Nanakuma, Jonan-ku, Fukuoka 814-0180, Japan b Department of Cardiology, Fukuoka University Chikushi Hospital, Chikushino, Fukuoka, Japan Received 14 April 2003; received in revised form 19 June 2003; accepted 30 June 2003

Abstract Left ventricular (LV) aneurysm has been recognized to frequently become a substrate of ventricular tachyarrhythmias. We report a case of a 66-year-old woman with symptomatic sustained monomorphic ventricular tachycardia (SMVT) originating from saccular apical LV aneurysm without definite underlying diseases. We performed catheter ablation using electroanatomical and conventional bipolar potential mapping. During SMVT, we found an area of fragmented potential 40 ms preceding the earliest wide QRS complex in the area of the apical LV aneurysm. Radiofrequency applications were delivered to this area. Since then, SMVT was no longer inducible by programmed electrical stimulation. The patient has remained free of VT recurrences during a subsequent 12-month follow-up period. D 2003 Elsevier Ireland Ltd. All rights reserved. Keywords: Electroanatomical mapping; Radiofrequency catheter ablation; Saccular apical left ventricular aneurysm; Sustained monomorphic ventricular tachycardia

1. Introduction Left ventricular (LV) aneurysm is known as one of the complications in patients with myocardial infarction, but rarely occurs in patients with intact coronary arteries, and LV aneurysm of unknown etiology is defined as idiopathic LV aneurysm and often becomes a substrate of ventricular arrhythmias [1,2]. Because ventricular arrhythmias complicated with LV aneurysm cannot be easily suppressed by medication, non-pharmacological therapy is necessarily performed [3– 5]. However, to our knowledge, there is no report of a successful catheter ablation of ventricular tachycardia complicated with idiopathic LV aneurysm. We describe here a case in which radiofrequency catheter ablation using electroanatomical mapping effectively treated sus-

* Corresponding author. Tel.: +81-92-801-1011; fax: +81-92-865-2692. E-mail address: [email protected] (M. Ogawa). 0167-5273/$ - see front matter D 2003 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/S0167-5273(03)00222-5

tained monomorphic ventricular tachycardia (SMVT) originating from LV aneurysm without definite underlying diseases.

2. Case report A 66-year-old woman suffering from palpitation with fainting dizziness was admitted to our hospital for evaluation and treatment of SMVT. She had no family history of heart disease or past history of systemic diseases. Seven years previously at another hospital, she was diagnosed as having both LV aneurysm and SMVT. Since then, although her arrhythmia was administered several medical treatments including class I or III antiarrhythmic agents, Ca channel blocker, and beta blocker, her SMVT frequency increased with its time course. Though she took sotalol and verapamil orally, her SMVT attacks occurred twice a week just before her current admission. On examination, left ventriculography revealed a large saccular aneurysm of

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LV apex (Fig. 1A and B) and coronary angiography showed intact coronary artery. Because further examinations could not demonstrate underlying diseases, we defined the present case as idiopathic LV aneurysm. During subsequent electrophysiological study, the SMVT with a cycle length of 380 ms and the same morphology as a clinical VT (Fig. 2B) was reproducibly induced by double extrastimuli after 280 and 270 ms during basic stimuli with a cycle length of 600 ms from the right ventricular (RV) apex without difficulty. During SMVT, endocardial electrogram recordings at the apical LV aneurysm showed fragmented potential 40 ms preceding the earliest wide QRS complex (Fig. 2C). Three-dimensional electroanatomical mapping (CARTOk; Biosense Webster) of the LV clearly demonstrated that the SMVT was originating from the apical LV aneurysm (Fig. 2D – F). At this site, one radiofrequency application of 90 s, 55 jC, and 50 W terminated the SMVT after 14 s, and then additional applications were delivered in the vicinity of this site in accordance with electroanatomical mapping. Thereafter, the SMVT was no longer inducible by a programmed electrical stimulation at the RV apex or RV outflow tract. The patient has remained free of VT recurrences during a subsequent 12-month follow-up period.

3. Discussion The present case was characterized by a large idiopathic saccular apical LV aneurysm complicated with

recurrent SMVT refractory to medical therapy. It has been reported that idiopathic LV aneurysm is often complicated with ventricular tachyarrhythmias, and its mechanism is due to a reentry [6]. Furthermore, VTs with idiopathic LV aneurysm are occasionally resistant to medical treatment. In order to treat them, non-pharmacological therapies are required, including implantable cardioverter defibrillator and surgical repairs [3 – 5]. However, there was no report of successful catheter ablation for VT originating from idiopathic LV aneurysm. In the present case, we performed electroanatomical and conventional bipolar potential mapping. These combined LV mappings during SMVT under decreased blood pressure were useful to identify a reentry circuit and a critical focus in a short time. Although the saccular apical LV aneurysm was large, the intracardiac abnormal potentials area was relatively small. This led us to apply a local radiofrequency catheter ablation. O’Callaghan et al. [7] reported that the presence of LV aneurysm followed by a prior myocardial infarction was one of the predictors of VT recurrence during long-term follow-up after catheter ablation, and Rajasinghe et al. [4] reported the necessity of surgical therapy for medically refractory arrhythmogenic LV aneurysm. These previous studies [4,7] suggest the necessity of careful observation for SMVT recurrence in the future, although catheter ablation for the patient was successful and no further episode of SMVT was observed during a 12-month follow-up. If medically refractory ventricular tachyarrhythmias recur, a surgical treatment should be considered.

Fig. 1. The diastolic (A) and systolic (B) phases of left ventriculographies (right anterior oblique 30j view) showed existence of saccular apical aneurysm.

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Fig. 2. Twelve-lead ECG at rest showed normal sinus rhythm (57 bpm) and negative T wave appeared in V2 to V6 (25 mm/s, 1 cm/mV) (A). Northwest axis deviation and right bundle branch block type SMVT with a cycle length of 380 ms was induced by programmed electrical stimulation, same as clinical VT (25 mm/s, l cm/mV) (B). Note the fragmented ventricular potential of 40 ms preceding the surface QRS complex recorded (100 mm/s) with distal successful ablation catheter (ABL d) (C). Three-dimensional electroanatomical map of the LV showed the endocardial activation sequence during SMVT in a right anterior oblique 30j view (D), a left anterior oblique 60j view (E) and a bottom view (F). Earliest activation (red color and arrows) occurred gradually from the part of the apical LV aneurysm. Red dots indicate radiofrequency applications.

References [1] Maloy WC, Arrants JE, Sowell BF, Hendrix GH. Left ventricular aneurysm of uncertain etiology with recurrent ventricular arrhythmias. N Engl J Med 1971;285:662 – 3. [2] Treisman B, Cooley DA, Lufschanowski R, Leachman RD. Diverticular aneurysm of left ventricule. Am J Cardiol 1973;32:119 – 23. [3] Fellows CL, Bardy GH, Ivey TD, Werner JA, Draheim JJ, Greene HL. Ventricular dysrhythmias associated with congenital left ventricular aneurysms. Am J Cardiol 1986;57:997 – 9. [4] Rajasinghe HA, Lorenz HP, Longaker MT, Scheinmann MM, Merrick SH. Arrhythmogenic ventricular aneurysms unrelated to coronary artery disease. Ann Thorac Surg 1995;59:1079 – 84.

[5] Proclemer A, Miani D, Basadonna PT, Rocco M, Nicotra G. Idiopathic left ventricular aneurysm: an unusual substrate of ventricular fibrillation and ventricular tachycardia. J Interv Card Electrophysiol 1998; 2:187 – 91. [6] Tada H, Kurita T, Ohe T, et al. Clinical and electrophysiologic features of idiopathic left ventricular aneurysm with sustained ventricular tachycardia. Int J Cardiol 1998;67:27 – 38. [7] O’Callaghan PA, Poloniecki J, Sosa-Suarez G, Ruskin JN, McGovern BA, Garan H. Long-term clinical outcome of patients with prior myocardial infarction after palliative radiofrequency catheter ablation for frequent ventricular tachycardia. Am J Cardiol 2001;87:975 – 9.

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Fig. 2 (continued).