Endovascular catheter ablation of ventricular tachycardia in a patient with a surgically repaired congenital left ventricular aneurysm

We present a patient with a congenital left ventricular aneurysm who visited our outpatient clinic for a routine check-up and, during this visit, lost consciousness due to sustained ventricular tachycardia. In our patient, endocardial mapping revealed extensive conduction abnormalities, and successful ablation was accomplished at the endocardial surface.

A 19-year-old male individual with a surgically corrected congenital left ventricular aneurysm (LVA) in the basal posterior wall visited our outpatient clinic for a routine checkup. Surgical resection of the aneurysm was performed 10 years ago. LVA recurrence was discovered only 1 year after surgery. The left ventricle was dilated (end-diastolic diameter 70 mm), and the ejection fraction was decreased (36 %). During this visit, the patient lost consciousness due to sustained ventricular tachycardia (VT; left upper part of Fig. 1). His ICD (implantable cardiac defibrillator), which was implanted earlier for non-sustained VT episodes, did not deliver therapy, as the cycle length of the VT was longer than the programmed detection interval. The VT seemed to be originating from the basal posterior wall of the left ventricle, most likely from the LVA. During external cardiover-

Discussion
Congenital LVA is a rare congenital defect. It is defined as the presence of an akinetic or dyskinetic structure with a wide connection to the left ventricle, which is normal in size and function [1]. Reports on VT associated with congenital LVA are limited to a few cases [2]. Patients with LVA are frequently asymptomatic but congestive heart failure, tachyarrhythmias and systemic embolisation may develop. Even sudden death has been observed in LVA patients and may be related to rupture of the LVA [3,4].
In a group of 108 patients with either LVA or diverticulum, who were followed during a median period of 50 months, VTs occurred in only ten patients [5]. Yamashiro et al. [6] described cryoablation during cardiac surgery in two adult LVA patients with sustained VT. However, they did not perform epicardial mapping prior to ablation. Only Ouyang et al. reported on cardiac mapping prior to ablation in four LVA patients with recurrent exercise-induced syncope attributable to sustained fast monomorphic VT. The aneurysm was located in the inferolateral part of the left ventricle in all patients. Mapping during sinus rhythm revealed abnormal signals (fractionated or late potentials) on the epicardium but not on the endocardium. In one patient with a stable VT, epicardial mapping showed a macrore-entrant VT with a focal pattern of activation at the endocardial surface. Epicardial ablation was successfully performed in three patients [7]. Hence, our case is the first LVA patient in whom (1) endocardial mapping revealed extensive conduction abnormalities (low voltage, double and fractionated potentials), and (2) successful ablation was accomplished at the endocardial surface. Our patient had a dilated left ventricle and depressed ejection fractionindicating a more advanced stage of LVA compared with the patients in the study by Ouyang et al. [7]. The underlying mechanism of the VT is most likely a microre-entry circuit at the endocardial surface. However, endocardial breakthrough of an epicardial wavefront cannot be excluded.

Conclusion
Ventricular tachycardia after cardiac surgery for LVAs can be treated by endocardial catheter ablation at the endocardial surface of the left ventricle. Extensive local conduction abnormalities are recorded within the endocardial surface of the aneurysm which may form the substrate of the ventricular tachycardia.
Funding None.

Conflict of interests None declared.
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