adiofrequency (RF) catheter ablation (CA) is estab-lished as an effective and curative therapy for idiopathic ventricular tachycardia (I-VT). [1][2][3][4][5][6][7][8] It is well known that some I-VTs can be eliminated by RFCA at the endocardium of the left ventricular outflow tract (LVOT) or the left sinus of Valsalva (LSV). [1][2][3]8 However, some that arise from the epicardial portion of the LVOT are remote from the LSV or left ventricular (LV) endocardium and are not amenable to ablation at those sites. 5,8,9 Several recent reports have demonstrated that I-VTs arising from the epicardial portion of the LVOT can be ablated from the distal portion of the coronary venous system that lies along the LV epicardial site. [10][11][12][13] However, the ECG and electrophysiologic characteristics of this type of ventricular tachycardia (VT) have not been sufficiently clarified.We describe here a case of an I-VT that was finally eliminated by RFCA within the great cardiac vein (GCV). We also present a summarized review of I-VTs that have been ablated from the coronary venous system or by percutaneous epicardial instrumentation.
Case ReportA 30-year-old man was admitted for a second session of RFCA of symptomatic, drug-refractory VT and premature ventricular contractions (PVCs). At the age of 27 in 2003, he complained of palpitations, and 24-h Holter ECG recording disclosed frequent nonsustained VTs and PVCs (total number of PVCs: 43,474 beats/day). He underwent a first session of RFCA for this tachycardia: the local ventricular activation recorded at the endocardial site of the LVOT
Circulation Journal Vol.71, December 2007(LVOT endocardium) and LSV both preceded the onset of the QRS complex by 16 ms, and RFCA at both sites eliminated the VTs. However, the PVCs, which had the same QRS morphology as the first beat of the clinical VT and PVCs, recurred a few hours after the ablation procedure. Although sporadic PVCs occurred (404 beats/day), he was asymptomatic and did not receive medications.Three years later at the age of 30 in 2006, he began to experience palpitations and the sensation of a pulse deficit. The 12-lead ECG at the time of admission demonstrated regular sinus rhythm with a narrow QRS complex and a normal axis (Fig 1). During the clinical arrhythmia, the surface ECG always revealed monomorphic VT or PVCs with a left bundle-branch block morphology and an inferior axis, which had the same QRS morphology as those occurring 3 years ago. Holter ECG monitoring revealed a nonsustained VT lasting up to 34 consecutive beats and a total number of PVCs consisting of 41,691 beats/day. Echocardiography disclosed a dilated LV with an end-diastolic internal dimension of 57 mm and a decreased LV wall motion with an ejection fraction of 39% during sinus rhythm. The chest X-ray revealed a cardiothoracic ratio of 51.2%, and the plasma level of brain natriuretic peptide (BNP) was 30 pg/ml (normal reference values in Japanese are <18.4 pg/ml).After informed written consent was given, a second electrophysiology study was perform...