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(Circulation. 2006;113:1659-1666.)
© 2006 American Heart Association, Inc.

Arrhythmia/Electrophysiology

Idiopathic Epicardial Left Ventricular Tachycardia Originating Remote From the Sinus of Valsalva

Electrophysiological Characteristics, Catheter Ablation, and Identification From the 12-Lead Electrocardiogram

David V. Daniels, MD; Yen-Yu Lu, MD; Joseph B. Morton, MD; Peter A. Santucci, MD; Joseph G. Akar, MD, PhD; Alex Green, MD; David J. Wilber, MD

From the Cardiovascular Institute, Loyola University Medical Center, Maywood, Ill.

Correspondence to David J. Wilber, MD, Cardiovascular Institute, Bldg 110, Room 6232, Loyola University Medical Center, 2160 S. First Ave, Maywood, IL 60153. E-mail dwilber{at}lumc.edu

Received September 13, 2005; de novo received December 31, 2005; revision received January 16, 2006; accepted January 31, 2006.

Background— Despite the success of catheter ablation for treatment of idiopathic ventricular tachycardia (VT), occasional patients have been reported in whom VT could not be ablated from the right or left ventricular endocardium or from the aortic sinus of Valsalva (ASOV).

Methods and Results— In 12 of 138 patients (9%) with idiopathic VT referred for ablation, an epicardial left ventricular site of origin was identified >10 mm from the ASOV. Coronary venous mapping demonstrated epicardial preceding endocardial activation by >10 ms (41±7 versus 15±11 ms before QRS onset; P<0.001). VT induction was facilitated by catecholamines and terminated by adenosine. Ablation through the coronary veins or via percutaneous transpericardial catheterization was successful in 9 patients; 2 required direct surgical ablation as a result of anatomic constraints. No ECG pattern was specific for epicardial VT. However, slowed initial precordial QRS activation, as quantified by a novel metric, the maximum deflection index, was more useful. A delayed precordial maximum deflection index 0.55 identified epicardial VT remote from the ASOV with a sensitivity of 100% and a specificity of 98.7% relative to all other sites of origin (P<0.001).

Conclusions— Although clinically underrecognized, idiopathic VT may originate from the perivascular sites on the left ventricular epicardium. The mechanism is consistent with triggered activity. It is amenable to ablation by transvenous or transpericardial approaches, although technical challenges remain. Recognition of a prolonged precordial maximum deflection index and early use of transvenous epicardial mapping are critical to avoid protracted and unsuccessful ablation elsewhere in the ventricles.

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