PMC6342335_01
During ablation in the left coronary cusp of the aorta, outflow ventricular tachycardia (VT) terminated and converted to a right ventricular apical VT. The second VT was then pace-terminated. At this point, it became evident that a more extensive process was involved.
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During the course of this study, a left bundle branch (LBB) morphology, inferior axis VT (Figure 1) was induced. During ablation in the left coronary cusp, the outflow tract VT converted to a more apically located VT origin (Figure 1). At the conclusion of the endocardial voltage mapping, isoproterenol was infused and VT with LBB morphology, left superior axis (similar to Figure 1) was induced following a single extrastimulation with a 500-ms drivetrain. Pace mapping revealed a region within the lateral RV epicardial surface with a 96% pace match (PASO algorithm, Biosense Webster) with the left superior axis LBB VT morphology seen in the latter half of Figure 1, but no clear late potentials were evident.
CARTO voltage maps, intracardiac electrogram, and computed tomography integration of aortic root and coronary arteries. A: Endocardial (upper left) and epicardial (upper right) voltage maps in the right anterior oblique (RAO) projection with normal tissue (purple) reference of 1.5 mV. A small region of endocardial scar is seen on the posterior aspect of the right ventricular (RV) outflow tract over the right coronary cusp corresponding to the region of prior endocardial/aortic root ablation. A significant region of epicardial scar is seen on the lateral RV wall extending to the posterior wall. The blue dots delineate atrioventricular groove points; the white circle marks a broad site of greater than 90% pace match points to the induced hemodynamically unstable ventricular tachycardia. B: Catheter positioning against the RV free wall, along with measured contact force (5 g). A large region of low voltage involving the lateral right ventricle is evident on voltage mapping. Simultaneous intracardiac electrogram (right) shows low voltage potentials (arrow, 0.28 V) suggesting possible scar. Intracardiac echocardiographic (below right) imaging shows no pericardial effusion. The presence of epicardial scar is not definitive in this region solely by low voltage owing to perivascular and RV epicardial fat in this region, and the absence of late and split potentials suggests the possibility of this being normal. This is equally as likely as there being scarring not detected by magnetic resonance imaging.
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Next, epicardial access was obtained percutaneously, and epicardial electroanatomic mapping was performed on the left and right ventricles (Figure 2).