Abstract 11288: Conduction Velocity is Slower in Corridors Traversing Lipomatous Metaplasia Than in Corridors Traversing Scar in Chronic Infarcts

Abstract

Introduction: We sought to examine the association of infarct scar versus lipomatous metaplasia (LM) with impulse conduction velocity (CV) in putative ventricular tachycardia (VT) corridors that traverse the infarct zone in patients with prior myocardial infarction (MI). Methods: The cohort included 31 patients from the prospective In tra-Myocardial F at Deposition and Ventricular Tachycardia in Ischemic Card i omyopa t h y (INFINITY) study. CV was calculated as the mean CV between that point and five adjacent points along the activation wavefront using an automated Python script in myocardial scar, border zone (BZ), and potential viable corridors defined by late gadolinium enhancement (LGE)-cardiac magnetic resonance (CMR), and LM identified by computed tomography (CT). Both image sets were registered with electroanatomic maps (EAM). Results: Regions with LM exhibited lower myocardial CV than scar (median 12.0 vs. 13.5 cm/s, P <0.001). Of 96 corridors computed from LGE-CMR and electrophysiologically confirmed to participate in VT reentry, 95 traversed through or near LM identified on CT. These critical corridors displayed slower CV {median 8.8 [interquartile range (IQR) 6.0, 15.4] vs. 39.0 (IQR 27.8, 56.5) cm/s, P <0.001, Figure 1}, and demonstrated low-peripheral-high-center (mountain-shaped, 25%), or mean low level (45.7%) CV patterns, when compared to 122 non-critical corridors distant from LM that displayed high-peripheral-low-center (valley-shaped, 20.5%) or mean high level (59%) CV patterns. Conclusion: Myocardial LM is a crucial contributor to VT propensity. Corridors traversing through or near LM exhibit significantly slower CV, which likely facilitate the presence and stability of the VT circuit reentry.