Lipomatous Metaplasia Facilitates Slow Conduction in Critical Ventricular Tachycardia Corridors Within Postinfarct Myocardium

Abstract

BackgroundMyocardial lipomatous metaplasia (LM) has been reported to be associated with post-infarct ventricular tachycardia (VT) circuitry. ObjectivesThis study examined the association of scar versus LM composition with impulse conduction velocity (CV) in putative VT corridors that traverse the infarct zone in post-infarct patients. MethodsThe cohort included 31 post-infarct patients from the prospective INFINITY (Intra-Myocardial Fat Deposition and Ventricular Tachycardia in Cardiomyopathy) study. Myocardial scar, border zone, and potential viable corridors were defined by late gadolinium enhancement cardiac magnetic resonance (LGE-CMR), and LM was defined by computed tomography. Images were registered to electroanatomic maps, and the CV at each electroanatomic map point was calculated as the mean CV between that point and 5 adjacent points along the activation wave front. ResultsRegions with LM exhibited lower CV than scar (median = 11.9 vs 13.5 cm/s; P < 0.001). Of 94 corridors computed from LGE-CMR and electrophysiologically confirmed to participate in VT circuitry, 93 traversed through or near LM. These critical corridors displayed slower CV (median 8.8 [IQR: 5.9-15.7] cm/s vs 39.2 [IQR: 28.1-58.5]) cm/s; P < 0.001) than 115 noncritical corridors distant from LM. Additionally, critical corridors demonstrated low-peripheral, high-center (mountain shaped, 23.3%) or mean low-level (46.7%) CV patterns compared with 115 noncritical corridors distant from LM that displayed high-peripheral, low-center (valley shaped, 19.1%) or mean high-level (60.9%) CV patterns. ConclusionsThe association of myocardial LM with VT circuitry is at least partially mediated by slowing nearby corridor CV thus facilitating an excitable gap that enables circuit re-entry.