Lipomatous Metaplasia Enables Ventricular Tachycardia by ReducingCurrent Loss Within theProtected Corridor.

Abstract

Post-myocardial infarction ventricular tachycardia (VT) is due to re-entry through surviving conductive myocardial corridors across infarcted tissue. However, not all conductive corridors participate in re-entry. This study sought to test the hypothesis that critical VT corridors are more likely to traverse near lipomatous metaplasia (LM) and that current loss is reduced during impulse propagation through such corridors. Among 30 patients in the Prospective 2-center INFINITY (Intra-Myocardial Fat Deposition and Ventricular Tachycardia in Cardiomyopathy) study, potential VT-viable corridors within myocardial scar or LM were computed from late gadolinium enhancement cardiac magnetic resonance images. Because late gadolinium enhancement highlights both scar and LM, LM was distinguished from scar by using computed tomography. The SD of the current along each corridor was measured. Scar exhibited lower impedance than LM (median Z-score -0.22 [IQR: -0.84 to 0.35] vs -0.07 [IQR: -0.67 to 0.54]; P< 0.001). Among all 381 corridors, 84 were proven to participate in VT re-entry circuits, 83 (99%) of which traversed or were adjacent to LM. In comparison, only 13 (4%) non-VT corridors were adjacent to LM. Critical corridors adjacent to LM displayed lower SD of current compared with noncritical corridors through scar but distant from LM (2.0[IQR: 1.0 to 3.4] μA vs 8.4 [IQR: 5.5 to 12.8] μA; P< 0.001). Corridors critical to VT circuitry traverse infarcted tissue through or near LM. This association is likely mediated by increased regional resistance and reduced current loss as impulses traverse corridors adjacent to LM.