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. 2022 Oct;8(10):1274-1285.
doi: 10.1016/j.jacep.2022.07.005. Epub 2022 Aug 31.

Lipomatous Metaplasia Enables Ventricular Tachycardia by Reducing Current Loss Within the Protected Corridor

Lingyu Xu  1 , Mirmilad Khoshknab  1 , Ronald D Berger  2 , Jonathan Chrispin  2 , Sanjay Dixit  1 , Pasquale Santangeli  1 , David Callans  1 , Francis E Marchlinski  1 , Stefan L Zimmerman  3 , Yuchi Han  1 , Natalia Trayanova  4 , Benoit Desjardins  5 , Saman Nazarian  6
Affiliations

Lipomatous Metaplasia Enables Ventricular Tachycardia by Reducing Current Loss Within the Protected Corridor

Lingyu Xu et al. JACC Clin Electrophysiol. 2022 Oct.

Abstract

Background: 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.

Objectives: 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.

Methods: 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.

Results: 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).

Conclusions: 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.

Keywords: current loss; fat; impedance; ischemic cardiomyopathy; lipomatous metaplasia; myocardial infarction; ventricular tachycardia.

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Conflict of interest statement

Funding Support and Author Disclosures The INFINITY study is funded by National Institutes of Health grant 1R01HL142893-01, as well as support from the Mark Marchlinski Electrophysiology Research and Education Fund. Dr. Marchlinski has served as consultant for Abbott Medical, Biosense Webster, Biotronik, and Medtronic Inc. Dr. Nazarian has served as a consultant for CardioSolv and Circle CVI; and principal investigator for research funding from Biosense Webster, ImriCor, Siemens, ADAS software, and the U.S. National Institutes of Health. The University of Pennsylvania Conflict of Interest Committee manages all commercial arrangements. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.

Figures

Figure 1.
Figure 1.. Electrogram Characteristics versus Tissue Types –
Violin plots of electrogram characteristics among myocardial tissue types. Bipolar and unipolar voltage amplitude, impedance and current are plotted with the absolute value in the left panel and the z-score in the right panel (circle represents the median, and the thick gray bar represents the interquartile range). *Significantly different from normal myocardium (P<0.05); † Significantly different from border zone (P <0.05); ‡ Significantly different from scar (P<0.05).
Figure 2.
Figure 2.. Preservation of Current in Corridors Traversing LM –
Current amplitude along viable corridors through scar and LM. Panels a1-4) corridors (white line) traversing LGE (combination of scar and LM as red) magnified in Panel b; Panel c1-4) visualization of LM (white area) from CT, with the corridor magnified in Panel d; Panel d1-4) relation of corridor (white line) to LM; Panel e1-4) plot of current amplitude along the corridors displayed in Panel a, showing stability along Corridors 1 and 3 (critical to VT) compared to Corridors 2 and 4 (not critical to VT). Panel f) Violin plot display of SD of current amplitude along viable corridors traversing LM versus distant from LM. White points: sampled points; red points: ablation sites; black points: delayed potential; magenta point in Corridor 1: exit of the VT reentry corridor; blue points in Corridor 3: isthmus of the VT reentry corridor. Lipomatous metaplasia = LM, ventricular tachycardia = VT.
Figure 3.
Figure 3.. Lipomatous Metaplasia and Circuit Sites –
LM patterns of electroanatomic mapping points identified as entrances, isthmuses and exits of VT reentry circuits. Lipomatous metaplasia = LM, ventricular tachycardia = VT.
Central Illustration.
Central Illustration.
Study Methodology. Panel a1) Representative LGE (scar/LM = red) and CT (LM = green) images segmented into shell (a2) with LGE (scar = red, border-zone = light blue, corridor = white line), and CT (LM = green) features, co-registered with electroanatomic mapping with VT isthmus (blue dot) at LM-scar interface. a3) Corridors (white line) are identified when >5 mm border-zone (stars) is surrounded by LGE (scar/LM, triangles) and connects healthy to healthy tissue (diamonds). b1) The hypothesis was that corridors traversing low impedance scar acting as current sink would exhibit higher standard deviation of current measurements with progressive drop (one-side activation of corridor) or U-shaped pattern (two-side activation); whereas (b2) corridors surrounded by LM (higher impedance than scar) would exhibit lower standard deviation due to reduced current loss. Late gadolinium enhancement = LGE, lipomatous metaplasia = LM, computed tomography = CT, ventricular tachycardia = VT.
See this image and copyright information in PMC

Comment in

  • Ventricular Tachycardia Corridors and Fat.
    Stevenson WG, Richardson TD, Kanagasundram AN. Stevenson WG, et al. JACC Clin Electrophysiol. 2022 Oct;8(10):1286-1288. doi: 10.1016/j.jacep.2022.08.005. JACC Clin Electrophysiol. 2022. PMID: 36266005 No abstract available.

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