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. 2023 Aug;9(8 Pt 1):1235-1245.
doi: 10.1016/j.jacep.2023.02.014. Epub 2023 May 24.

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

Lingyu Xu  1 , Sohail Zahid  2 , Mirmilad Khoshknab  3 , Juwann Moss  3 , Ronald D Berger  4 , Jonathan Chrispin  4 , David Callans  3 , Francis E Marchlinski  3 , Stefan L Zimmerman  5 , Yuchi Han  3 , Benoit Desjardins  6 , Natalia Trayanova  7 , Saman Nazarian  8
Affiliations

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

Lingyu Xu et al. JACC Clin Electrophysiol. 2023 Aug.

Abstract

Background: Myocardial lipomatous metaplasia (LM) has been reported to be associated with post-infarct ventricular tachycardia (VT) circuitry.

Objectives: This 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.

Methods: The 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.

Results: Regions 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.

Conclusions: The 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.

Keywords: conduction velocity; 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 the National Institute of Health grant 1R01HL142893-01. The authors received support from support from ADAS Software and from the Mark Marchlinski Electrophysiology Research and Education Fund. Dr Xu is funded by an American Heart Association postdoctoral fellowship. The University of Pennsylvania Conflict of Interest Committee manages all commercial arrangements. Dr Nazarian is a consultant for CardioSolv and Circle CVI; and is a principal investigator for research funding from Biosense Webster, ImriCor, Siemens, ADAS software, and the U.S. National Institutes of Health. Dr Marchlinski has served as consultant for Abbott Medical, Biosense Webster, Biotronik, and Medtronic Inc. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.

Figures

Figure 1.
Figure 1.. Conduction velocity was compared among four types of cardiac tissue by violin plots –
The absolute value and the modified z score of conduction velocity was plotted according to four types of cardiac tissue, healthy myocardium, border zone (BZ) tissue, scar and lipomatous metaplasia (LM) in the left and right panel, respectively. * means significantly different from normal myocardium; # means significantly different from border zone tissue; ¶ means significantly different from scar; Abbreviation: LM = lipomatous metaplasia; BZ = border zone; CV = conduction velocity.
Figure 2.
Figure 2.. The conduction velocity pattern of the consecutive points along corridors participating in VT reentry circuits and traversing or adjacent to lipomatous metaplasia versus corridors not participating in VT circuits distant from lipomatous metaplasia.
Abbreviations: VT = ventricular tachycardia; CV = conduction velocity; LM = lipomatous metaplasia; SD = standard deviation. * in the figure means significant different from the critical corridors traversing LM.
Central Illustration.
Central Illustration.. Examples of conduction velocity along corridors participating in VT reentry circuits versus corridors not participating in VT circuits.
-Panels a 1–4) corridors (white line) computed in LGE image with the corridor (white square) magnified in Panel c); Panel b 1~4) the 3D visualization of lipomatous metaplasia (LM, white area) in computed tomography image, with the corresponding part of the corridor from the Panel a) magnified in Panel d); Panel d 1~4) the corridor (white line) in relation to LM; Panel e 1~4) conduction velocity (CV) measurements of intracardiac electrogram points along the corridors were displayed in a scatter plot, showing substantially lower average level and less fluctuation of the CV along Corridors 1 & 3 (critical to VT circuitry) than that of Corridors 2 & 4 (not critical to VT circuitry ). Panel f). The mean and standard deviation of CV measurements at multiple points along corridors traversing or adjacent to the LM found to participate in VT reentry on entrainment or pace-mapping are significantly lower (indicated as #) than those of corridors not adjacent to LM and not participating in VT reentry. white points: mapping spots; red points: ablation sites; black points: delayed potential; yellow points: pacing sites; Green dot in Corridor #1: entrance site of VT reentry; Purple dot in Corridor #1: exit site of VT reentry. Abbreviation: LM = lipomatous metaplasia; CV = conduction velocity. 1
See this image and copyright information in PMC

Comment in

  • Scar, Fat, and Fibrosis: Rethinking Re-Entry.
    Tung R, Tamarappoo B, Morris MF. Tung R, et al. JACC Clin Electrophysiol. 2023 Aug;9(8 Pt 1):1246-1247. doi: 10.1016/j.jacep.2023.06.007. JACC Clin Electrophysiol. 2023. PMID: 37558286 No abstract available.

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