ArticleJACC. Clinical electrophysiology2023
Lipomatous Metaplasia Facilitates Slow Conduction in Critical Ventricular Tachycardia Corridors Within Postinfarct Myocardium.
Article in JACC. Clinical electrophysiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 17 citations in OpenAlex.
- Predicting Sudden Cardiac Death in Heart Failure with Mildly Reduced/Preserved Left Ventricular Ejection Fraction: A Clinical Review.Journal of clinical medicine · 2026Review
- CMR-quantified epicardial adipose tissue heterogeneity and its predictive value for ventricular and atrial arrhythmias after myocardial infarction.BMC medical imaging · 2026Article
- Prognostic significance and influencing factors of lipomatous metaplasia in patients after myocardial infarction.Insights into imaging · 2025Article
- The Role of Imaging in Ventricular Tachycardia Ablation.Diagnostics (Basel, Switzerland) · 2025Review
- Cardiovascular imaging techniques for electrophysiologists.Nature cardiovascular research · 2025Review
- Reply to: Stochastic virtual heart model predictions.Nature cardiovascular research · 2025Article
- Up digital and personal: How heart digital twins can transform heart patient care.Heart rhythm · 2024Review
- Noninvasive Assessment of Lipomatous Metaplasia as a Substrate for Ventricular Tachycardia in Chronic Infarct.Circulation. Cardiovascular imaging · 2023Review
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Authors and funding
13 authors at 4 institutions in 1 country.
Funding
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.
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