Dataset Information

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

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.

SUBMITTER: Xu L

PROVIDER: S-EPMC11168467 | biostudies-literature | 2023 Aug

REPOSITORIES: biostudies-literature

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Publications

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

Xu Lingyu L Zahid Sohail S Khoshknab Mirmilad M Moss Juwann J Berger Ronald D RD Chrispin Jonathan J Callans David D Marchlinski Francis E FE Zimmerman Stefan L SL Han Yuchi Y Desjardins Benoit B Trayanova Natalia N Nazarian Saman S

JACC. Clinical electrophysiology 20230524 8 Pt 1

<h4>Background</h4>Myocardial lipomatous metaplasia (LM) has been reported to be associated with post-infarct ventricular tachycardia (VT) circuitry.<h4>Objectives</h4>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.<h4>Methods</h4>The cohort included 31 post-infarct patients from the prospective INFINITY (Intra-Myocardial Fat Deposition and Ventricular Tachyca ...[more]

PMID: 37227343

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Project description:BACKGROUND:Ripple mapping displays every deflection of a bipolar electrogram and enables the visualization of conduction channels (RMCC) within postinfarction ventricular scar to guide ventricular tachycardia (VT) ablation. The utility of RMCC identification for facilitation of VT ablation in the setting of arrhythmogenic right ventricular cardiomyopathy (ARVC) has not been described. OBJECTIVE:We sought to (a) identify the slow conduction channels in the endocardial/epicardial scar by ripple mapping and (b) retrospectively analyze whether the elimination of RMCC is associated with improved VT-free survival, in ARVC patients. METHODS:High-density right ventricular endocardial and epicardial electrograms were collected using the CARTO 3 system in sinus rhythm or ventricular pacing and reviewed for RMCC. Low-voltage zones and abnormal myocardium in the epicardium were identified by using standardized late-gadolinium-enhanced (LGE) magnetic resonance imaging (MRI) signal intensity (SI) z-scores. RESULTS:A cohort of 20 ARVC patients that had undergone simultaneous high-density right ventricular endocardial and epicardial electrogram mapping was identified (age 44 ± 13 years). Epicardial scar, defined as bipolar voltage less than 1.0 mV, occupied 47.6% (interquartile range [IQR], 30.9-63.7) of the total epicardial surface area and was larger than endocardial scar, defined as bipolar voltage less than 1.5 mV, which occupied 11.2% (IQR, 4.2 ± 17.8) of the endocardium (P < 0.01). A median 1.5 RMCC, defined as continuous corridors of sequential late activation within scar, were identified per patient (IQR, 1-3), most of which were epicardial. The median ratio of RMCC ablated was 1 (IQR, 0.6-1). During a median follow-up of 44 months (IQR, 11-49), the ratio of RMCC ablated was associated with freedom from recurrent VT (hazard ratio, 0.01; P = 0.049). Among nine patients with adequate MRI, 73% of RMCC were localized in LGE regions, 24% were adjacent to an area with LGE, and 3% were in regions without LGE. CONCLUSION:Slow conduction channels within endocardial or epicardial ARVC scar were delineated clearly by ripple mapping and corresponded to critical isthmus sites during entrainment. Complete elimination of RMCC was associated with freedom from VT.

Dataset Information

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

Background

Objectives

Methods

Results

Conclusions

Publications

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

Similar Datasets

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