Lipomatous metaplasia prolongs repolarization and increases repolarization dispersion within post-infarct ventricular tachycardia circuit cites

Abstract

Aims Post-infarct myocardium contains viable corridors traversing scar or lipomatous metaplasia (LM). Ventricular tachycardia (VT) circuitry has been separately reported to associate with corridors that traverse LM and with repolarization heterogeneity. We examined the association of corridor activation recovery interval (ARI) and ARI dispersion with surrounding tissue type. Methods and results The cohort included 33 post-infarct patients from the prospective Intra-Myocardial Fat Deposition and Ventricular Tachycardia in Cardiomyopathy (INFINITY) study. We co-registered scar and corridors from late gadolinium enhanced magnetic resonance, and LM from computed tomography with intracardiac electrogram locations. Activation recovery interval was calculated during sinus or ventricular pacing, as the time interval from the minimum derivative within the QRS to the maximum derivative within the T-wave on unipolar electrograms. Regional ARI dispersion was defined as the standard deviation (SD) of ARI per AHA segment (ARISD). Lipomatous metaplasia exhibited higher ARI than scar [325 (interquartile range 270–392) vs. 313 (255–374), P < 0.001]. Corridors critical to VT re-entry were more likely to traverse through or near LM and displayed prolonged ARI compared with non-critical corridors [355 (319–397) vs. 302 (279–333) ms, P < 0.001]. ARISD was more closely associated with LM than with scar (likelihood ratio χ2 50 vs. 12, and 4.2-unit vs. 0.9-unit increase in 0.01*Log(ARISD) per 1 cm2 increase per AHA segment). Additionally, LM and scar exhibited interaction (P < 0.001) in their association with ARISD. Conclusion Lipomatous metaplasia is closely associated with prolonged local action potential duration of corridors and ARI dispersion, which may facilitate the propensity of VT circuit re-entry.

Noninvasive Assessment of Lipomatous Metaplasia as a Substrate for Ventricular Tachycardia in Chronic Infarct

“…3 We reported that, via registering the LGE-CMR images and the cardiac CECT images, 33% of LM detected from the cardiac CECT was located within the border zone, while 60% of LM was located within the dense LGE area. 31 Although LGE images are the gold standard for evaluating scar, 30 other CMR sequences or other modalities (eg, CT) are required to differentiate LM from scar or edema on LGE images. Segmentation of LGE images should be performed cautiously, because the bright EAT can obscure the subepicardial contour in the presence of subepicardial LGE and ventricular blood pool can obscure the subendocardial border in the presence of subendocardial LGE.…”

“…Using image to electroanatomic map registration, our group and others have reported the electrophysiological features of LM. LM exhibits significantly lower intracardiac electrogram voltage amplitude, 3,6 higher electrical impedance, 3 lower current amplitude, 3 prolonged repolarization time, increased regional repolarization variation, 31 and slower conduction velocity, 4,53 and subtantial colocolization with the deceleration zone 54 compared with scar 54 (Table S2). Therefore, LM appears to be a vital contributor to VT circuitry in patients with prior MI.…”

Fat deposition and repolarization: another brick in the wall promoting ventricular tachycardia?

“…Still, several clinical studies have shown that VT circuits are associated with repolarization heterogeneity. 3 , 8 , 9 Thus, targeting the regions exhibiting repolarization heterogeneities may represent a potential strategy to eliminate ventricular arrhythmia. 10 …”

“…In this issue of Europace , Xu et al . 9 report on the relationship between fat deposition and ARIs in patients presenting with post-infarction VT. They further explore how these two parameters (one structural and one functional) relate to VT circuits, in a series of 33 patients referred for VT ablation with available pre-operative CMR and CT studies.…”

The Silent Player

“…Lipomatous metaplasia (LM) refers to the replacement of myocardial scar with adipose tissue, commonly following myocardial infarction (MI). 16 According to Ichikawa et al, 17 the volume of LM increases over time following an MI. Similarly, monomorphic VT in ischemic cardiomyopathy can occur years after an MI.…”