Why the study?
LGE-CMR identifies structural properties linked to ventricular tachycardia but lacks functional data; ECGI-based identification of slow conduction during sinus rhythm could complement LGE-CMR for risk stratification.
Does noninvasive electrocardiographic imaging (ECGI) during sinus rhythm identify ventricular arrhythmogenic substrate in patients with ischemic cardiomyopathy?
Observational (n=72)
Does noninvasive electrocardiographic imaging (ECGI) during sinus rhythm identify ventricular arrhythmogenic substrate in patients with ischemic cardiomyopathy?
Noninvasive electrocardiographic imaging during sinus rhythm can identify regional activation dispersion associated with arrhythmogenic scar, potentially complementing LGE-CMR for VT risk stratification.
Answers are grounded in this paper and cite their sources.
ECGI may identify arrhythmogenic substrate in ICM; hypothesis-generating for VT risk stratification, prospective validation needed.
BACKGROUND: Late gadolinium enhancement cardiac magnetic resonance (LGE-CMR) identifies structural properties associated with ventricular tachycardia (VT) but lacks functional information. Noninvasive identification of slow conduction regions using electrocardiographic imaging (ECGI) could complement LGE-CMR to aid VT risk stratification. OBJECTIVE: This study aimed to evaluate the relationship between ventricular arrhythmogenic substrate and regional ECGI markers during sinus rhythm in patients with ischemic cardiomyopathy (ICM). METHODS: Seventy-two patients were included: 29 with ICM evidenced by LGE-CMR referred for VT ablation, 17 with ICM with implantable cardioverter-defibrillator for primary prevention without documented VT, and 26 controls. ECGI-derived regional activation dispersion (rAD) and pseudo-regional conduction velocity (pseudo-rCV) were analyzed and compared between scarred and healthy regions based on LGE, and between patients with ICM with and without previous VT. In a subgroup with electroanatomic mapping (n = 16), deceleration zones were correlated with ECGI. RESULTS: Scarred regions showed higher rAD (46.3 ± 2.2 vs 30.1 ± 1.7 ms, P < .001) and reduced pseudo-rCV (149.9 ± 3.0 vs 165.7 ± 2.4 cm/s, P < .001) than healthy regions. In the subgroup with sinus rhythm electroanatomic mapping, regions containing deceleration zones showed increased rAD (64.9 ± 5.4 vs 43.1 ± 3.1 ms, P < .001), and ECGI identified 70.4% of those zones. At the patient level, the mean of the 3 regions with the highest activation dispersion differentiated patients with ICM with and without previous VT (rAD ≥60.0 ms, sensitivity 75.9%, area under the curve [AUC] 0.75, P = .005) and identified patients with ICM from controls (rAD ≥39.5 ms, AUC 0.93). CONCLUSION: This study introduces a novel regional ECGI methodology demonstrating that rAD identifies abnormalities linked to arrhythmogenic substrate and could help identify patients at risk of VT. These findings highlight ECGI's potential as a complementary tool to LGE-CMR.
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Reventos-Presmanes et al. (2025) conducted an observational in Ischemic cardiomyopathy (n=72). Electrocardiographic imaging (ECGI) vs. Healthy regions / Controls was evaluated on Regional activation dispersion (rAD) in scarred versus healthy regions (p=<.001).
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