Dataset Information

Evaluation of the reentry vulnerability index to predict ventricular tachycardia circuits using high-density contact mapping.

ABSTRACT: BACKGROUND:Identifying arrhythmogenic sites to improve ventricular tachycardia (VT) ablation outcomes remains unresolved. The reentry vulnerability index (RVI) combines activation and repolarization timings to identify sites critical for reentrant arrhythmia initiation without inducing VT. OBJECTIVE:The purpose of this study was to provide the first assessment of RVI's capability to identify VT sites of origin using high-density contact mapping and comparison with other activation-repolarization markers of functional substrate. METHODS:Eighteen VT ablation patients (16 male; 72% ischemic) were studied. Unipolar electrograms were recorded during ventricular pacing and analyzed offline. Activation time (AT), activation-recovery interval (ARI), and repolarization time (RT) were measured. Vulnerability to reentry was mapped based on RVI and spatial distribution of AT, ARI, and RT. The distance from sites identified as vulnerable to reentry to the VT site of origin was measured, with distances <10 mm and >20 mm indicating accurate and inaccurate localization, respectively. RESULTS:The origins of 18 VTs (6 entrainment, 12 pace-mapping) were identified. RVI maps included 1012 (408-2098) (median, 1st-3rd quartiles) points per patient. RVI accurately localized 72.2% VT sites of origin, with median distance of 5.1 (3.2-10.1) mm. Inaccurate localization was significantly less frequent for RVI than AT (5.6% vs 33.3%; odds ratio 0.12; P = .035). Compared to RVI, distance to VT sites of origin was significantly larger for sites showing prolonged RT and ARI and were nonsignificantly larger for sites showing highest AT and ARI gradients. CONCLUSION:RVI identifies vulnerable regions closest to VT sites of origin. Activation-repolarization metrics may improve VT substrate delineation and inform novel ablation strategies.

SUBMITTER: Orini M

PROVIDER: S-EPMC7105818 | biostudies-literature | 2020 Apr

REPOSITORIES: biostudies-literature

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Evaluation of the reentry vulnerability index to predict ventricular tachycardia circuits using high-density contact mapping.

Orini Michele M Graham Adam J AJ Srinivasan Neil T NT Campos Fernando O FO Hanson Ben M BM Chow Anthony A Hunter Ross J RJ Schilling Richard J RJ Finlay Malcolm M Earley Mark J MJ Sporton Simon S Dhinoja Mehul M Lowe Martin M Porter Bradley B Child Nicholas N Rinaldi Christopher A CA Gill Jaswinder J Bishop Martin M Taggart Peter P Lambiase Pier D PD

Heart rhythm 20191118 4

<h4>Background</h4>Identifying arrhythmogenic sites to improve ventricular tachycardia (VT) ablation outcomes remains unresolved. The reentry vulnerability index (RVI) combines activation and repolarization timings to identify sites critical for reentrant arrhythmia initiation without inducing VT.<h4>Objective</h4>The purpose of this study was to provide the first assessment of RVI's capability to identify VT sites of origin using high-density contact mapping and comparison with other activation ...[more]

PMID: 31751771

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Project description:Exit sites associated with scar-related reentrant arrhythmias represent important targets for catheter ablation therapy. However, their accurate location in a safe and robust manner remains a significant clinical challenge. We recently proposed a novel quantitative metric (termed the Reentry Vulnerability Index, RVI) to determine the difference between activation and repolarisation intervals measured from pairs of spatial locations during premature stimulation to accurately locate the critical site of reentry formation. In the clinic, the method showed potential to identify regions of low RVI corresponding to areas vulnerable to reentry, subsequently identified as ventricular tachycardia (VT) circuit exit sites. Here, we perform an in silico investigation of the RVI metric in order to aid the acquisition and interpretation of RVI maps and optimise its future usage within the clinic. Within idealised 2D sheet models we show that the RVI produces lower values under correspondingly more arrhythmogenic conditions, with even low resolution (8 mm electrode separation) recordings still able to locate vulnerable regions. When applied to models of infarct scars, the surface RVI maps successfully identified exit sites of the reentrant circuit, even in scenarios where the scar was wholly intramural. Within highly complex infarct scar anatomies with multiple reentrant pathways, the identified exit sites were dependent upon the specific pacing location used to compute the endocardial RVI maps. However, simulated ablation of these sites successfully prevented the reentry re-initiation. We conclude that endocardial surface RVI maps are able to successfully locate regions vulnerable to reentry corresponding to critical exit sites during sustained scar-related VT. The method is robust against highly complex and intramural scar anatomies and low resolution clinical data acquisition. Optimal location of all relevant sites requires RVI maps to be computed from multiple pacing locations.

Project description:BackgroundThe optimal method to identify the arrhythmogenic substrate of scar-related ventricular tachycardia (VT) is unknown. Sites of activation slowing during sinus rhythm (SR) often colocalize with the VT circuit. However, the utility and limitations of such approach for guiding ablation are unknown.MethodsWe conducted a multicenter study in patients with infarct-related VT. The left ventricular (LV) was mapped during activation from 3 directions: SR (or atrial pacing), right ventricular, and LV pacing at 600 ms. Ablation was applied selectively to the cumulative area of slow activation, defined as the sum of all regions with activation times of ≥40 ms per 10 mm. Hemodynamically tolerated VTs were mapped with activation or entrainment. The primary outcome was a composite of appropriate implanted cardioverter-defibrillator therapies and cardiovascular death.ResultsIn 85 patients, the LV was mapped during activation from 2.4±0.6 directions. The direction of LV activation influenced the location and magnitude of activation slowing. The spatial overlap of activation slowing between SR and right ventricular pacing was 84.2±7.1%, between SR and LV pacing was 61.4±8.8%, and between right ventricular and LV pacing was 71.3±9.6% (P<0.05 between all comparisons). Mapping during SR identified only 66.2±8.2% of the entire area of activation slowing and 58% critical isthmus sites. Activation from other directions by right ventricular and LV stimulation unmasked an additional 33% of slowly conducting zones and 25% critical isthmus sites. The area of maximal activation slowing often corresponded to the site where the wavefront first interacted with the infarct. During a follow-up period of 3.6 years, the primary end point occurred in 14 out of 85 (16.5%) patients.ConclusionsThe spatial distribution of activation slowing is dependent on the direction of LV activation with the area of maximal slowing corresponding to the site where the wavefront first interacts with the infarct. This data may have implications for VT substrate mapping strategies.

Dataset Information

Evaluation of the reentry vulnerability index to predict ventricular tachycardia circuits using high-density contact mapping.

Publications

Evaluation of the reentry vulnerability index to predict ventricular tachycardia circuits using high-density contact mapping.

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