Abstract
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.
Highlights
Ischemic heart disease remains a significant cause of world-wide mortality and morbidity, primarily due to ventricular arrhythmia
We demonstrate the basic use of the RVI algorithm in both a situation of induced reentry and failed reentry in which only the dynamic electrophysiological properties of the tissue are altered between the two cases to produce different induced outcomes, as originially shown in Child et al (2015) [10]
The findings from our study suggest that a combination of different pacing sites may be utilised in order to create multiple RVI maps which may identify a number of anatomicallydistinct target sites for catheter ablation
Summary
Ischemic heart disease remains a significant cause of world-wide mortality and morbidity, primarily due to ventricular arrhythmia. Isthmuses, of surviving tracts of myocardium interspersed with fibrosis [5] may exist through an otherwise dense scar Such channels provide a slow, yet viable, conduit for activation to propagate due to the tortuous pathways the wavefront is forced to take [6]. The resulting conduction delay [7] allows the tissue at the exit point of the isthmus to repolarise, such that it may be reactivated by these anomalous waves, providing the necessary requirement for self-sustained reentrant activity. Such mechanisms underlie the majority of incidences of scar-related VT
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