Mechanisms underlying morphological changes in recorded electrical signals by micro-anatomical arrhythmogenic substrates

Aim Arrhythmogenic substrates responsible for lethal ventricular arrhythmias may be too small to be detected by commonly used medical imaging. However, they may still alter the morphology of electrical signals, allowing their detection and/or inference of their arrhythmogenesis. The aim of the study is to understand how micro-anatomical arrhythmogenic substrates (µAASs) give rise to pathological morphologies in the traces of recorded electrical signals. Methods and results Eleven human biventricular models with a µAAS were created by varying the location of the µAAS and the volume of weakly coupled myocardium surrounding it. Electrograms (EGMs) and body surface potential maps (BSPMs) were simulated from the biventricular models under sinus activation within a torso. Sinus activation was achieved through either stimulating the His-Purkinje network or early activation sites (EAS). EGMs and BSPMs simulated in ventricular models with and without a µAAS were compared. A qualitative analysis showed that under sinus beat, EGMs from epicardial electrodes had more pronounced morphological changes than those from endocardial electrodes. Also, sinus activation through the His-Purkinje network resulted in EGMs with more pronounced morphological changes than sinus activation through EAS. All ventricular models with a µAAS caused morphological changes in BSPM but only one resulted in changes large enough to be distinguishable from noise. These changes were restricted to the torso area around the sternum. Conclusions The electrophysiological and structural properties of a substrate are more important for its effects on traces of measured electrical signal tracings than its size or location. µAASs significantly change BSPMs in regions closest to the heart.