Introduction: As the location of the accessory pathway in Wolff-Parkinson-White (WPW) may serve as a bio-marker for patient morbidity, recent clinical studies have aimed to understand the influence of location on the 12 lead electrocardiogram (ECG) used for patient diagnostics, as well as patient outcome. Furthermore, simulation studies have also been conducted to better elucidate the poorly understood mechanisms of the disease. However, clinical studies only provide limited information due to experimental and ethical limitations, and simulations studies have only been performed on simplified models. We therefore aimed to investigate the influence of the location of accessory pathways on the 12 lead ECG using a physiologically-detailed whole heart model of electrophysiology (EP) that is capable of providing in-depth information on the underlying electrical mechanisms of WPW.
Methods: In previous work, a physiologically-detailed model of whole heart EP had been built and personalized for a single subject to generate a realistic normal sinus rhythm. Locations of accessory pathways were automatically inserted within the electrically-isolated basal surface of the heart using universal ventricular coordinates (UVCs). For every location, cardiac sources and 12 lead ECGs were computed using an efficient cardiac simulator. 12 lead ECGs were evaluated for clinical markers of WPW. Electrical mechanisms are explored for two locations exhibiting highest and lowest morphological differences in the 12 lead ECG.
Results: Not all accessory pathways resulted in 12 lead ECGs exhibiting morphological markers for WPW in agreement with clinical evaluation. This may be due to the representation of the accessory pathway or inherent dynamics of WPW. Investigation into cardiac sources reveals a pre-excitation wavefront within the affected ventricles, causing retrograde activation of the His-Purkinje System, that later merges with the wave-front stemming from normal activation of the His-Purkinje System.