K. Gillette, M. Gsell, S. Kurath-Koller, M. Manninger, A. Prassl, D. Scherr, G. Plank
{"title":"Exploring Role of Accessory Pathway Location in Wolff-Parkinson-White Syndrome in a Model of Whole Heart Electrophysiology","authors":"K. Gillette, M. Gsell, S. Kurath-Koller, M. Manninger, A. Prassl, D. Scherr, G. Plank","doi":"10.22489/CinC.2022.057","DOIUrl":null,"url":null,"abstract":"Introduction: The location of the accessory pathway $(AP)$ in Wolff-Parkinson-White $(WPW)$ may serve as a bio-marker for patient morbidity. We therefore aimed to investigate the influence of the location of a typical $AV$ bypass tract 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 $EP$ was built and personalized for a single subject to generate a realistic normal sinus rhythm. Locations of APs used were automatically inserted within the heart using universal ventricular coordinates (UVCs) to model a typical AV bypass tract. 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: Retrograde activation of the His-Purkinje System (HPS) that later merges with the wave-front stemming from normal activation of the $HPS$ is observed. Not all $APs$ resulted in 12 lead ECGs exhibiting morphological markers for $WPW$ under clinical evaluation. This may be due to the representation of the $AP$ or inherent dynamics of $WPW$","PeriodicalId":117840,"journal":{"name":"2022 Computing in Cardiology (CinC)","volume":"29 1","pages":"0"},"PeriodicalIF":0.0000,"publicationDate":"2022-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"1","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"2022 Computing in Cardiology (CinC)","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.22489/CinC.2022.057","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 1
Abstract
Introduction: The location of the accessory pathway $(AP)$ in Wolff-Parkinson-White $(WPW)$ may serve as a bio-marker for patient morbidity. We therefore aimed to investigate the influence of the location of a typical $AV$ bypass tract 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 $EP$ was built and personalized for a single subject to generate a realistic normal sinus rhythm. Locations of APs used were automatically inserted within the heart using universal ventricular coordinates (UVCs) to model a typical AV bypass tract. 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: Retrograde activation of the His-Purkinje System (HPS) that later merges with the wave-front stemming from normal activation of the $HPS$ is observed. Not all $APs$ resulted in 12 lead ECGs exhibiting morphological markers for $WPW$ under clinical evaluation. This may be due to the representation of the $AP$ or inherent dynamics of $WPW$