Intercellular Coupling Abnormalities in the Heart: Quantification from Surface Measurements and Impact on Arrhythmia Vulnerability

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atmire.migration.oldid4457
dc.contributor.advisorNygren, Anders
dc.contributor.authorGhazanfari, Amin
dc.contributor.committeememberVigmond, Edward
dc.contributor.committeememberDalton, Colin
dc.contributor.committeememberFederico, Salvatore
dc.contributor.committeememberVinet, Alain
dc.date.accessioned2016-05-31T15:07:47Z
dc.date.available2016-05-31T15:07:47Z
dc.date.issued2016
dc.date.submitted2016en
dc.description.abstractCardiac conduction velocity is one of the most important electrophysiological characteristics of the heart. Several cardiac dysfunctions and arrhythmia are caused by slowed conduction velocity. Measurement of cardiac conduction velocity and other physiological characteristics of the heart such as anisotropy ratio are challenged by complex cardiac tissue structure and inaccurate measurement techniques. Diabetes mellitus is an example of a condition that can alter conduction velocity by reducing the electrical coupling between cardiac cells. Diabetes is also known to increase the risk of arrhythmia by increasing the action potential duration of cardiac myocytes. This thesis discusses a measurement method based on fitting ellipses to activation isochrones. Our results show that the intramural fiber rotation caused error in conventional measurement methods used to estimate fiber orientation and anisotropy ratio specially in thinner tissues. These errors are increased by optical mapping measurements specifically in thicker tissues. We developed a mathematical model for the diabetic rabbit ventricular action potential and also used an existing model of the diabetic rat ventricular action potential. We demonstrated the window of vulnerability to reentrant arrhythmia for healthy and diabetic models of both rabbit and rat. Connexin lateralization was modelled in the diabetic models by reducing the gap junction conductivity in the lateral direction. Results demonstrated that window of vulnerability in diabetic rat is smaller than in healthy rat. On the contrary, diabetic rabbit was more vulnerable to reentry than healthy rabbit. The ATP-dependent potassium channel was added to the models and the results demonstrated that diabetic models are more vulnerable to reentry when ischemia occurs and Ikatp channels open consequently.en_US
dc.identifier.citationGhazanfari, A. (2016). Intercellular Coupling Abnormalities in the Heart: Quantification from Surface Measurements and Impact on Arrhythmia Vulnerability (Doctoral thesis, University of Calgary, Calgary, Canada). Retrieved from https://prism.ucalgary.ca. doi:10.11575/PRISM/26609en_US
dc.identifier.doihttp://dx.doi.org/10.11575/PRISM/26609
dc.identifier.urihttp://hdl.handle.net/11023/3037
dc.language.isoeng
dc.publisher.facultyGraduate Studies
dc.publisher.institutionUniversity of Calgaryen
dc.publisher.placeCalgaryen
dc.rightsUniversity of Calgary graduate students retain copyright ownership and moral rights for their thesis. You may use this material in any way that is permitted by the Copyright Act or through licensing that has been assigned to the document. For uses that are not allowable under copyright legislation or licensing, you are required to seek permission.
dc.subjectEngineering--Biomedical
dc.subjectEngineering--Electronics and Electrical
dc.titleIntercellular Coupling Abnormalities in the Heart: Quantification from Surface Measurements and Impact on Arrhythmia Vulnerability
dc.typedoctoral thesis
thesis.degree.disciplineElectrical and Computer Engineering
thesis.degree.grantorUniversity of Calgary
thesis.degree.nameDoctor of Philosophy (PhD)
ucalgary.item.requestcopytrue
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