Hypertrophic cardiomyopathy (HCM) is the most common monogenic disorder and the leading cause of sudden arrhythmic death in children and young adults. It is typically asymptomatic and first manifests itself during cardiac arrest, making it a challenge to diagnose in advance. Computational models can explore and reveal underlying molecular mechanisms in cardiac electrophysiology by allowing researchers to alter various parameters such as tissue size or ionic current amplitudes. The goal of this thesis is to develop a computational model in MATLAB and to determine if this model can accurately indicate cases of hypertrophic cardiomyopathy. This goal is achieved by combining a three-dimensional network of the bidomain model with the Beeler-Reuter model and then by manually varying the thickness of that tissue and recording the resulting membrane potential with respect to time. The results of this analysis demonstrated that the developed model is able to depict variations in tissue thickness through the difference in membrane potential recordings. A one-way ANOVA analysis confirmed that the membrane potential recordings of the different thicknesses were significantly different from one another. This study assumed continuum behavior, which may not be indicative of diseased tissue. In the future, such a model might be validated through in vitro experiments that measure electrical activity in hypertrophied cardiac tissue. This model may be useful in future applications to study the ionic mechanisms related to hypertrophic cardiomyopathy or other related cardiac diseases.
","abstract_html":"<p>Hypertrophic cardiomyopathy (HCM) is the most common monogenic disorder and the leading cause of sudden arrhythmic death in children and young adults. It is typically asymptomatic and first manifests itself during cardiac arrest, making it a challenge to diagnose in advance. Computational models can explore and reveal underlying molecular mechanisms in cardiac electrophysiology by allowing researchers to alter various parameters such as tissue size or ionic current amplitudes. The goal of this thesis is to develop a computational model in MATLAB and to determine if this model can accurately indicate cases of hypertrophic cardiomyopathy. This goal is achieved by combining a three-dimensional network of the bidomain model with the Beeler-Reuter model and then by manually varying the thickness of that tissue and recording the resulting membrane potential with respect to time. The results of this analysis demonstrated that the developed model is able to depict variations in tissue thickness through the difference in membrane potential recordings. A one-way ANOVA analysis confirmed that the membrane potential recordings of the different thicknesses were significantly different from one another. This study assumed continuum behavior, which may not be indicative of diseased tissue. In the future, such a model might be validated through in vitro experiments that measure electrical activity in hypertrophied cardiac tissue. This model may be useful in future applications to study the ionic mechanisms related to hypertrophic cardiomyopathy or other related cardiac diseases.</p>","abstract_has_math":false,"creators":["Kelley, Julia Elizabeth"],"institution":null,"degree_name":"MS in Biomedical Engineering","degree_level":null,"degree_discipline":"Biomedical Engineering","degree_department":null,"school":null,"contributors":["Robert Szlavik","Biomedical Engineering","College of Engineering"],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2021,"date_issued":"2021-06-01T07:00:00Z","date_published":"2021-06-01T07:00:00Z","updated_at":"2026-07-24T01:32:55Z","subjects":["Hypertrophic Cardiomyopathy","Beeler Reuter","Bidomain","Computational Modeling","Bioelectrical and Neuroengineering","Other Biomedical Engineering and Bioengineering"],"languages":[],"rights":[],"rights_urls":[],"identifier_entries":[{"key":"dc:identifier","label":"Identifier","values":["10.15368/theses.2021.175"],"render_values":[{"text":"10.15368/theses.2021.175","href":"https://doi.org/10.15368/theses.2021.175","code":true}]}]},"links":{"outbound_url":"https://digitalcommons.calpoly.edu/theses/2407","outbound_label":"Repository record","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["Robert Szlavik","Biomedical Engineering","College of Engineering"]},{"key":"dc:creator","label":"Author","values":["Kelley, Julia Elizabeth"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date.available","label":"Dc Date Available","values":["2022-07-18T07:00:00Z"]},{"key":"thesis:degree_discipline","label":"Discipline","values":["Biomedical Engineering"]},{"key":"thesis:degree_name","label":"Degree Name","values":["MS in Biomedical Engineering"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["Hypertrophic Cardiomyopathy","Beeler Reuter","Bidomain","Computational Modeling","Bioelectrical and Neuroengineering","Other Biomedical Engineering and Bioengineering"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["https://digitalcommons.calpoly.edu/theses/2407","10.15368/theses.2021.175"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description.abstract","label":"Abstract","values":["Hypertrophic cardiomyopathy (HCM) is the most common monogenic disorder and the leading cause of sudden arrhythmic death in children and young adults. It is typically asymptomatic and first manifests itself during cardiac arrest, making it a challenge to diagnose in advance. Computational models can explore and reveal underlying molecular mechanisms in cardiac electrophysiology by allowing researchers to alter various parameters such as tissue size or ionic current amplitudes. The goal of this thesis is to develop a computational model in MATLAB and to determine if this model can accurately indicate cases of hypertrophic cardiomyopathy. This goal is achieved by combining a three-dimensional network of the bidomain model with the Beeler-Reuter model and then by manually varying the thickness of that tissue and recording the resulting membrane potential with respect to time. The results of this analysis demonstrated that the developed model is able to depict variations in tissue thickness through the difference in membrane potential recordings. A one-way ANOVA analysis confirmed that the membrane potential recordings of the different thicknesses were significantly different from one another. This study assumed continuum behavior, which may not be indicative of diseased tissue. In the future, such a model might be validated through in vitro experiments that measure electrical activity in hypertrophied cardiac tissue. This model may be useful in future applications to study the ionic mechanisms related to hypertrophic cardiomyopathy or other related cardiac diseases.
"]},{"key":"dc:title","label":"Title","values":["Modeling Action Potential Propagation During Hypertrophic Cardiomyopathy Through a Three-Dimensional Computational Model"]}]}],"canonical_facts":{"dc:contributor":["Robert Szlavik","Biomedical Engineering","College of Engineering"],"dc:creator":["Kelley, Julia Elizabeth"],"dc:date.available":["2022-07-18T07:00:00Z"],"dc:description.abstract":["Hypertrophic cardiomyopathy (HCM) is the most common monogenic disorder and the leading cause of sudden arrhythmic death in children and young adults. It is typically asymptomatic and first manifests itself during cardiac arrest, making it a challenge to diagnose in advance. Computational models can explore and reveal underlying molecular mechanisms in cardiac electrophysiology by allowing researchers to alter various parameters such as tissue size or ionic current amplitudes. The goal of this thesis is to develop a computational model in MATLAB and to determine if this model can accurately indicate cases of hypertrophic cardiomyopathy. This goal is achieved by combining a three-dimensional network of the bidomain model with the Beeler-Reuter model and then by manually varying the thickness of that tissue and recording the resulting membrane potential with respect to time. The results of this analysis demonstrated that the developed model is able to depict variations in tissue thickness through the difference in membrane potential recordings. A one-way ANOVA analysis confirmed that the membrane potential recordings of the different thicknesses were significantly different from one another. This study assumed continuum behavior, which may not be indicative of diseased tissue. In the future, such a model might be validated through in vitro experiments that measure electrical activity in hypertrophied cardiac tissue. This model may be useful in future applications to study the ionic mechanisms related to hypertrophic cardiomyopathy or other related cardiac diseases.
"],"dc:identifier":["https://digitalcommons.calpoly.edu/theses/2407","10.15368/theses.2021.175"],"dc:subject":["Hypertrophic Cardiomyopathy","Beeler Reuter","Bidomain","Computational Modeling","Bioelectrical and Neuroengineering","Other Biomedical Engineering and Bioengineering"],"dc:title":["Modeling Action Potential Propagation During Hypertrophic Cardiomyopathy Through a Three-Dimensional Computational Model"],"thesis:degree_discipline":["Biomedical Engineering"],"thesis:degree_name":["MS in Biomedical Engineering"]},"updated_at":"2026-07-24T01:32:55Z"}