Impact of Calcium Store Overload and Electrical Dynamics on Cardiac Myocytes

dc.contributor.authorAlexander, Amanda M.
dc.contributor.authorDeNardo, Erin K.
dc.contributor.authorFrazier III, Eric
dc.contributor.authorMcCauley, Michael
dc.contributor.authorRojina, Nicholas
dc.contributor.authorCoulibaly, Zana
dc.contributor.authorPeercy, Bradford E.
dc.contributor.authorIzu, Leighton T.
dc.date.accessioned2018-09-25T19:37:28Z
dc.date.available2018-09-25T19:37:28Z
dc.date.issued2015
dc.description.abstractThe heart's main function of pumping blood to the body is a complicated process separated into two major steps. Initially, the heart is relaxed and blood flows freely into the ventricles and atria from the veins, then the atria contracts and pumps more blood to the ventricles. The atria relaxes and the inlet valves between these and the ventricles close, producing the initial thump of the heartbeat, as pressure builds while the ventricles contract. This pressure also forces the outlet valves open, allowing blood to ow into the arteries and aorta. As the ventricles relax, the outlet valves then close, producing the second thump of the heartbeat. Once the atria and ventricles are relaxed, the inlet valves reopen, allowing the compartments to ll with blood again as the process repeats. If the heart's contractile abilities are impaired in any way, the rest of the body cannot perform properly. Despite advances in cardiology research, cardiac arrhythmia remains an influential cause of morbidity and mortality in the United States. Recent advances involve the application of devices, such as pacemakers or de brillators, and the outlook of antiarrhythmic drug therapy up to this point is grim, so it is necessary to understand how some pathological conditions within cardiac myocytes can lead to dysfunction of these cells. Calcium mishandling can play a major role in disruption of overall cardiac function by preventing the ability of the heart muscles to relax between heartbeats and thus impair their pumping blood to the bodyen_US
dc.description.sponsorshipThese results were obtained as part of the REU Site: Interdisciplinary Program in High Performance Computing (hpcreu.umbc.edu) in the Department of Mathematics and Statistics at the University of Maryland, Baltimore County (UMBC) in Summer 2015. This program is funded by the National Science Foundation (NSF), the National Security Agency (NSA), and the Department of Defense (DOD), with additional support from UMBC, the Department of Mathematics and Statistics, the Center for Interdisciplinary Research and Consulting (CIRC), and the UMBC High Performance Computing Facility (HPCF). HPCF is supported by the U.S. National Science Foundation through the MRI program (grant nos. CNS{0821258) and CNS{1228778) and the SCREMS program (grant no. DMS{0821311), with additional substantial support from UMBC. Co-author Michael McCauley was supported, in part, by the UMBC National Security Agency (NSA) Scholars Program through a contract with the NSA. Graduate assistant Zana Coulibaly was supported during Summer 2015 by UMBC.en_US
dc.description.urihttps://userpages.umbc.edu/~gobbert/papers/REU2015Team5.pdfen_US
dc.format.extent20 pagesen_US
dc.genretechnical reporten_US
dc.identifierdoi:10.13016/M2VQ2SF17
dc.identifier.urihttp://hdl.handle.net/11603/11376
dc.language.isoen_USen_US
dc.relation.isAvailableAtThe University of Maryland, Baltimore County (UMBC)
dc.relation.ispartofUMBC Mathematics Department Collection
dc.relation.ispartofUMBC Faculty Collection
dc.relation.ispartofUMBC Student Collection
dc.relation.ispartofseriesHPCF Technical Report;HPCF-2015-24
dc.rightsThis item is likely protected under Title 17 of the U.S. Copyright Law. Unless on a Creative Commons license, for uses protected by Copyright Law, contact the copyright holder or the author.
dc.subjectUMBC High Performance Computing Facility (HPCF)en_US
dc.subjectcardiac arrhythmia
dc.subjectpathological conditions within cardiac myocytes
dc.subjectcalcium mishandling and cardiac function
dc.subjectsarcoplasmic reticulum (SR)
dc.subjectcalcium channels
dc.subjectfinite element method (FEM)
dc.titleImpact of Calcium Store Overload and Electrical Dynamics on Cardiac Myocytesen_US
dc.typeTexten_US

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