000061844 001__ 61844
000061844 005__ 20190219123620.0
000061844 037__ $$aTESIS-2017-072
000061844 041__ $$aeng
000061844 080__ $$a519.876.5:57.08
000061844 1001_ $$aMena Tobar, Andrés
000061844 24500 $$aModeling and simulation of the electric activity of the heart using graphic processing units
000061844 260__ $$aZaragoza$$bUniversidad de Zaragoza, Prensas de la Universidad$$c2017
000061844 300__ $$a135
000061844 4900_ $$aTesis de la Universidad de Zaragoza$$v2017-072$$x2254-7606
000061844 500__ $$aPresentado: 23 06 2017
000061844 502__ $$aTesis-Univ. Zaragoza, Instituto de Investigación en Ingeniería de Aragón (I3A), 2017$$bZaragoza, Universidad de Zaragoza$$c2017
000061844 506__ $$aby-nc-nd$$bCreative Commons$$c3.0$$uhttps://creativecommons.org/licenses/by-nc-nd/3.0/
000061844 520__ $$aMathematical modelling and simulation of the electric activity of the heart (cardiac electrophysiology) offers and ideal framework to combine clinical and experimental data in order to help understanding the underlying mechanisms behind the observed respond under physiological and pathological conditions. In this regard, solving the electric activity of the heart possess a big challenge, not only because of the structural complexities inherent to the heart tissue, but also because of the complex electric behaviour of the cardiac cells. The multi- scale nature of the electrophysiology problem makes difficult its numerical solution, requiring temporal and spatial resolutions of 0.1 ms and 0.2 mm respectively for accurate simulations, leading to models with millions degrees of freedom that need to be solved for thousand time steps. Solution of this problem requires the use of algorithms with higher level of parallelism in multi-core platforms. In this regard the newer programmable graphic processing units (GPU) has become a valid alternative due to their tremendous computational horsepower. This thesis develops around the implementation of an electrophysiology simulation software entirely developed in Compute Unified Device Architecture (CUDA) for GPU computing. The software implements fully explicit and semi-implicit solvers for the monodomain model, using operator splitting and the finite element method for space discretization. Performance is compared with classical multi-core MPI based solvers operating on dedicated high-performance computer clusters. Results obtained with the GPU based solver show enormous potential for this technology with accelerations over 50× for three-dimensional problems when using an implicit scheme for the parabolic equation, whereas accelerations reach values up to 100× for the explicit implementation. The implemented solver has been applied to study pro-arrhythmic mechanisms during acute ischemia. In particular, we investigate on how hyperkalemia affects the vulnerability window to reentry and the reentry patterns in the heterogeneous substrate caused by acute regional ischemia using an anatomically and biophysically detailed human biventricular model. A three dimensional geometrically and anatomically accurate regionally ischemic human heart model was created. The ischemic region was located in the inferolateral and posterior side of the left ventricle mimicking the occlusion of the circumflex artery, and the presence of a washed-out zone not affected by ischemia at the endocardium has been incorporated. Realistic heterogeneity and fi er anisotropy has also been considered in the model. A highly electrophysiological detailed action potential model for human has been adapted to make it suitable for modeling ischemic conditions (hyperkalemia, hipoxia, and acidic conditions) by introducing a formulation of the ATP-sensitive K+ current. The model predicts the generation of sustained re-entrant activity in the form single and double circus around a blocked area within the ischemic zone for K+ concentrations bellow 9mM, with the reentrant activity associated with ventricular tachycardia in all cases. Results suggest the washed-out zone as a potential pro-arrhythmic substrate factor helping on establishing sustained ventricular tachycardia.<br />Colli-Franzone P, Pavarino L. A parallel solver for reaction-diffusion systems in computational electrocardiology, Math. Models Methods Appl. Sci. 14 (06):883-911, 2004.<br />Colli-Franzone P, Deu hard P, Erdmann B, Lang J, Pavarino L F. Adaptivity in space and time for reaction-diffusion systems in electrocardiology, SIAM J. Sci. Comput. 28 (3):942-962, 2006.<br />Ferrero J M(Jr), Saiz J, Ferrero J M, Thakor N V. Simulation of action potentials from metabolically impaired cardiac myocytes: Role of atp-sensitive K+ current. Circ Res, 79(2):208-221, 1996.<br />Ferrero J M (Jr), Trenor B. Rodriguez B, Saiz J. Electrical acticvity and reentry during acute regional myocardial ischemia: Insights from simulations.Int J Bif Chaos, 13:3703-3715, 2003.<br />Heidenreich E, Ferrero J M, Doblare M, Rodriguez J F. Adaptive macro finite elements for the numerical solution of monodomain equations in cardiac electrophysiology, Ann. Biomed. Eng. 38 (7):2331-2345, 2010.<br />Janse M J, Kleber A G. Electrophysiological changes and ventricular arrhythmias in the early phase of regional myocardial ischemia. Circ. Res. 49:1069-1081, 1981.<br />ten Tusscher K HWJ, Panlov A V. Alternans and spiral breakup in a human ventricular tissue model. Am. J.Physiol. Heart Circ. Physiol. 291(3):1088-1100, 2006.<br />
000061844 520__ $$a<br />
000061844 6531_ $$asimulación
000061844 700__ $$aRodríguez Matas, José Félix$$edir.
000061844 7102_ $$aUniversidad de Zaragoza$$bInstituto de Investigación en Ingeniería de Aragón (I3A)
000061844 8560_ $$fchperez@unizar.es
000061844 8564_ $$s4808613$$uhttps://zaguan.unizar.es/record/61844/files/TESIS-2017-072.pdf$$zTexto completo (eng)
000061844 909CO $$ooai:zaguan.unizar.es:61844$$pdriver
000061844 909co $$ptesis
000061844 9102_ $$aIngeniería de sistemas y automática$$bInstituto de Investigación en Ingeniería de Aragón (I3A)
000061844 980__ $$aTESIS