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National Repository of Grey Literature 2 records found  Search took 0.01 seconds. 
Computational modelling of heart contraction
 Vaverka, Jiří ; Polzer, Stanislav (referee) ; Burša, Jiří (advisor)
This thesis aims to determine the impact of slowed myocardial conduction velocity and depressed myocyte contractility on the duration of isovolumic contraction time (ICT) of the left ventricle by carrying out simulations using finite element method. A 3D finite element model enabling to simulate both physiological and pathological states of myocardium was created. The model is based on simplified ellipsoidal geometry and accounts for anisotropic behavior of myocardium, its asynchronous contraction and variations in the arrangement of muscle fibers. Slowing of conduction velocity to a half of its physiological value resulted in prolongation of ICT by 27 %; slowing of shortening velocity of myocytes by the same percentage prolonged ICT by 73 %. It is therefore concluded that ICT can be much more prolonged due to depressed contractility than due to conduction slowing. The presented results give an idea of the extent to which ICT can be prolonged due to depressed contractility and conduction slowing and therefore can be useful in identifying the causes of decreased myocardial performance in heart disease.
Detailed record
Computational modelling of heart contraction
 Vaverka, Jiří ; Polzer, Stanislav (referee) ; Burša, Jiří (advisor)
This thesis aims to determine the impact of slowed myocardial conduction velocity and depressed myocyte contractility on the duration of isovolumic contraction time (ICT) of the left ventricle by carrying out simulations using finite element method. A 3D finite element model enabling to simulate both physiological and pathological states of myocardium was created. The model is based on simplified ellipsoidal geometry and accounts for anisotropic behavior of myocardium, its asynchronous contraction and variations in the arrangement of muscle fibers. Slowing of conduction velocity to a half of its physiological value resulted in prolongation of ICT by 27 %; slowing of shortening velocity of myocytes by the same percentage prolonged ICT by 73 %. It is therefore concluded that ICT can be much more prolonged due to depressed contractility than due to conduction slowing. The presented results give an idea of the extent to which ICT can be prolonged due to depressed contractility and conduction slowing and therefore can be useful in identifying the causes of decreased myocardial performance in heart disease.
Detailed record

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