Přehled o publikaci
2018
Paced Electrical Field Modeling Within Ischemic Myocardium
KORPAS, David and Pavel BÁRTABasic information
Original name
Paced Electrical Field Modeling Within Ischemic Myocardium
Authors
KORPAS, David (203 Czech Republic, guarantor, belonging to the institution) and Pavel BÁRTA (203 Czech Republic)
Edition
IFMBE Proceedings, 2018, 1680-0737
Other information
Language
English
Type of outcome
Article in a journal
Field of Study
20600 2.6 Medical engineering
Country of publisher
United States of America
Confidentiality degree
is not subject to a state or trade secret
RIV identification code
RIV/47813059:19510/18:A0000102
Organization
Fakulta veřejných politik v Opavě – Slezská univerzita v Opavě – Repository
UT WoS
000450908300090
Keywords in English
Cardiac modeling; Pacing; Ischemic tissue; FitzHugh-Nagumo model
Changed: 25/4/2019 09:38, Bc. Nikol Maďová
Abstract
In the original language
Cardiac pacing in an ischemic area is very disadvantageous because of higher pacing thresholds and lower sensed intrinsic signal. An irregular propagation of myocardial activation in the ventricles is also a clinical problem of ischemia. The aim of this paper is to model the theoretical electrical depolarization propagation within the paced ventricular myocardium, using mathematical and computation methods. For numerical simulation of different biological or physiological systems, models utilizing the differential equation are appropriate. The basic model is Hodgkin-Huxley, describing the action potentials on the basis of varying channel permeability for different ions. Our characteristics of modeled tissues are described according to the FitzHugh-Nagumo model which is a simplification of Hodgkin-Huxley. The computation was performed using the Comsol Multiphysics software. The results are composed of several models of paced ventricles: a physiological one, one with apical ischemia, and one with left lateral ischemia as well as a combination of all three with low or high energy right ventricular or biventricular pacing. The results of the simulations of right ventricular pacing are consistent with the clinical experience. They confirm an increase in ischemic dyssynchrony because of different activation times in the right ventricle in comparison with the left ventricle. Apical pacing in the ischemic area shows the latest activation times in comparison with the physiological reference. In this case, lead reposition would be recommended in the practice. The location of an ischemic lesion within the model is adjustable and can also be used for the assessment and planning of pacing effectiveness.