Abstract
Under diseased conditions, remodeling of the cardiac tissue properties (“passive properties”) takes place; these are aspects of electrophysiological behavior that are not associated with active ion transport across cell membranes. Remodeling of the passive electrophysiological properties most often results from structural remodeling, such as gap junction down-regulation and lateralization, fibrotic growth infiltrating the myocardium, or the development of an infarct scar. Such structural remodeling renders atrial or ventricular tissue as a major substrate for arrhythmias. The current review focuses on these aspects of cardiac arrhythmogenesis. Due to the inherent complexity of cardiac arrhythmias, computer simulations have provided means to elucidate interactions pertinent to this spatial scale. Here we review the current state-of-the-art in modeling atrial and ventricular arrhythmogenesis as arising from the disease-induced changes in the passive tissue properties, as well as the contributions these modeling studies have made to our understanding of the mechanisms of arrhythmias in the heart. Because of the rapid advance of structural imaging methodologies in cardiac electrophysiology, we chose to present studies that have used such imaging methodologies to construct geometrically realistic models of cardiac tissue, or the organ itself, where the regional remodeling properties of the myocardium can be represented in a realistic way. We emphasize how the acquired knowledge can be used to pave the way for clinical applications of cardiac organ modeling under the conditions of structural remodeling.
Highlights
Computer modeling has emerged as a powerful platform for the investigation of lethal heart rhythm disorders
Because of this inherent complexity of cardiac arrhythmias, it is often difficult to dissect the contributions of individual players, and to elucidate interactions at a particular spatial scale
The passive electrical properties of the myocardium (Figure 1A) can be regionally remodeled in disease, with the regional change originating from several major sources: (1) changes in gap junction resistance between cells resulting in changes in conductivity values; (2) deposition of collagen forming either local resistive barriers between fibers or replacing myocytes; (3) formation of an infarction scar in the ventricles as a result of ischemic cardiac disease; and (4) abnormal proliferation, under diseased conditions, of non-myocyte cells, such as myofibroblasts, which may or may not interact with the cardiomyocytes electrically
Summary
Computer modeling has emerged as a powerful platform for the investigation of lethal heart rhythm disorders.
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
