Fractional Diffusion Modulates Distribution of Action Potential Duration in Fibrotic Atrial Strands
Background: Fibroblast proliferation, as a component of the fibrotic process, plays a role in structural remodeling, but also can alter the electrophysiology of the cardiomyocytes. Aim: To study the action potential duration dispersion (dAPD) in fibrotic atrial strands, where fibroblasts exerts both...
- Autores:
- Tipo de recurso:
- Fecha de publicación:
- 2018
- Institución:
- Universidad de Medellín
- Repositorio:
- Repositorio UDEM
- Idioma:
- eng
- OAI Identifier:
- oai:repository.udem.edu.co:11407/5721
- Acceso en línea:
- http://hdl.handle.net/11407/5721
- Palabra clave:
- Cardiology
Cell culture
Diffusion
Dispersion (waves)
Electrophysiology
Action potential durations
Electrical components
Fibroblast proliferation
Fractional derivatives
Fractional diffusion
Spatial characteristics
Structural component
Structural remodeling
Fibroblasts
- Rights
- License
- http://purl.org/coar/access_right/c_16ec
Summary: | Background: Fibroblast proliferation, as a component of the fibrotic process, plays a role in structural remodeling, but also can alter the electrophysiology of the cardiomyocytes. Aim: To study the action potential duration dispersion (dAPD) in fibrotic atrial strands, where fibroblasts exerts both, structural and electrical influence on the propagation, using a fractional diffusion model. Methods: The Courtemanche model of human atrial cell is implemented under chronic atrial fibrillation (AF) remodeling conditions. The atrial strands are designed as 1D domains, having a fibrotic portion localized in the middle. Fibrosis is modeled taking into account an electrical component, implemented by coupling a number of fibroblasts to a single cardiomyocyte, and a structural component, implemented through a q-order fractional derivative. Results: The variations of q define two dAPD dispersion regimes. For q < 1.4, the fibrosis density and the number of fibroblast per cardiomyocyte do not alter the dAPD. For q ? 1.4, the dAPD depends on the fibrosis spatial characteristics. Conclusion: This study shows that the structural component of fibrosis, modeled using fractional diffusion, modulates the spatial dAPD in a domain including electrical coupling of cardiomyocytes and fibroblasts, under chronic AF conditions. © 2018 Creative Commons Attribution. |
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