TY - GEN
T1 - Fractional Diffusion Modulates Distribution of Action Potential Duration in Fibrotic Atrial Strands
AU - Ugarte, Juan P.
AU - Tobon, Catalina
AU - Palacio, Laura C.
AU - Andrade-Caicedo, Henry
AU - Saiz, Javier
N1 - Funding Information:
This work was supported by the “Departamento Administrativo de Ciencia, Tecnología e Innovación” – COLCIENCIAS of Colombia, by research project #121065741044, and by the UdeM research project #890.
Publisher Copyright:
© 2018 Creative Commons Attribution.
PY - 2018/9/1
Y1 - 2018/9/1
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=85068799331&partnerID=8YFLogxK
U2 - 10.22489/CinC.2018.228
DO - 10.22489/CinC.2018.228
M3 - Contribución a la conferencia
AN - SCOPUS:85068799331
T3 - Computing in Cardiology
BT - Computing in Cardiology Conference, CinC 2018
PB - IEEE Computer Society
Y2 - 23 September 2018 through 26 September 2018
ER -