title: In vivo porcine left atrial wall stress: Effect of ventricular tachypacing on spatial and temporal stress distribution.
abstract: Animal models of ventricular tachypacing (VTP) have been successfully used to reproduce the relevant features observed in patients with atrial fibrillation, such as increased atrial pressure and volume, ion-channel alterations and fibrosis. After performing VTP on a healthy Yorkshire pig, we measured an increase in volume of 60%, a two-fold rise in pressure, and a complex pattern of local mechanical, histological and biochemical changes, including a generalized stiffening of the wall. A protocol recently developed was employed to generate computational models of the porcine left atrium mechanics in healthy conditions and after VTP. Comparison of the stress distribution in the healthy vs. VTP case provided a map of how pressure overload affects and modifies left atrium mechanics. Overall, a positive increase in stress was computed after the VTP treatment. Regions of large increase in the stresses post-VTP were the appendage boundaries, the area around the lower pulmonary vein and the area in the front of the atrium towards the appendage. Due to the elevated stress, the back of the atrium mainly modified its mechanical response, while the appendage remodeled both its shape and its mechanical properties. Large changes in the shape of the mitral valve annulus could be observed as a consequence of the remodeling in the front of the atrium. The relation between local mechanical stress and remodeling that emerges from the results is in agreement with our hypothesis that the structural changes in the atrium are a consequence of a stress-mediated mechanism.
authors.affiliation: Department of Civil Engineering and Centre for Bioengineering Research and Education, The University of Calgary, 2500 University Drive NW, Calgary, Alberta, Canada T2N1N4. edimarti@ucalgary.ca
authors.forename: Elena S
authors.initials: ES
authors.lastname: Di Martino
authors.forename: Chiara
authors.initials: C
authors.lastname: Bellini
authors.forename: David S
authors.initials: DS
authors.lastname: Schwartzman
mesh_terms: D000818:Animals; D001281:Atrial Fibrillation / Q000473:pathology / Q000503:physiopathology*; D005260:Female; D006325:Heart Atria / Q000473:pathology / Q000503:physiopathology*; D006801:Humans; D008955:Models, Cardiovascular; D009206:Myocardium / Q000473:pathology; D013312:Stress, Physiological; D013552:Swine