Kwan Eugene, Hunt Bram, Paccione Eric N, Orkild Ben A, Bergquist Jake A, Ishidoya Yuki, Yazaki Kyoichiro, Mendes Jason K, DiBella Ed V R, MacLeod Rob S, Dosdall Derek J, Ranjan Ravi
Division of Cardiovascular Medicine, Department of Internal Medicine, University of Utah, Salt Lake City, Utah, USA; Department of Biomedical Engineering, University of Utah, Salt Lake City, Utah, USA; Nora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah, Salt Lake City, Utah, USA.
Division of Cardiovascular Medicine, Department of Internal Medicine, University of Utah, Salt Lake City, Utah, USA; Department of Biomedical Engineering, University of Utah, Salt Lake City, Utah, USA; Nora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah, Salt Lake City, Utah, USA; Scientific Computing and Imaging Institute, University of Utah, Salt Lake City, Utah, USA.
JACC Clin Electrophysiol. 2025 Apr;11(4):720-734. doi: 10.1016/j.jacep.2024.10.001. Epub 2024 Nov 27.
Contractile, electrical, and structural remodeling has been associated with atrial fibrillation (AF), but the progression of functional and structural changes as AF sustains has not been previously evaluated serially.
Using a rapid-paced persistent AF canine model, the authors aimed to evaluate the structural and functional changes serially as AF progresses.
Serial electrophysiological studies in a chronic rapid-paced canine model (n = 19) prior to AF sustaining and repeated at 1, 3, and 6 months of sustained AF were conducted to measure changes in atrial conduction speed and direction. Cardiac late gadolinium enhancement magnetic resonance imaging was performed prior to and following sustained AF to evaluate structural remodeling.
As AF progressed, the overall area of the left atrium with fibrosis increased. Over time, conduction speeds slowed, with speeds decreasing by 0.15 m/s after 3 months and 0.26 m/s after 6 months of sustained AF. Regions that developed fibrosis experienced greater slowing compared with healthy regions (0.32 ± 0.01 m/s decrease vs 0.21 ± 0.01 m/s decrease; P < 0.001). Conduction directions became more aligned (conduction direction heterogeneity decreased from 19.7 ± 0.1° to 17.5 ± 0.1° after 6 months of sustained AF; P < 0.001). Fibrotic regions had a greater decrease in conduction direction heterogeneity (2.7 ± 0.3° vs 2.0 ± 0.2°; P = 0.008).
As AF progressed, functional changes occurred globally throughout the left atrium. Conduction speed slowed, and conduction directions became more aligned over time, with the greatest changes occurring within regions that developed fibrosis.
收缩、电和结构重塑与心房颤动(AF)相关,但随着房颤持续,功能和结构变化的进展此前尚未进行连续评估。
作者使用快速起搏持续性房颤犬模型,旨在评估随着房颤进展的结构和功能变化。
在慢性快速起搏犬模型(n = 19)中,于房颤持续前进行系列电生理研究,并在房颤持续1、3和6个月时重复进行,以测量心房传导速度和方向的变化。在房颤持续前后进行心脏延迟钆增强磁共振成像,以评估结构重塑。
随着房颤进展,左心房纤维化的总面积增加。随着时间推移,传导速度减慢,房颤持续3个月后速度降低0.15m/s,持续6个月后降低0.26m/s。与健康区域相比,发生纤维化的区域减慢更明显(降低0.32±0.01m/s vs 0.21±0.01m/s;P<0.001)。传导方向变得更加一致(房颤持续6个月后传导方向异质性从19.7±0.1°降至17.5±0.1°;P<0.001)。纤维化区域的传导方向异质性降低更大(2.7±0.3° vs 2.0±0.2°;P = 0.008)。
随着房颤进展,左心房整体发生功能变化。传导速度减慢,传导方向随时间变得更加一致,最大变化发生在发生纤维化的区域。