Biomedical Signal and Image Processing Laboratory, Department of Electrical, Computer, and Biomedical Engineering, Faculty of Engineering and Architectural Science, Toronto Metropolitan University, 350 Victoria St, Toronto, M5B 2K3, ON, Canada.
Toby Hull Cardiac Fibrillation Management, Toronto General Hospital, University Health Network, 200 Elizabeth Street, Toronto, M5G 2C4, ON, Canada.
Comput Biol Med. 2024 Nov;182:109195. doi: 10.1016/j.compbiomed.2024.109195. Epub 2024 Sep 26.
Sympathetic hyperactivity via spatially dense adrenergic stimulation may create pro-arrhythmic substrates even without structural remodelling. However, the effect of sympathetic hyperactivity on arrhythmic activity, such as rotors, is unknown. Using simulations, we examined the effects of gradually increasing the spatial density of adrenergic stimulation (AS) in atrial sheets on rotors. We compared their characteristics against rotors hosted in atrial sheets with increasing spatial density of minimally conductive (MC) elements to simulate structural remodelling due to injury or disease. We generated rotors using an S1-S2 stimulation protocol. Then, we created phase maps to identify phase singularities and map their trajectory over time. We measured each rotor's duration (s), angular speed (rad/s), and spatiotemporal organization. We demonstrated that atrial sheets with increased AS spatial densities could maintain rotors longer than with MC elements (2.6 ± 0.1 s vs. 1.5 ± 0.2 s, p<0.001). Moreover, rotors have higher angular speed (70 ± 7 rads/s vs. 60 ± 15 rads/s, p<0.05) and better spatiotemporal organization (0.56 ± 0.05 vs. 0.58 ± 0.18, p<0.05) in atrial sheets with less than 25% AS elements compared to MC elements. Our findings may help elucidate electrophysiological potential alterations in atrial substrates due to sympathetic hyperactivity, particularly among individuals with autonomic derangements caused by chronic distress.
通过空间密集的肾上腺素刺激产生的交感神经兴奋,即使没有结构重塑,也可能产生致心律失常的基质。然而,交感神经兴奋对心律失常活动(如转子)的影响尚不清楚。我们使用模拟,研究了在心房片上逐渐增加肾上腺素刺激(AS)的空间密度对转子的影响。我们将它们的特征与由于损伤或疾病导致结构重塑而增加最小传导(MC)元件空间密度的心房片中的转子进行了比较。我们使用 S1-S2 刺激方案产生转子。然后,我们生成相位图以识别相位奇点并随时间映射它们的轨迹。我们测量了每个转子的持续时间(s)、角速度(rad/s)和时空组织。我们证明,与 MC 元件相比,增加 AS 空间密度的心房片可以维持转子更长时间(2.6 ± 0.1 s 与 1.5 ± 0.2 s,p<0.001)。此外,与 MC 元件相比,AS 元件少于 25%的心房片中的转子具有更高的角速度(70 ± 7 rad/s 与 60 ± 15 rad/s,p<0.05)和更好的时空组织(0.56 ± 0.05 与 0.58 ± 0.18,p<0.05)。我们的发现可能有助于阐明由于交感神经兴奋导致的心房基质电生理潜在变化,特别是在那些由于慢性压力引起自主神经紊乱的个体中。