Carrick Richard T, Benson Bryce E, Bates Oliver R J, Spector Peter S
College of Medicine, University of Vermont, Burlington, VT, United States.
College of Engineering and Mathematical Sciences, University of Vermont, Burlington, VT, United States.
Front Physiol. 2021 Mar 16;12:633643. doi: 10.3389/fphys.2021.633643. eCollection 2021.
There is debate whether human atrial fibrillation is driven by focal drivers or multiwavelet reentry. We propose that the changing activation sequences surrounding a focal driver can at times self-sustain in the absence of that driver. Further, the relationship between focal drivers and surrounding chaotic activation is bidirectional; focal drivers can generate chaotic activation, which may affect the dynamics of focal drivers.
In a propagation model, we generated tissues that support structural micro-reentry and moving functional reentrant circuits. We qualitatively assessed (1) the tissue's ability to support self-sustaining fibrillation after elimination of the focal driver, (2) the impact that structural-reentrant substrate has on the duration of fibrillation, the impact that micro-reentrant (3) frequency, (4) excitable gap, and (5) exposure to surrounding fibrillation have on micro-reentry in the setting of chaotic activation, and finally the likelihood fibrillation will end in structural reentry based on (6) the distance between and (7) the relative lengths of an ablated tissue's inner and outer boundaries. We found (1) focal drivers produced chaotic activation when waves encountered heterogeneous refractoriness; chaotic activation could then repeatedly initiate and terminate micro-reentry. Perpetuation of fibrillation following elimination of micro-reentry was predicted by tissue properties. (2) Duration of fibrillation was increased by the presence of a structural micro-reentrant substrate only when surrounding tissue had a low propensity to support self-sustaining chaotic activation. Likelihood of micro-reentry around the structural reentrant substrate increased as (3) the frequency of structural reentry increased relative to the frequency of fibrillation in the surrounding tissue, (4) the excitable gap of micro-reentry increased, and (5) the exposure of the structural circuit to the surrounding tissue decreased. Likelihood of organized tachycardia following termination of fibrillation increased with (6) decreasing distance and (7) disparity of size between focal obstacle and external boundary.
Focal drivers such as structural micro-reentry and the chaotic activation they produce are continuously interacting with one another. In order to accurately describe cardiac tissue's propensity to support fibrillation, the relative characteristics of both stationary and moving drivers must be taken into account.
关于人类心房颤动是由局灶驱动因素还是多小波折返引起，存在争议。我们提出，围绕局灶驱动因素的激活序列变化有时在该驱动因素不存在的情况下也能自我维持。此外，局灶驱动因素与周围混沌激活之间的关系是双向的；局灶驱动因素可产生混沌激活，这可能影响局灶驱动因素的动力学。
在一个传播模型中，我们生成了支持结构性微折返和移动功能性折返环路的组织。我们定性评估了：（1）消除局灶驱动因素后组织支持自我维持颤动的能力；（2）结构性折返基质对颤动持续时间的影响；（3）微折返频率、（4）可兴奋间隙以及（5）在混沌激活情况下周围颤动对微折返的影响；最后基于（6）消融组织的内边界和外边界之间的距离以及（7）相对长度，评估颤动以结构性折返结束的可能性。我们发现：（1）当波遇到异质性不应期时，局灶驱动因素产生混沌激活；混沌激活随后可反复启动和终止微折返。微折返消除后颤动的持续存在可由组织特性预测。（2）仅当周围组织支持自我维持混沌激活的倾向较低时，结构性微折返基质的存在才会增加颤动持续时间。随着（3）结构性折返频率相对于周围组织颤动频率增加、（4）微折返的可兴奋间隙增加以及（5）结构性环路与周围组织的接触减少，结构性折返基质周围微折返的可能性增加。随着（6）局灶障碍物与外部边界之间距离减小以及（7）大小差异减小，颤动终止后出现有组织心动过速的可能性增加。
结构性微折返等局灶驱动因素及其产生的混沌激活相互之间持续相互作用。为了准确描述心脏组织支持颤动的倾向，必须考虑固定和移动驱动因素的相对特征。
