Ciaccio Edward J, Coromilas James, Ashikaga Hiroshi, Cervantes Daniel O, Wit Andrew L, Peters Nicholas S, McVeigh Elliot R, Garan Hasan
Division of Cardiology, Department of Medicine, Columbia University Medical Center, New York, NY, United States.
Division of Cardiovascular Diseases & Hypertension, Rutgers Robert Wood Johnson Medical School, New Brunswick, NJ, United States.
Comput Biol Med. 2015 Jul;62:254-63. doi: 10.1016/j.compbiomed.2015.04.032. Epub 2015 Apr 29.
When the infarct border zone is stimulated prematurely, a unidirectional block line (UBL) can form and lead to double-loop (figure-of-eight) reentrant ventricular tachycardia (VT) with a central isthmus. The isthmus is composed of an entrance, center, and exit. It was hypothesized that for certain stimulus site locations and coupling intervals, the UBL would coincide with the isthmus entrance boundary, where infarct border zone thickness changes from thin-to-thick in the travel direction of the premature stimulus wavefront.
A quantitative model was developed to describe how thin-to-thick changes in the border zone result in critically convex wavefront curvature leading to conduction block, which is dependent upon coupling interval. The model was tested in 12 retrospectively analyzed postinfarction canine experiments. Electrical activation was mapped for premature stimulation and for the first reentrant VT cycle. The relationship of functional conduction block forming during premature stimulation to functional block during reentrant VT was quantified.
For an appropriately placed stimulus, in accord with model predictions: (1) The UBL and reentrant VT isthmus lateral boundaries overlapped (error: 4.8±5.7mm). (2) The UBL leading edge coincided with the distal isthmus where the center-entrance boundary would be expected to occur. (3) The mean coupling interval was 164.6±11.0ms during premature stimulation and 190.7±20.4ms during the first reentrant VT cycle, in accord with model calculations, which resulted in critically convex wavefront curvature with functional conduction block, respectively, at the location of the isthmus entrance boundary and at the lateral isthmus edges.
Reentrant VT onset following premature stimulation can be explained by the presence of critically convex wavefront curvature and unidirectional block at the isthmus entrance boundary when the premature stimulation interval is sufficiently short. The double-loop reentrant circuit pattern is a consequence of wavefront bifurcation around this UBL followed by coalescence, and then impulse propagation through the isthmus. The wavefront is blocked from propagating laterally away from the isthmus by sharp increases in border zone thickness, which results in critically convex wavefront curvature at VT cycle lengths.
当梗死边缘区被过早刺激时,可形成单向阻滞线(UBL),并导致带有中央峡部的双环(8字形)折返性室性心动过速(VT)。峡部由入口、中心和出口组成。据推测,对于某些刺激部位和偶联间期,UBL将与峡部入口边界重合,在此处梗死边缘区厚度在过早刺激波前的传播方向上从薄变厚。
建立了一个定量模型,以描述边缘区从薄到厚的变化如何导致临界凸形波前曲率,从而导致传导阻滞,这取决于偶联间期。该模型在12个经回顾性分析的心肌梗死后犬实验中进行了测试。绘制了过早刺激和第一个折返性VT周期的电激活图。对过早刺激期间形成的功能性传导阻滞与折返性VT期间的功能性阻滞之间的关系进行了量化。
对于放置适当的刺激,与模型预测一致:(1)UBL与折返性VT峡部外侧边界重叠(误差:4.8±5.7mm)。(2)UBL前沿与预期会出现中心-入口边界的峡部远端重合。(3)过早刺激期间的平均偶联间期为164.6±11.0ms,第一个折返性VT周期期间为190.7±20.4ms,与模型计算结果一致,分别在峡部入口边界位置和峡部外侧边缘处导致临界凸形波前曲率和功能性传导阻滞。
当过早刺激间期足够短时,过早刺激后折返性VT的发作可通过峡部入口边界处存在临界凸形波前曲率和单向阻滞来解释。双环折返电路模式是波前围绕该UBL分叉然后合并,随后冲动通过峡部传播的结果。波前因边缘区厚度急剧增加而被阻止从峡部横向传播,这导致在VT周期长度时出现临界凸形波前曲率。