Department of Physiology, Faculty of Medicine, Maastricht University, Maastricht, the Netherlands.
Department of Cardiology, University Medical Centre Hamburg, Hamburg, Germany.
Europace. 2021 Jul 18;23(7):1114-1123. doi: 10.1093/europace/euab026.
Complex propagation patterns are observed in patients and models with stable atrial fibrillation (AF). The degree of this complexity is associated with AF stability. Experimental work suggests reduced wavefront turning as an important mechanism for widening of the excitable gap. The aim of this study was to investigate how sodium channel inhibition by vernakalant affects turning behaviour and propagation patterns during AF.
Two groups of 8 goats were instrumented with electrodes on the left atrium, and AF was maintained by burst pacing for 3 or 22 weeks. Measurements were performed at baseline and two dosages of vernakalant. Unipolar electrograms were mapped (249 electrodes/array) on the left and right atrium in an open-chest experiment. Local activation times and conduction vectors, flow lines, the number of fibrillation waves, and local re-entries were determined. At baseline, fibrillation patterns contained numerous individual fibrillation waves conducting in random directions. Vernakalant induced conduction slowing and cycle length prolongation and terminated AF in 13/15 goats. Local re-entries were strongly reduced. Local conduction vectors showed increased preferential directions and less beat-to-beat variability. Breakthroughs and waves were significantly reduced in number. Flow line curvature reduced and waves conducted more homogenously in one direction. Overall, complex propagation patterns were strongly reduced. No substantial differences in drug effects between right and left atria or between goats with different AF durations were observed.
Destabilization of AF by vernakalant is associated with a lowering of fibrillation frequency and inhibition of complex propagation patterns, wave turning, local re-entries, and breakthroughs.
在患有稳定型心房颤动（AF）的患者和模型中观察到复杂的传播模式。这种复杂性的程度与 AF 的稳定性有关。实验工作表明，波阵面转向减少是扩宽可兴奋间隙的重要机制。本研究旨在探讨维纳卡兰对钠通道的抑制作用如何影响 AF 期间的转向行为和传播模式。
两组 8 只山羊在左心房放置电极，并通过爆发起搏维持 AF 3 或 22 周。在基线和 vernakalant 的两种剂量下进行测量。在开胸实验中，在左心房和右心房上进行单极电图映射（249 个电极/数组）。确定局部激活时间和传导向量、流线、纤颤波的数量和局部折返。在基线时，纤颤模式包含许多随机方向传导的单个纤颤波。Vernakalant 诱导传导减慢和周期长度延长，并终止了 15 只山羊中的 13 只 AF。局部折返明显减少。局部传导向量显示出增加的优先方向和更少的逐拍变化。突破和波的数量明显减少。流线曲率降低，波沿一个方向更均匀地传播。总的来说，复杂的传播模式大大减少。在右心房和左心房之间或 AF 持续时间不同的山羊之间，药物作用没有明显差异。
Vernakalant 使 AF 不稳定与纤颤频率降低以及复杂传播模式、波转向、局部折返和突破的抑制有关。
