Department of Physics and BioTech, University of Trento, Povo-Trento, Italy.
Am J Physiol Heart Circ Physiol. 2012 Nov 15;303(10):H1219-28. doi: 10.1152/ajpheart.00228.2012. Epub 2012 Sep 21.
The genesis of complex ventricular rhythms during atrial tachyarrhythmias in humans is not fully understood. To clarify the dynamics of atrioventricular (AV) conduction in response to a regular high-rate atrial activation, 29 episodes of spontaneous or pacing-induced atrial flutter (AFL), covering a wide range of atrial rates (cycle lengths from 145 to 270 ms), were analyzed in 10 patients. AV patterns were identified by applying firing sequence and surrogate data analysis to atrial and ventricular activation series, whereas modular simulation with a difference-equation AV node model was used to correlate the patterns with specific nodal properties. AV node response at high atrial rate was characterized by 1) AV patterns of decreasing conduction ratios at the shortening of atrial cycle length (from 236.3 ± 32.4 to 172.6 ± 17.8 ms) according to a Farey sequence ordering (conduction ratio from 0.34 ± 0.12 to 0.23 ± 0.06; P < 0.01); 2) the appearance of high-order alternating Wenckebach rhythms, such as 6:2, 10:2, and 12:2, associated with ventricular interval oscillations of large amplitude (407.7 ± 150.4 ms); and 3) the deterioration of pattern stability at advanced levels of block, with the percentage of stable patterns decreasing from 64.3 ± 35.2% to 28.3 ± 34.5% (P < 0.01). Simulations suggested these patterns to originate from the combined effect of nodal recovery, dual pathway physiology, and concealed conduction. These results indicate that intrinsic nodal properties may account for the wide spectrum of AV block patterns occurring during regular atrial tachyarrhythmias. The characterization of AV nodal function during different AFL forms constitutes an intermediate step toward the understanding of complex ventricular rhythms during atrial fibrillation.
在人类的房性心动过速期间,复杂室性节律的发生机制尚不完全清楚。为了阐明在规则的高频率心房激动时房室(AV)传导的动力学,我们分析了 10 例患者的 29 阵自发性或起搏诱导的房扑(AFL),心房率(周长从 145 到 270 毫秒)范围很广。通过将发放序列和替代数据分析应用于心房和心室激动序列,确定了 AV 模式,而房室结模型的差分方程模块模拟则用于将这些模式与特定的结区特性相关联。在高心房率时,AV 结的反应特征为:1)根据 Farey 序列排序,随着心房周长的缩短,传导比率降低的 AV 模式(从 236.3 ± 32.4 到 172.6 ± 17.8 毫秒)(传导比率从 0.34 ± 0.12 到 0.23 ± 0.06;P < 0.01);2)出现高阶交替文氏型节律,如 6:2、10:2 和 12:2,伴有大振幅的心室间隔波动(407.7 ± 150.4 毫秒);3)在阻滞的高级水平时,模式稳定性恶化,稳定模式的百分比从 64.3 ± 35.2%下降到 28.3 ± 34.5%(P < 0.01)。模拟表明这些模式源于结区恢复、双径路生理学和隐匿性传导的综合作用。这些结果表明,固有结区特性可能是在规则的房性心动过速期间出现的广泛的 AV 阻滞模式的原因。在不同的 AFL 形式下对 AV 结功能的描述构成了理解心房颤动期间复杂室性节律的中间步骤。