Ravelli Flavia, Masè Michela, Disertori Marcello
Laboratory of Biophysics and Biosignals, Department of Physics, University of Trento, Via Sommarive 14, Povo-Trento, Italy.
Prog Biophys Mol Biol. 2008 Jun-Jul;97(2-3):417-34. doi: 10.1016/j.pbiomolbio.2008.02.018. Epub 2008 Feb 16.
Although atrial flutter (AFL) is considered a highly regular rhythm, small fluctuations in cycle length have been described. The mechanisms responsible for these interval oscillations have been investigated by recent studies in humans which have shown that cyclic variations in atrial volume and pressure following ventricular contraction may account for the spontaneous variability of AFL. Other studies have shown that variations in the dimensions of the atria, caused by hemodynamical alterations due to imposed manoeuvres, directly modify the rate of AFL. All this evidence has led to the development of the mechano-electrical feedback (MEF) hypothesis, which assumes that changes in atrial volume directly affect AFL cycle length variability by modifying the conduction properties of the circulating impulse in the atrium. In the present study, we re-examined the variability pattern of typical AFL by spectral analysis aiming to support the MEF hypothesis for AFL cycle length variability. In a study population of 30 patients with typical AFL, we observed that AFL cycle length presented a spontaneous beat-to-beat variability, composed of two oscillations: a main oscillation at the frequency of ventricular contraction (1.70+/-0.48 Hz, spectral power: 15.4+/-17.6 ms2) and a second oscillation at the frequency of respiration (0.32+/-0.07 Hz, spectral power: 2.9+/-2.6 ms2). Both ventricular and respiratory oscillations persisted after pharmacologic autonomic blockade (ventricular spectral power: 17.7+/-14.7 ms2 (before block) vs 20.2+/-18.3 ms2 (after block), p=NS; respiratory spectral power: 6.0+/-3.8 ms2 (before block) vs 5.0+/-3.4 ms2 (after block), p=NS), suggesting a non-neurally mediated underlying mechanism. Contrary to respiratory modulation of heart rate during sinus rhythm, respiratory AFL cycle length oscillations displayed a reverse pattern, with longer cycle lengths during inspiration and shorter during expiration (AA insp=223.2+/-28.6 ms vs AA exp=221.1+/-28.2 ms, p<0.0005), which was consistent with a mechanical modulation of AFL reentry. The use of spectral analysis techniques applied to ventricular interval series and combined with computer simulations of atrioventricular conduction showed that the respiratory oscillation of atrial cycle length determined an oscillation in ventricular intervals with longer intervals during inspiration and shorter during expiration (VV insp=639.9+/-186.0 ms vs VV exp=634.8+/-182.9 ms, p<0.05). Ventricular interval oscillations resulted amplified by a factor 1.8 with respect to corresponding atrial cycle length oscillations. Thus, the mechanical fluctuations in AFL cycle length, although of small amplitude, might become clinically relevant through a magnified effect on ventricular variability.
尽管心房扑动（AFL）被认为是一种高度规则的节律，但已有研究描述了其周期长度的微小波动。近期针对人类的研究对这些间期振荡的机制进行了探究，结果表明心室收缩后心房容积和压力的周期性变化可能是AFL自发变异性的原因。其他研究表明，因人为操作导致的血流动力学改变引起的心房尺寸变化，会直接改变AFL的速率。所有这些证据促使了机械 - 电反馈（MEF）假说的提出，该假说认为心房容积的变化通过改变心房中循环冲动的传导特性，直接影响AFL周期长度的变异性。在本研究中，我们通过频谱分析重新审视了典型AFL的变异性模式，旨在支持MEF假说对AFL周期长度变异性的解释。在一个由30例典型AFL患者组成的研究群体中，我们观察到AFL周期长度呈现出自发的逐搏变异性，由两种振荡组成：一种主要振荡频率为心室收缩频率（1.70±0.48Hz，频谱功率：15.4±17.6ms²），另一种次要振荡频率为呼吸频率（0.32±0.07Hz，频谱功率：2.9±2.6ms²）。在药物自主神经阻滞之后，心室和呼吸振荡均持续存在（心室频谱功率：阻滞前为17.7±14.7ms²，阻滞后为20.2±18.3ms²，p = 无显著差异；呼吸频谱功率：阻滞前为6.0±3.8ms²，阻滞后为5.0±3.4ms²，p = 无显著差异），这表明存在一种非神经介导的潜在机制。与窦性心律期间心率的呼吸调制相反，呼吸性AFL周期长度振荡呈现出相反的模式，吸气时周期长度较长，呼气时较短（吸气时AA = 223.2±28.6ms，呼气时AA = 221.1±28.2ms，p < 0.0005），这与AFL折返的机械调制一致。应用于心室间期序列的频谱分析技术与房室传导的计算机模拟相结合的研究表明，心房周期长度的呼吸振荡决定了心室间期的振荡，吸气时间期较长，呼气时较短（吸气时VV = 639.9±186.0ms，呼气时VV = 634.8±182.9ms，p < 0.05）。心室间期振荡相对于相应的心房周期长度振荡放大了1.8倍。因此，AFL周期长度的机械波动尽管幅度较小，但可能通过对心室变异性的放大作用而在临床上具有相关性。
