Mechanical modulation of atrial flutter cycle length.

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.