Iwasa Atsushi, Hwa Michael, Hassankhani Alborz, Liu Taylor, Narayan Sanjiv M
University of California, Veterans Administration Medical Centers, San Diego, CA 92161, USA.
Pacing Clin Electrophysiol. 2005 Nov;28(11):1189-97. doi: 10.1111/j.1540-8159.2005.50186.x.
Abnormal heart rate turbulence (HRT) reflects autonomic derangements predicting all-cause mortality, yet has not been shown to predict ventricular arrhythmias in at-risk patients. We hypothesized that HRT at programmed ventricular stimulation (PVS) would predict arrhythmia initiation in patients with left ventricular dysfunction.
We studied 27 patients with coronary disease, left ventricular ejection fraction (LVEF) 26.7 +/- 9.1%, and plasma B-type natriuretic peptide (BNP) 461 +/- 561 pg/mL. Prior to arrhythmia induction at PVS, we measured sinus cycles after spontaneous or paced premature ventricular contractions (PVCs) for turbulence onset (TO; % cycle length change following PVC) and slope (TS; greatest slope of return to baseline cycle). T-wave alternans (TWA) was also measured during atrial pacing.
At PVS, abnormal TO (> or =0%) predicted inducible ventricular tachycardia (VT; n = 10 patients; P < 0.05). TO was greater in inducible than in noninducible patients (2.3 +/- 3.1% vs -0.02 +/- 2.8%, P < 0.05) and correlated with LVEF (P < 0.05) but not with BNP. TS did not differ between groups. Conversely, ambulatory HRT differed significantly from HRT at PVS (TO -0.55 +/- 1.08% vs 0.85 +/- 3.02%, P < 0.05; TS 2.63 +/- 2.09 ms/RR vs 8.70 +/- 6.56 ms/RR, P < 0.01), and did not predict inducible VT but trended (P = 0.05) to predict sustained VT on 739 +/- 179 days follow-up. TWA predicted inducible (P < 0.05) and spontaneous (P = 0.0001) VT but did not co-migrate with HRT.
Abnormal HRT measured at PVS predicted the induction of sustained ventricular arrhythmias in patients with ischemic cardiomyopathy. However, HRT at PVS did not correlate with ambulatory HRT, nor with TWA, both of which predicted spontaneous ventricular arrhythmias. Thus, HRT may reflect the influence of autonomic milieu on arrhythmic susceptibility and is likely complementary to traditional arrhythmic indices.
异常心率震荡（HRT）反映自主神经功能紊乱，可预测全因死亡率，但尚未证实其能预测高危患者的室性心律失常。我们假设在程控心室刺激（PVS）时的HRT可预测左心室功能障碍患者心律失常的发生。
我们研究了27例冠心病患者，左心室射血分数（LVEF）为26.7±9.1%，血浆B型利钠肽（BNP）为461±561 pg/mL。在PVS诱发心律失常之前，我们测量了自发或起搏诱发室性早搏（PVC）后的窦性周期，以计算震荡起始（TO；PVC后周期长度变化的百分比）和斜率（TS；恢复至基线周期的最大斜率）。在心房起搏期间还测量了T波交替（TWA）。
在PVS时，异常TO（≥0%）可预测可诱发的室性心动过速（VT；10例患者；P<0.05）。可诱发VT的患者TO大于不可诱发VT的患者（2.3±3.1%对-0.02±2.8%，P<0.05），且与LVEF相关（P<0.05），但与BNP无关。两组间TS无差异。相反，动态HRT与PVS时的HRT有显著差异（TO -0.55±1.08%对0.85±3.02%，P<0.05；TS 2.63±2.09 ms/RR对8.70±6.56 ms/RR，P<0.01），且不能预测可诱发的VT，但在739±179天的随访中对预测持续性VT有趋势性意义（P = 0.05）。TWA可预测可诱发的（P<0.05）和自发的（P = 0.0001）VT，但与HRT不共同变化。
在PVS时测量的异常HRT可预测缺血性心肌病患者持续性室性心律失常的诱发。然而，PVS时的HRT与动态HRT无关，也与TWA无关，后两者均可预测自发性室性心律失常。因此，HRT可能反映自主神经环境对心律失常易感性的影响，且可能是传统心律失常指标的补充。
