Choy A M, Lang C C, Roden D M, Robertson D, Wood A J, Robertson R M, Biaggioni I
Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tenn 37232-2195, USA.
Am Heart J. 1998 Oct;136(4 Pt 1):664-71. doi: 10.1016/s0002-8703(98)70014-6.
Experimental evidence shows that activation of the autonomic nervous system influences ventricular repolarization and, therefore, the QT interval on the ECG. To test the hypothesis that the QT interval is abnormal in autonomic dysfunction, we examined ECGs in patients with severe primary autonomic failure and in patients with congenital dopamine beta-hydroxylase (DbetaH) deficiency who are unable to synthesize norepinephrine and epinephrine.
Maximal QT and rate-corrected QT (QTc) intervals and adjusted QTc dispersion [(maximal QTc - minimum QTc on 12 lead ECG)/square root of the number of leads measured] were determined in blinded fashion from ECGs of 67 patients with primary autonomic failure (36 patients with multiple system atrophy [MSA], and 31 patients with pure autonomic failure [PAF]) and 17 age- and sex-matched healthy controls. ECGs of 5 patients with congenital DbetaH deficiency and 6 age- and sex-matched controls were also analyzed.
Patients with MSA and PAF had significantly prolonged maximum QTc intervals (492+/-58 ms(1/2) and 502+/-61 ms(1/2) [mean +/- SD]), respectively, compared with controls (450+/-18 ms(1/2), P < .05 and P < .01, respectively). A similar but not significant trend was observed for QT. QTc dispersion was also increased in MSA (40+/-20 ms(1/2), P < .05 vs controls) and PAF patients (32+/-19 ms(1/2), NS) compared with controls (21+/-5 ms(1/2)). In contrast, patients with congenital DbetaH deficiency did not have significantly different RR, QT, QTc intervals, or QTc dispersion when compared with controls.
Patients with primary autonomic failure who have combined parasympathetic and sympathetic failure have abnormally prolonged QT interval and increased QT dispersion. However, QT interval in patients with congenital DbetaH deficiency was not significantly different from controls. It is possible, therefore, that QT abnormalities in patients with primary autonomic failure are not solely caused by lesions of the sympathetic nervous system, and that the parasympathetic nervous system is likely to have a modulatory role in ventricular repolarization.
实验证据表明，自主神经系统的激活会影响心室复极，进而影响心电图上的QT间期。为了验证自主神经功能障碍患者QT间期异常这一假说，我们检查了严重原发性自主神经功能衰竭患者以及先天性多巴胺β-羟化酶（DβH）缺乏症患者（这些患者无法合成去甲肾上腺素和肾上腺素）的心电图。
采用盲法从67例原发性自主神经功能衰竭患者（36例多系统萎缩[MSA]患者和31例纯自主神经功能衰竭[PAF]患者）以及17例年龄和性别匹配的健康对照者的心电图中测定最大QT间期和心率校正QT（QTc）间期以及校正后的QTc离散度[（12导联心电图上的最大QTc - 最小QTc）/测量导联数的平方根]。还分析了5例先天性DβH缺乏症患者和6例年龄和性别匹配的对照者的心电图。
与对照组相比，MSA患者和PAF患者的最大QTc间期显著延长，分别为（492±58毫秒（1/2）和502±61毫秒（1/2）[均值±标准差]），而对照组为（450±18毫秒（1/2），P分别<.05和<.01）。QT间期也有类似但不显著的趋势。与对照组（21±5毫秒（1/2））相比，MSA患者（40±20毫秒（1/2），与对照组相比P<.05）和PAF患者（32±19毫秒（1/2），无显著性差异）的QTc离散度也增加。相比之下，先天性DβH缺乏症患者与对照组相比，RR、QT、QTc间期或QTc离散度无显著差异。
原发性自主神经功能衰竭患者同时存在副交感神经和交感神经功能衰竭，其QT间期异常延长，QT离散度增加。然而，先天性DβH缺乏症患者的QT间期与对照组相比无显著差异。因此，原发性自主神经功能衰竭患者的QT异常可能并非仅由交感神经系统病变引起，副交感神经系统可能在心室复极中起调节作用。
