Abnormalities of the QT interval in primary disorders of autonomic failure
Abnormalities of the QT interval in primary disorders of autonomic failure
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DOI：
10.1016/s0002-8703(98)70014-6
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发表时间：
1998-10-01
影响因子：
4.8
通讯作者：
Biaggioni, I
中科院分区：
文献类型：
--
作者：
Choy, AMJ;Lang, CC;Biaggioni, I
实验证据表明，自主神经系统的激活影响心室复极，从而影响心电图的QT间期。为了验证自主神经功能障碍患者QT间期异常的假设，我们检查了严重原发性自主神经衰竭患者和先天性多巴胺β -羟化酶（D β H）缺乏症患者的心电图，这些患者无法合成去甲肾上腺素和肾上腺素。受试者和方法采用盲法对67例原发性自主神经衰竭患者（36例多系统萎缩[MSA]， 31例纯粹自主神经衰竭[PAF]）和17例年龄和性别匹配的健康对照进行心电图测定，测定最大QT间期、率校正QT （QTc）间期和调整后的QTc离散度[(12导联心电图上最大QTc -最小QTc) /测得导联根数]。分析了5例先天性D - β H缺乏症患者和6例年龄和性别匹配的对照组的心电图。结果与对照组（450 +/- 18 ms1/2, P < 0.05和P < 0.01）相比，MSA和PAF患者QTc最大间隔时间（492 +/- 58 ms1/2和502 +/- 61 ms1/2 [mean +/- SD]）显著延长（P < 0.05和P < 0.01）。QTc离散度在MSA患者（40 +/- 20 ms1/2，与对照组相比P < 0.05）和PAF患者（32 +/- 19 ms1/2， NS）中也比对照组（21 +/- 5 ms1/2）增加。相比之下，与对照组相比，先天性D β H缺乏症患者的RR、QT、QTc间隔或QTc离散度无显著差异。结论原发性自主神经衰竭合并副交感神经和交感神经衰竭患者QT间期异常延长，QT离散度增高。然而，先天性DPH缺乏症患者的QT间期与对照组没有显著差异，因此，原发性自主神经衰竭患者的QT异常可能不仅仅是由交感神经系统病变引起的，副交感神经系统可能在心室复极中起调节作用。
Background Experimental evidence shows that activation of the autonomic nervous system influences ventricular repolarization and, therefore, the QT interval on the EGG. 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 (D beta H) deficiency who are unable to synthesize norepinephrine and epinephrine.Subjects and methods Maximal QT and rate-corrected QT (QTc) intervals and adjusted QTc dispersion [(maximal QTc - minimum QTc on 12 lead ECG)/root 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 D beta H deficiency and 6 age- and sex-matched controls were also analyzed.Results Patients with MSA and PAF had significantly prolonged maximum QTc intervals (492 +/- 58 ms1/2 and 502 +/- 61 m1/2 [mean +/- SD]), respectively, compared with controls (450 +/- 18 ms1/2, 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 ms1/2, P < .05 vs controls) and PAF patients (32 +/- 19 ms1/2, NS) compared with controls (21 +/- 5 ms1/2). In contrast, patients with congenital D beta H deficiency did not have significantly different RR, QT, QTc intervals, or QTc dispersion when compared with controls.Conclusions 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 DPH 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.