The neuropathic postural tachycardia syndrome

The neuropathic postural tachycardia syndrome
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DOI:
10.1056/nejm200010053431404
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发表时间:
2000-10-05
影响因子:
158.5
通讯作者:
Robertson, D
Robertson, D
中科院分区:
医学1区
文献类型:
--
作者:
Jacob, G;Costa, F;Robertson, D

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背景资料:体位性心动过速综合征是一种常见的疾病,其特征是慢性直立性症状和站立时心率急剧增加,但不涉及直立性低血压。几条证据表明,这种疾病可能是由于交感神经的腿。方法:我们测量了去甲肾上腺素溢出(去甲肾上腺素进入静脉循环的速率)在暴露于三种刺激之前和响应于暴露于三种刺激时在手臂和腿部中的变化(冷加压试验,硝普钠输注,10例体位性心动过速综合征患者和8例年龄和性别匹配的正常人。在底线,体位性心动过速综合征患者股静脉血浆去甲肾上腺素浓度低于正常人(135+/-30 vs. 215+/-55 pg/ml [0.80+/-0.18 vs. 1.27+/-0.32 nmol/L],P=0.001)。两组受试者手臂中的去甲肾上腺素溢出在对三种刺激的反应中增加的程度相似,但体位性心动过速综合征患者下肢的增加幅度小于正常人(0.001+/-0.09对0.12+/-0.12 ng/min/dl组织[0.006+/-0.53对0.71+/-0.71 nmol/min/dl]与冷加压试验,P=0.02;硝普钠输注组0.02+/-0.07 vs 0.23+/-0.17 ng/min/dl [0.12+/-0.41 vs 1.36+/-1.00 nmol/min/dl],P=0.01;酪胺输注时每分钟0.008+/-0.09和0.19+/-0.25 ng/分升[每分钟0.05+/-0.53和1.12+/-1.47 nmol/分升],P=0.04)。神经性体位性心动过速综合征是由部分交感神经失神经支配引起的,尤其是在腿部。(N Engl J Med 2000;343:1008-14.)(C)2000年,马萨诸塞州医学会。
Background: The postural tachycardia syndrome is a common disorder that is characterized by chronic orthostatic symptoms and a dramatic increase in heart rate on standing, but that does not involve orthostatic hypotension. Several lines of evidence indicate that this disorder may result from sympathetic denervation of the legs.Methods: We measured norepinephrine spillover (the rate of entry of norepinephrine into the venous circulation) in the arms and legs both before and in response to exposure to three stimuli (the cold pressor test, sodium nitroprusside infusion, and tyramine infusion) in 10 patients with the postural tachycardia syndrome and in 8 age- and sex-matched normal subjects.Results: At base line, the mean (+/-SD) plasma norepinephrine concentration in the femoral vein was lower in the patients with the postural tachycardia syndrome than in the normal subjects (135+/-30 vs. 215+/-55 pg per milliliter [0.80+/-0.18 vs. 1.27+/-0.32 nmol per liter], P=0.001). Norepinephrine spillover in the arms increased to a similar extent in the two groups in response to each of the three stimuli, but the increases in the legs were smaller in the patients with the postural tachycardia syndrome than in the normal subjects (0.001+/-0.09 vs. 0.12+/-0.12 ng per minute per deciliter of tissue [0.006+/-0.53 vs. 0.71+/-0.71 nmol per minute per deciliter] with the cold pressor test, P=0.02; 0.02+/-0.07 vs. 0.23+/-0.17 ng per minute per deciliter [0.12+/-0.41 vs. 1.36+/-1.00 nmol per minute per deciliter] with nitroprusside infusion, P=0.01; and 0.008+/-0.09 vs. 0.19+/-0.25 ng per minute per deciliter [0.05+/-0.53 vs. 1.12+/-1.47 nmol per minute per deciliter] with tyramine infusion, P=0.04).Conclusions: The neuropathic postural tachycardia syndrome results from partial sympathetic denervation, especially in the legs. (N Engl J Med 2000;343:1008-14.) (C) 2000, Massachusetts Medical Society.