Autoimmune Basis for Postural Tachycardia Syndrome
Autoimmune Basis for Postural Tachycardia Syndrome
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DOI：
10.1161/jaha.113.000755
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发表时间：
2014-02-01
影响因子：
5.4
通讯作者：
Kem, David C.
中科院分区：
文献类型：
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作者：
Li, Hongliang;Yu, Xichun;Kem, David C.
背景-体位性心动过速综合征（POTS）患者常在病毒性疾病后出现夸大的直立性心动过速，提示自身免疫可能在POTS中起病理生理作用。我们测试的假设，他们窝藏功能性自身抗体肾上腺素能受体（AR）。方法和结果14例POTS患者（7个来自2个机构）和10名健康受试者进行了检查α 1 AR自身抗体介导的收缩性使用灌注大鼠提睾肌小动脉测定。使用基于受体转染细胞的试验检测β 1 AR和β 2 AR自身抗体的存在。将数据标准化并表示为基线的百分比。所有14名POTS患者的血清均显示出显著的小动脉收缩活性（69 +/- 3%，而健康对照组为基线的91 +/- 1%，P
Background-Patients with postural tachycardia syndrome (POTS) have exaggerated orthostatic tachycardia often following a viral illness, suggesting autoimmunity may play a pathophysiological role in POTS. We tested the hypothesis that they harbor functional autoantibodies to adrenergic receptors (AR).Methods and Results-Fourteen POTS patients (7 each from 2 institutions) and 10 healthy subjects were examined for alpha 1AR autoantibody-mediated contractility using a perfused rat cremaster arteriole assay. A receptor-transfected cell-based assay was used to detect the presence of beta 1AR and beta 2AR autoantibodies. Data were normalized and expressed as a percentage of baseline. The sera of all 14 POTS patients demonstrated significant arteriolar contractile activity (69 +/- 3% compared to 91 +/- 1% of baseline for healthy controls, P