サトウ キヨウコ   SATO Kyoko
  佐藤 恭子
   所属   医学部 医学科(東医療センター)
   職種   講師
論文種別 原著
言語種別 英語
査読の有無 査読あり
表題 Vagal and Sympathetic Function in Neuropathic Postural Tachycardia Syndrome.
掲載誌名 正式名:Hypertension (Dallas, Tex. : 1979)
略  称:Hypertension
ISSNコード:(1524-4563)0194-911X(Linking)
掲載区分国外
巻・号・頁 HYPERTENSIONAHA11811803頁
著者・共著者 Jacob Giris, Diedrich Laura, Sato Kyoko, Brychta Robert J, Raj Satish R, Robertson David, Biaggioni Italo, Diedrich André
発行年月 2019/03
概要 The diagnosis of neuropathic postural tachycardia syndrome (POTS) requires research techniques not available clinically. We hypothesized that these patients will have impaired vagal and sympathetic cardiovascular control that can be characterized with clinical autonomic tests. We included 12 POTS patients with possible neuropathic subtype because of normal plasma norepinephrine and no increase in upright blood pressure. We compared them to 10 healthy subjects. We assessed hemodynamics, heart rate and blood pressure variability, baroreflex sensitivity, raw and integrated muscle sympathetic nerve activity, and blood volume. To understand the vagal/sympathetic control, we dissected the phase 2 of Valsalva maneuver (VM) into early (VM2e) and late (VM2l). POTS' upright heart rate increased 43±3 bpm. Patients had normal plasma volume but reduced red blood cell volume (1.29 L versus predicted normal values 1.58 L; P=0.02). Vagal indices of heart rate variability, HFRRI (430±130 versus 1680±900; P=0.04), PNN50, and root mean squared of successive differences were lower in POTS. Patients showed a decrease in vagal baroreflex sensitivity (VM2e; P=0.04). In POTS, integrated muscle sympathetic nerve activity was lower at rest (12±1.5 versus 20±2 burst/min; P=0.004) and raw muscle sympathetic nerve activity spike analysis showed blunted responses during VM2e, despite a greater drop in systolic blood pressure (34±5 in POTS and 14±6 mm Hg in controls; P=0.01). This cohort of POTS patients enriched for possible neuropathic subtype had lower resting muscle sympathetic nerve activity, impaired vagal cardiac control, and exaggerated drop in blood pressure in response to VM and a delay in the sympathetic cardiovascular responsiveness during hypotensive challenge.
DOI 10.1161/HYPERTENSIONAHA.118.11803
PMID 30879357