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August 20, 2007

The hemodynamic and neurohumoral phenotype of postural tachycardia syndrome

August 21, 2007 issue
69 (8) 790-798

Abstract

Background: Previous studies of patients with postural tachycardia syndrome (POTS) have been hampered by relatively small cohorts, failure to control medications and diet, and inconsistent testing procedures.
Methods: The Vanderbilt Autonomic Dysfunction Center Database provided results of posture studies performed in 165 patients and 66 normal controls after dietary and medication restrictions. All posture studies were performed after an overnight fast and ≥30 minutes of supine rest.
Results: In both the supine and standing positions, heart rate (HR) and plasma concentrations of norepinephrine (NE), epinephrine, and dopamine were higher in patients with POTS compared with the healthy controls. Supine diastolic blood pressure (BP) was also elevated in POTS, whereas supine plasma l-3,4-dihydroxyphenyalanine was reduced. In an analysis of patient subgroups with either an upright plasma NE ≥ 3.54 nM (high NE) or an upright plasma NE < 3.54 nM (normal NE), HR and BP were greater in the patient subgroup with high NE. In addition to these significant differences in hemodynamic and catechol measurements, we demonstrated that supine and standing plasma aldosterone and the aldosterone/renin ratio were decreased in patients with POTS. Plasma renin activity (PRA) tended to be higher in patients, and standing HR for those in the highest PRA quartile was significantly greater than for those in the lowest PRA quartile.
Conclusions: Our results from larger cohorts of patients and controls than previously studied confirm published findings and contribute additional evidence of sympathetic activation in postural tachycardia syndrome (POTS). Abnormalities in the renin–angiotensin–aldosterone system may also contribute to the POTS phenotype.

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Information & Authors

Information

Published In

Neurology®
Volume 69Number 8August 21, 2007
Pages: 790-798
PubMed: 17709712

Publication History

Published online: August 20, 2007
Published in print: August 21, 2007

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Authors

Affiliations & Disclosures

E. M. Garland, PhD
From the Autonomic Dysfunction Center, Vanderbilt University, Nashville, TN.
S. R. Raj, MD
From the Autonomic Dysfunction Center, Vanderbilt University, Nashville, TN.
B. K. Black, RN
From the Autonomic Dysfunction Center, Vanderbilt University, Nashville, TN.
P. A. Harris, PhD
From the Autonomic Dysfunction Center, Vanderbilt University, Nashville, TN.
D. Robertson, MD
From the Autonomic Dysfunction Center, Vanderbilt University, Nashville, TN.

Notes

Address correspondence and reprint requests to Dr. Emily M. Garland, Autonomic Dysfunction Center, AA3228 Medical Center North, Vanderbilt University, 1161 21st Avenue South, Nashville, TN 37232-2195 [email protected]

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