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The hemodynamic and neurohumoral phenotype of postural tachycardia syndrome.

Authors :
Garland EM
Raj SR
Black BK
Harris PA
Robertson D
Source :
Neurology [Neurology] 2007 Aug 21; Vol. 69 (8), pp. 790-8.
Publication Year :
2007

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.<br />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 > or =30 minutes of supine rest.<br />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 > or = 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.<br />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.

Details

Language :
English
ISSN :
1526-632X
Volume :
69
Issue :
8
Database :
MEDLINE
Journal :
Neurology
Publication Type :
Academic Journal
Accession number :
17709712
Full Text :
https://doi.org/10.1212/01.wnl.0000267663.05398.40