Neurology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Figures Only
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Correspondence:
Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when Correspondence are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Garland, E. M.
Right arrow Articles by Robertson, D.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Garland, E. M.
Right arrow Articles by Robertson, D.
Related Collections
Right arrow All Medical/Systemic disease
Right arrow Endocrine
Right arrow Syncope
Right arrow Autonomic diseases
Right arrow Cardiac; see Cerebrovascular Disease/Cardiac
NEUROLOGY 2007;69:790-798
© 2007 American Academy of Neurology

The hemodynamic and neurohumoral phenotype of postural tachycardia syndrome

E. M. Garland, PhD, S. R. Raj, MD, B. K. Black, RN, P. A. Harris, PhD and D. Robertson, MD

From the Autonomic Dysfunction Center, Vanderbilt University, Nashville, TN.

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 emily.garland{at}vanderbilt.edu

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.

Supported in part by NIH grants MO1 RR00095, R01 HL071784, K23 RR020783, and PO1 HL56693.

Disclosure: The authors report no conflicts of interest.

Received December 5, 2006. Accepted in final form March 23, 2007.






HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 2007 by AAN Enterprises, Inc.