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August 20, 2007Neurology163 citations

The hemodynamic and neurohumoral phenotype of postural tachycardia syndrome

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EGEmily M. GarlandSRSatish R. RajBBBonnie K. Black

Key Result

Patients with POTS had higher heart rates and plasma catecholamines, and decreased aldosterone and aldosterone/renin ratios compared to healthy controls, indicating sympathetic activation.

Study Design

Type

Case-Control (n=231)

Structured PICO

What are the hemodynamic and neurohumoral phenotypic differences between patients with postural tachycardia syndrome and healthy controls?

P
Population
231 participants, comprising 165 patients with postural tachycardia syndrome and 66 normal controls, evaluated for hemodynamic and neurohumoral responses to posture.
E
Exposure
Posture studies (supine and standing positions) after dietary and medication restrictions, overnight fast, and ≥30 minutes of supine rest
C
Comparator
Healthy normal controls (n=66)
O
Outcome
Hemodynamic (heart rate, blood pressure) and neurohumoral (norepinephrine, epinephrine, dopamine, aldosterone, renin) measurements in supine and standing positionssurrogate

Patients with postural tachycardia syndrome exhibit significant sympathetic activation and abnormalities in the renin-angiotensin-aldosterone system compared to healthy controls.

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 > or =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 > 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. 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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Cite This Study

Garland et al. (2007) conducted a case-control in Postural tachycardia syndrome (POTS) (n=231). Postural tachycardia syndrome (POTS) vs. Normal controls was evaluated on Hemodynamic and neurohumoral responses (heart rate, blood pressure, catecholamines, aldosterone, renin). Patients with POTS had higher heart rates and plasma catecholamines, and decreased aldosterone and aldosterone/renin ratios compared to healthy controls, indicating sympathetic activation.

synapsesocial.com/papers/6a557efecae1d55e053ea8a5https://doi.org/10.1212/01.wnl.0000267663.05398.40
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