Cited by 358Cardiovascular Syncope and Autonomic DisordersHeart Rate Variability and Autonomic ControlLong-Term Effects of COVID-19

The DOI matches its Crossref record; 47 of the 48 references it cites were found in a registry or an index.

Postural Tachycardia Syndrome (POTS)

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LOW, PHILLIP A., SANDRONI, PAOLA, JOYNER, MICHAEL, SHEN, WIN‐KUANG·2009·Journal of Cardiovascular Electrophysiology

Abstract

Postural Tachycardia Syndrome. Introduction: POTS is defined as the development of orthostatic symptoms associated with a heart rate (HR) increment ≥30, usually to ≥120 bpm without orthostatic hypotension. Symptoms of orthostatic intolerance are those due to brain hypoperfusion and those due to sympathetic overaction. Methods: We provide a review of POTS based primarily on work from the Mayo Clinic. Results: Females predominate over males by 5:1. Mean age of onset in adults is about 30 years and most patients are between the ages of 20–40 years. Pathophysiologic mechanisms (not mutually exclusive) include peripheral denervation, hypovolemia, venous pooling, β‐receptor supersensitivity, psychologic mechanisms, and presumed impairment of brain stem regulation. Prolonged deconditioning may also interact with these mechanisms to exacerbate symptoms. The evaluation of POTS requires a focused history and examination, followed by tests that should include HUT, some estimation of volume status and preferably some evaluation of peripheral denervation and hyperadrenergic state. All patients with POTS require a high salt diet, copious fluids, and postural training. Many require β‐receptor antagonists in small doses and low‐dose vasoconstrictors. Somatic hypervigilance and psychologic factors are involved in a significant proportion of patients. Conclusions: POTS is heterogeneous in presentation and mechanisms. Major mechanisms are denervation, hypovolemia, deconditioning, and hyperadrenergic state. Most patients can benefit from a pathophysiologically based regimen of management. (J Cardiovasc Electrophysiol, Vol. 20, pp. 352‐358, March 2009)

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  1. 10.1007/978-1-4684-8962-0 · DOI
  2. 10.1002/mus.20853 · DOI

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Metadata

Authors
LOW, P. A., SANDRONI, P., JOYNER, M., & SHEN, W.
Affiliations
Mayo Clinic (US)
Venue
Journal of Cardiovascular Electrophysiology
Publisher
Wiley
Published
2009-02-20
Volume
20
Issue
3
Pages
352-358
ISSN
  • 1045-3873 (ISSN-L)
  • 1540-8167
OpenAlex
W2061811312
Cited by
358
References
48
Citations by year
2026: 10 · 2025: 25 · 2024: 21 · 2023: 19 · 2022: 27 · 2021: 18 · 2020: 32 · 2019: 19 · 2018: 20 · 2017: 25 · 2016: 17 · 2015: 25 · 2014: 22 · 2013: 18 · 2012: 21
FWCI
2.82
Type
journal article
Language
en
Open access
Locations
  • Journal of Cardiovascular Electrophysiology (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
  • Data Archiving and Networked Services (DANS) (submittedVersion)
  • Pure Amsterdam UMC (submittedVersion)
Funders
  • National Institutes of Health (n01ns032352-003)
  • National Institute of Neurological Disorders and Stroke (P01NS044233, P50NS032352, NS-44233, N01 NS032352)
Topics
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Syncope and Autonomic Disorders
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Heart Rate Variability and Autonomic Control
  • Health Sciences › Medicine › Clinical Neurology › Long-Term Effects of COVID-19
Keywords
postural orthostatic tachycardia syndrome, orthostatic intolerance, heart rate increase, peripheral denervation, hypovolemia, venous pooling, hyperadrenergic state, head-up tilt, volume status, high-salt diet, postural training, beta-receptor antagonists, vasoconstrictors, psychological factors
MeSH terms
Humans, Postural Orthostatic Tachycardia Syndrome

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