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Recent advances in the understanding of the mechanisms underlying postural tachycardia syndrome in children: practical implications for treatment

Published online by Cambridge University Press:  12 December 2016

Xiaochun Zheng
Affiliation:
Department of Pediatrics, Peking University First Hospital, Beijing, P. R. China
Yonghong Chen
Affiliation:
Department of Pediatrics, Peking University First Hospital, Beijing, P. R. China
Junbao Du*
Affiliation:
Department of Pediatrics, Peking University First Hospital, Beijing, P. R. China
*
Correspondence to: Professor J. Du, Department of Pediatrics, Peking University First Hospital, Beijing 100034, P. R. China. Tel: +86 10 8357 3165; Fax: +86 10 6653 0532; E-mail: [email protected]

Abstract

Postural tachycardia syndrome is defined by a heart rate increment of 40 beats/minute (bpm) (or a heart rate that exceeds 125 bpm) within 10 minutes of change from the supine position to an upright position in the absence of obvious orthostatic hypotension. There are multiple pathophysiological mechanisms that underlie postural tachycardia syndrome, including peripheral denervation, β-receptor supersensitivity, hypovolaemia, and impaired muscle pump. Some children afflicted with postural orthostatic tachycardia syndrome and hypovolaemic dysregulation have been found to have perturbed renin–angiotensin–aldosterone profile, disturbed vascular endothelial function, and abnormal vasodilation. The hyperadrenergic state in some postural tachycardia syndrome patients is likely a driver for orthostatic tachycardia. Other mechanisms include the presence of treatable autonomic neuropathies. An understanding of these pathophysiological mechanisms might be helpful for the effective treatment of postural tachycardia syndrome.

Type
Review Article
Copyright
© Cambridge University Press 2016 

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Footnotes

*

Xiaochun Zheng and Yonghong Chen contributed equally to this work.

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