Postural Tachycardia Syndrome (POTS)

Raj, Satish R.

doi:10.1161/circulationaha.112.144501

Cited by 215 publications

(222 citation statements)

References 21 publications

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“…It is frequently accompanied by other vascular and nonvascular symptoms. The syndrome affects predominantly young women (70–80%), but its cause has not been established 3, 4, 5. In 2014, our laboratory demonstrated that a marked relationship of activating autoantibodies (AAbs) to the α1‐adrenergic (α1AR) and β1/2‐adrenergic (β1/2AR) receptors existed in 14 of 14 such patients 6.…”

Section: Introductionmentioning

confidence: 99%

Angiotensin II Type 1 Receptor Autoantibodies in Postural Tachycardia Syndrome

Murphy

et al. 2018

JAHA

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BackgroundBoth the adrenergic and renin‐angiotensin systems contribute to orthostatic circulatory homeostasis, which is impaired in postural orthostatic tachycardia syndrome (POTS). Activating autoantibodies to the α1‐adrenergic and β1/2‐adrenergic receptors have previously been found in sera from patients with POTS. We hypothesized that patients with POTS might also harbor activating autoantibodies to the angiotensin II type 1 receptor (AT1R) independently of antiadrenergic autoimmunity. This study examines a possible pathophysiological role for AT1R autoantibodies in POTS.Methods and ResultsSerum immunoglobulin G from 17 patients with POTS, 6 patients with recurrent vasovagal syncope, and 10 normal controls was analyzed for the ability to activate AT1R and alter AT1R ligand responsiveness in transfected cells in vitro. Of 17 subjects with POTS, 12 demonstrated significant AT1R antibody activity in immunoglobulin G purified from their serum. No significant AT1R antibody activity was found in the subjects with vasovagal syncope or healthy subjects. AT1R activation by POTS immunoglobulin G was specifically blocked by the AT1R blocker losartan. Moreover, POTS immunoglobulin G significantly shifted the angiotensin II dosage response curve to the right, consistent with an inhibitory effect. All subjects with POTS were positive for one or both autoantibodies to the AT1R and α1‐adrenergic receptor.ConclusionsMost patients with POTS harbor AT1R antibody activity. This supports the concept that AT1R autoantibodies and antiadrenergic autoantibodies, acting separately or together, may exert a significant impact on the cardiovascular pathophysiological characteristics in POTS.

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Section: Introductionmentioning

confidence: 99%

Angiotensin II Type 1 Receptor Autoantibodies in Postural Tachycardia Syndrome

Murphy

et al. 2018

JAHA

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“…Pharmacological treatment of PoTS patients involves fludrocortisone (volume expansion), midodrine (vasoconstriction), beta-adrenergic blockers (reduce sympathetic influence on sinus node) and/or pyridostigmine (increases synaptic acetylcholine) [10;14]. Even though there are small studies describing positive effects of these drugs [10], the Food and Drug Administration (FDA) hasn't approved any of these drugs for the treatment of PoTS because of the lack of large randomized clinical studies [10]. The currents case reflects the challenge clinicians may face for timely diagnosis of PoTS.…”

Section: Discussionmentioning

confidence: 99%

Postural Tachycardia Syndrome

Saïd¹

2017

IJCC

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“…This is more common as a secondary mechanism in patients with POTS who have hypovolaemia or peripheral sympathetic denervation, but in some cases it is the primary cause 13. They often have increased sympathetic activity at rest, which becomes markedly exaggerated when upright 14…”

Section: Proposed Pathophysiologymentioning

confidence: 99%

Clinical challenges in the diagnosis and management of postural tachycardia syndrome

2016

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Postural tachycardia syndrome (POTS) is a multifactorial clinical syndrome defined by an increase in heart rate of ≥30 bpm on standing from supine position (or ≥40 bpm in children). It is associated with symptoms of cerebral hypoperfusion that are worse when upright and improve when in supine position. Patients often have additional symptoms including severe fatigue and difficulty concentrating. There are several possible pathophysiologic mechanisms including hypovolaemia, small-fibre peripheral neuropathy and hyperadrenergic states. POTS can also be associated with several disorders including mastocytosis, Ehlers-Danlos syndrome (hypermobility type) and autoimmune disorders. The treatment is focused on symptom relief and not solely on reducing tachycardia. Given its varying presentations, it is important to employ a practical, mechanism-focused approach to the diagnosis and management of POTS.

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Postural Tachycardia Syndrome (POTS)

Cited by 215 publications

References 21 publications

Angiotensin II Type 1 Receptor Autoantibodies in Postural Tachycardia Syndrome

Angiotensin II Type 1 Receptor Autoantibodies in Postural Tachycardia Syndrome

Postural Tachycardia Syndrome

Clinical challenges in the diagnosis and management of postural tachycardia syndrome

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