Pyridostigmine in the Treatment of Postural Orthostatic Tachycardia: A Single‐Center Experience

Kanjwal, Khalil; Karabin, Beverly; Sheikh, Mujeeb; Elmer, Lawrence; Kanjwal, Yousuf; Saeed, Bilal; Grubb, Blair P.

doi:10.1111/j.1540-8159.2011.03047.x

Cited by 91 publications

(60 citation statements)

References 9 publications

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“…24 Although syncope occurs in patients with POTS, it is relatively infrequent, and there is little evidence that the syncope is due to POTS. 24,514 Treatments that improve symptoms of POTS might decrease the occurrence of syncope, although this is unknown. 24 Some reports suggest that patients benefit from being informed of the suspected diagnosis in a clear but sympathetic manner that also acknowledges the involuntary nature of the attacks.…”

Section: Orthostatic Intolerancementioning

confidence: 99%

2017 ACC/AHA/HRS Guideline for the Evaluation and Management of Patients With Syncope: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society

Sheldon²,

et al. 2017

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Section: Orthostatic Intolerancementioning

confidence: 99%

2017 ACC/AHA/HRS Guideline for the Evaluation and Management of Patients With Syncope: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society

Sheldon²,

et al. 2017

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“…Drug therapy of POTS includes the mineralocorticoid fludrocortisone 90 to promote intravascular volume expansion, the ␣ 1 -adrenergic agonist midodrine 87,91 to elicit peripheral vasoconstriction and reduce venous pooling, ␤-blockers including propranolol 87,92 and cardioselective agents such as bisprostol 90,93 to control the excessive sinus tachycardia, and the cholinesterase inhibitor pyridostigmine [94][95][96] to prolong the phasic effects of acetylcholine on the autonomic ganglia, leading to peripheral sympathetic vasoconstrictor output (and potentiating vagal effects) on standing (Table 3). However, adverse effects of these drugs can limit their use in patients with POTS because of the presence of comorbid symptoms.…”

Section: Pharmacological Therapymentioning

confidence: 99%

Postural Tachycardia Syndrome: A Heterogeneous and Multifactorial Disorder

Benarroch

2012

Mayo Clinic Proceedings

315

354

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Postural tachycardia syndrome (POTS) is defined by a heart rate increment of 30 beats/min or more within 10 minutes of standing or head-up tilt in the absence of orthostatic hypotension; the standing heart rate is often 120 beats/min or higher. POTS manifests with symptoms of cerebral hypoperfusion and excessive sympathoexcitation. The pathophysiology of POTS is heterogeneous and includes impaired sympathetically mediated vasoconstriction, excessive sympathetic drive, volume dysregulation, and deconditioning. POTS is frequently included in the differential diagnosis of chronic unexplained symptoms, such as inappropriate sinus tachycardia, chronic fatigue, chronic dizziness, or unexplained spells in otherwise healthy young individuals. Many patients with POTS also report symptoms not attributable to orthostatic intolerance, including those of functional gastrointestinal or bladder disorders, chronic headache, fibromyalgia, and sleep disturbances. In many of these cases, cognitive and behavioral factors, somatic hypervigilance associated with anxiety, depression, and behavioral amplification contribute to symptom chronicity. The aims of evaluation in patients with POTS are to exclude cardiac causes of inappropriate tachycardia; elucidate, if possible, the most likely pathophysiologic basis of postural intolerance; assess for the presence of treatable autonomic neuropathies; exclude endocrine causes of a hyperadrenergic state; evaluate for cardiovascular deconditioning; and determine the contribution of emotional and behavioral factors to the patient's symptoms. Management of POTS includes avoidance of precipitating factors, volume expansion, physical countermaneuvers, exercise training, pharmacotherapy (fludrocortisone, midodrine, ␤-blockers, and/or pyridostigmine), and behavioral-cognitive therapy. A literature search of PubMed for articles published from January 1, 1990, to June 15, 2012, was performed using the following terms (or combination of terms): POTS; postural tachycardia syndrome, orthostatic; orthostatic; syncope; sympathetic; baroreceptors; vestibulosympathetic; hypovolemia; visceral pain; chronic fatigue; deconditioning; headache; Chiari malformation; Ehlers-Danlos; emotion; amygdala; insula; anterior cingulate; periaqueductal gray; fludrocortisone; midodrine; propranolol; ␤-adrenergic; and pyridostigmine. Studies were limited to those published in English. Other articles were identified from bibliographies of the retrieved articles. 1,2 According to current criteria for adults, 3 POTS is defined by a heart rate increment of 30 beats/min or more within 10 minutes of standing or head-up tilt (HUT) in the absence of orthostatic hypotension; the standing heart rate is often 120 beats/min or higher. These criteria may not be applicable for individuals with low resting heart rate. For individuals aged 12 to 19 years, the required increment is at least 40 beats/min.3 The orthostatic tachycardia may be accompanied by symptoms of cerebral hypoperfusion and sympathetic hyperactivity that are reliev...

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“…It decreases the heart rate in response to standing and reduces the symptom burden in patients with POTS 32. When used longitudinally in outpatients with POTS, most patients report improvement, although 20% of patients had to stop medication due to diarrhoea 33. Doses of 30–60 mg three times a day may be effective, without decreasing the blood pressure.…”

Section: Treatmentsmentioning

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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Pyridostigmine in the Treatment of Postural Orthostatic Tachycardia: A Single‐Center Experience

Abstract: The subgroup of POTS patients who can tolerate oral pyridostigmine may demonstrate improvement in their standing HR, standing diastolic blood pressure, and clinical symptoms of orthostatic intolerance.

Cited by 91 publications

References 9 publications

2017 ACC/AHA/HRS Guideline for the Evaluation and Management of Patients With Syncope: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society

2017 ACC/AHA/HRS Guideline for the Evaluation and Management of Patients With Syncope: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society

Postural Tachycardia Syndrome: A Heterogeneous and Multifactorial Disorder

Clinical challenges in the diagnosis and management of postural tachycardia syndrome

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