Review: Postural orthostatic tachycardia syndrome: clinical presentation, aetiology and management, 2018, Fedorowski

Andy

Retired committee member
Abstract
Postural orthostatic tachycardia syndrome (POTS) is a variant of cardiovascular autonomic disorder characterized by an excessive heart rate increase on standing and orthostatic intolerance. POTS affects younger individuals 15–45 years old with a distinct female predominance (≈80%). The prevalence ranges between 0.2% and 1.0% in developed countries. The onset of POTS is typically precipitated by immunological stressors such as viral infection, vaccination, trauma, pregnancy, surgery or psychosocial stress. The most common complaints are dizziness, weakness, rapid heartbeat and palpitation on standing. Moreover, patients often report physical deconditioning and reduced exercise capacity as well as headache, ‘brain fog’, dyspnoea, gastrointestinal disorders and musculoskeletal pain.

The aetiology of POTS is largely unknown and three main hypotheses include an autoimmune disorder, abnormally increased sympathetic activity and catecholamine excess, and sympathetic denervation leading to central hypovolaemia and reflex tachycardia. The golden standard for POTS diagnosis is head‐up tilt test with a non‐invasive beat‐to‐beat haemodynamic monitoring. Although long‐term prognosis of POTS is poorly explored, around 50% of patients spontaneously recover within 1–3 years. After the diagnosis has been established, patient should be thoroughly educated about non‐pharmacological measures alleviating the symptoms. Exercise training may be very effective and counteract deconditioning. In more symptomatic patients, different drugs directed at controlling heart rate, increasing peripheral vasoconstriction and intravascular volume can be tested.

However, the overall effects of pharmacological therapy are modest and the most affected patients remain handicapped. Future efforts should focus on better understanding of POTS pathophysiology and designing randomized controlled trials for selection of more effective therapy.
Open access at https://onlinelibrary.wiley.com/doi/full/10.1111/joim.12852
 
I have so far just read through the review once and may be unfair in my comments but two things struck me in an otherwise clear and appearantly well argued review:

1. In relation to 'CFS' the authors say:

Interestingly, a substantial proportion of POTS patients (20–50%) share diagnoses with chronic fatigue syndrome (CFS) and Ehlers–Danlos syndrome (EDS)31, 33. Among all CFS patients, around 10–15% meet diagnostic POTS criteria 58, 59. These patients are typically younger and have shorter disease duration 59. In EDS, characteristic POST symptoms can be found in up to 40% of patients and the onset is typically not precipitated by viral infection 60.

however given the limited resources for diagnosis, mentioned by the authors, and the fact that many people with more severe ME do not have adequate access to medical assesment isn't it likely that any research involves under reporting and a potentially skewed sample.

I suspect that POTS in severe ME may be more prevalent, not confined to younger patients and longer lasting than suggested here. Also I am interested in the possibility that the symptom of orthostatic intolerance that may occur in ME in the absence of full blown POTS, though unfortunately this area is so little investigated. Indeed how common is the symptom of orthostatic intolerance outside what would fit the formal diagnostic criteria of POTS?

2. In relation to exercise they say in the abstract:

After the diagnosis has been established, patient should be thoroughly educated about non‐pharmacological measures alleviating the symptoms. Exercise training may be very effective and counteract deconditioning.

and in the text they say

Exercise training may be very effective and has been shown to alleviate the symptoms of POTS‐related deconditioning 66, 67.

Exercise training - There are different programmes available. A regular, structured, graduated, and supervised exercise programme featuring aerobic reconditioning with some resistance training for the thighs is preferable. Initial training should avoid upright position. Mild‐to‐moderate‐intensity endurance training, progressing from semi‐recumbent to upright position plus strength training is recommended. Rowing machines, recumbent bicycles and swimming may be applied. Class IIA recommendation 3, 67, 78-80

however they do not discuss any limitations that perhaps should be placed on exercise in relation to those patients with comorbid ME. Also, though I have not checked their cited studies, because of ME research's unjustified assertions of deconditioning and often totally inadequate evaluation of exercise interventions, I feel wary of taking these assertions at face value.

The current medical belief that exercise is a universal panacea, may 'all things being equal' be a justified assumption, but it should not be allowed to be an excuse for assuming that exercise is always appropriate even when 'all things are not equal'.
 
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