A case report of postural tachycardia syndrome after COVID-19

Miglis, Mitchell G.; Prieto, Thomas; Shaik, Ruba; Muppidi, Srikanth; Sinn, Dong In; Jaradeh, Safwan

doi:10.1007/s10286-020-00727-9

Cited by 154 publications

(153 citation statements)

References 6 publications

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“…Other studies have reported that viral infections and molecular mimicry are likely associated with autoimmune diseases [ 68 , 69 ]. A number of recent reports have identified POTS as a sequela of COVID-19 infection [ 70 , 71 , 72 ]. One might postulate that molecular mimicry might induce antibodies that target adrenergic and cholinergic muscarinic receptors via receptor stoichiometry similar to an unknown antigenic epitope seen in infection and/or inflammation.…”

Section: Resultsmentioning

confidence: 99%

Inflammatory Biomarkers in Postural Orthostatic Tachycardia Syndrome with Elevated G-Protein-Coupled Receptor Autoantibodies

Gunning

Stepkowski

Kramer

et al. 2021

JCM

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A growing body of evidence suggests that postural orthostatic tachycardia syndrome (POTS) may be an autoimmune disorder. We have reported in a previous manuscript that 89% of POTS patients (n = 55) had elevations in G-protein-coupled adrenergic A1 receptor autoantibodies and 53% had elevations in muscarinic acetylcholine M4 receptor autoantibodies, as assessed by ELISA. Patients with autoimmune disorders have been reported with a variety of elevated cytokines and cytokines (such as rheumatoid arthritis); thus, we evaluated a limited number of cytokines/chemokines in POTS patients with elevated adrenergic and muscarinic receptor autoantibodies. We utilized the plasma of 34 patients from a previous study; all of the patients (100%) had autoantibodies against the A1 adrenergic receptor and 55.9% (19/34) had autoantibodies against the M4 muscarinic acetylcholine receptor. In particular, the plasma cytokine/chemokine levels were measured as biomarkers of inflammation by Quantibody® technology (Raybiotech, Peachtree Corners, GA, USA). We also evaluated the platelet dense granule numbers, as these patients frequently complain of symptoms related to platelet dysfunction. Patients were predominantly young females who displayed a multitude of co-morbidities but generally reported viral-like symptoms preceding episodes of syncope. Eighty five percent (29/34) had platelet storage pool deficiency. Patients had elevations in five of ten cytokine/chemokines biomarkers (IL1β, IL21, TNFα, INFγ, and CD30), whereas two biomarkers had decreased levels (CD40L and RANTES). Our observations demonstrate that POTS patients known to have autoantibodies against the G-protein-coupled adrenergic A1 receptor have abnormal plasma concentrations of inflammatory cytokines.

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Section: Resultsmentioning

confidence: 99%

Inflammatory Biomarkers in Postural Orthostatic Tachycardia Syndrome with Elevated G-Protein-Coupled Receptor Autoantibodies

Gunning

Stepkowski

Kramer

et al. 2021

JCM

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“…Authors suggest that these symptoms are compatible with dysautonomia due to microangiopathy and endothelial injury. Miglis et al (2020a , b) also described a subset of COVID-19 survivors presenting symptoms of autonomic dysfunction such as orthostatic intolerance and postural orthostatic tachycardia. Such symptoms are frequently reported after other viral infections and might be related to gastrointestinal fluid loss, prolonged bed rest and deconditioning of the cardiovascular system.…”

Section: Persisting Cariorespiratory Symptoms In Coronavirus Survivormentioning

confidence: 99%

Hyperventilation: A Possible Explanation for Long-Lasting Exercise Intolerance in Mild COVID-19 Survivors?

et al. 2021

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Since the outbreak of the coronavirus (COVID-19) pandemic, most attention has focused on containing transmission and addressing the surge of critically ill patients in acute care settings. As we enter the second phase of the pandemic, emphasis must evolve to post-acute care of COVID-19 survivors. Persisting cardiorespiratory symptoms have been reported at several months after the onset of the infection. Information is lacking on the pathophysiology of exercise intolerance after COVID-19. Previous outbreaks of coronaviruses have been associated with persistent dyspnea, muscle weakness, fatigue and reduced quality of life. The extent of Covid-19 sequelae remains to be evaluated, but persisting cardiorespiratory symptoms in COVID-19 survivors can be described as two distinct entities. The first type of post-Covid symptoms are directly related to organ injury in the acute phase, or the complications of treatment. The second type of persisting symptoms can affect patients even with mild initial disease presentation without evidence of organ damage. The mechanisms are still poorly qualified to date. There is a lack of correlation between initial symptom severity and residual symptoms at exertion. We report exercise hyperventilation as a major limiting factor in COVID-19 survivors. The origin of this hyperventilation may be related to an abnormality of ventilatory control, by either hyperactivity of activator systems (automatic and cortical ventilatory control, peripheral afferents, and sensory cortex) or failure of inhibitory systems (endorphins) in the aftermath of pulmonary infection. Hyperventilation-induced hypocapnia can cause a multitude of extremely disabling symptoms such as dyspnea, tachycardia, chest pain, fatigue, dizziness and syncope at exertion.

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“…have shown multi-organ dysfunction using MRI that is suggestive of an ongoing inflammatory process in recovering patients [ 6 ], but its aetiology still needs to be ascertained. Additionally, certain rare syndromes such as Guillain–Barré syndrome [ 12 ], myasthenia gravis [ 13 ], postural–orthostatic tachycardia syndrome [ 14 ] and others may account for some patients' symptoms.…”

mentioning

confidence: 99%