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      A case report of postural tachycardia syndrome after COVID-19

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          Abstract

          Dear Editors, The most common symptoms of coronavirus disease 19 (COVID-19) from severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection include fever, cough, sore throat, and fatigue. As case numbers grow, neurological symptoms have been reported with increasing frequency, including those of autonomic dysfunction [1]. Most neurological reports detail symptoms in hospitalized patients during the para-infectious period; thus, understanding of longer-term, post-infectious sequalae is limited. We report the case of a patient who developed postural tachycardia syndrome (POTS) several months after confirmed SARS-CoV-2 infection. In early March of 2020, a 26-year-old emergency department nurse in Orange County, California developed a mild cough and an itchy throat. She woke the next day with palpitations, fatigue, and mild shortness of breath. On day 3 she presented to urgent care and had a nasopharyngeal swab which returned negative for SARS-CoV-2 PCR. On day 7 she woke up with palpitations, shortness of breath, and anorexia. She noted that her resting seated HR was 110 bpm and would increase to 190 bpm after walking up a flight of stairs. Her cough worsened and she developed burning chest pains on inhalation. She presented to the emergency department for evaluation, where her temperature was 100.4 ℉ and her SaO2 98%. A chest CT was performed and demonstrated moderate bronchitis with right lower lobe atelectasis. Her SARS-CoV nasopharyngeal swab was repeated and returned positive. IgG and IgM antibodies to the SARS-CoV-2 spike receptor binding domain (RBD) also returned positive. She was given IV fluids, a 5-day prescription of azithromycin, and discharged home. Over the following week she noted continued tachycardia (standing HR of 150 bpm after showering), chest pains, shortness of breath, fatigue and exercise intolerance, along with subjective fevers and insomnia. Her seated, resting BP increased to 156/112 mmHg (her typical seated, resting BP was 110/60 mmHg). On day 19 she developed orthostatic lightheadedness and presyncope. She returned to the emergency department for evaluation, where her seated BP was 146/100 mmHg, HR was 125 bpm, and SaO2 dropped from 98% to 94% with minimal exertion. She was given IV fluids, kept overnight, and discharged the following day. On day 22 she developed symptoms of hyperactivity with pressured speech and a feeling of inner restlessness. On day 24 she developed episodic sensations of “adrenaline surges” characterized by diarrhea, tremors, and worsening restlessness. Over the following month her orthostatic intolerance worsened, despite ongoing ability to exercise. Increased fluid and salt intake and compression garments were utilized, with minimal improvement in symptoms. On day 45 she developed episodic facial flushing, dermatographia, and non-pruritic hives. She presented to our autonomic clinic for evaluation at this time. Her past medical history included exercise-induced asthma and obsessive–compulsive disorder, diagnosed at age 16, which resolved without pharmacological treatment by age 18. She had no history of autonomic symptoms or syncope. Her family history was notable for similar symptoms in her twin sister, a close contact, who experienced a similar infectious prodrome during the same time period; however, her sister tested negative for SARS-CoV-2, twice, by the same lab that analyzed the patient’s samples. Physical examination of our patient, including a detailed neurological examination, was normal. There was no evidence of joint hypermobility. We prescribed propranolol and clonidine which led to some improvement of her hyperadrenergic symptoms. Despite these medications, her symptoms of orthostatic intolerance and spells of sympathetic hyperactivity continued, and on day 107, over 3 months after symptom onset, she underwent autonomic reflex testing in our laboratory, including quantitative sudomotor axon reflex testing (QSART), heart rate variability with deep breathing, Valsalva maneuver, and a 10-min head-up tilt (HUT) at an angle of 70°. Beat-to-beat BP was measured with finger plethysmography and confirmed with an automated cuff sphygmomanometer over the brachial artery. An intravenous catheter was placed, and supine and upright norepinephrine (NE) levels were collected. All medications were held 1 week prior to testing. Autonomic testing demonstrated an exaggerated postural tachycardia with an HR increase of 65 bpm on HUT, episodic hypertensive systolic BP surges to 170 mmHg in an oscillatory pattern, and robust BP responses to Valsalva maneuver pattern in the absence of hyperventilation, suggestive of a hyperadrenergic state (Fig. 1). The heart rate response to HUT demonstrated a sustained increase of greater than 30 bpm which persisted for the duration of the tilt, arguing against an anxiety response. The remainder of her autonomic testing and NE levels were normal (supplementary table). Her nasopharyngeal swab was repeated and was negative for SARS-CoV-2. IgM and IgG RBD antibodies were repeated and were also negative, as were ganglionic acetylcholine receptor antibodies. At the time of this report, approximately 5.5 months after symptom onset, the patient’s symptoms remain, and she has not yet returned to work. Fig. 1 a Valsalva maneuver demonstrating a robust BP and HR response. b Head-up tilt testing at 70° demonstrating an exaggerated postural tachycardia with an HR increase of 65 bpm and episodic hypertensive systolic BP surges in an oscillatory pattern in the absence of hyperventilation We report the first case, to our knowledge, of POTS developing after SARS-CoV-2 infection. Our patient developed tachycardia along with common respiratory symptoms of COVID-19 in the acute phase of her illness; however, these symptoms resolved within 3 weeks, while her tachycardia and other symptoms of autonomic impairment persisted and intensified over the following several months. Hyperadrenergic symptoms were a prominent feature in our patient, and her autonomic testing demonstrated features often reported in hyperadrenergic POTS; however, her serum NE levels returned normal, and in fact lower than typically reported in POTS, which deserves further investigation in future cases. It should also be noted that our patient’s symptoms have now persisted for 5.5 months, and some definitions of POTS require a symptom duration of at least 6 months. Infection is a well-described trigger of POTS, with 28–41% of patients reporting onset after a viral prodrome [2, 3]. In addition, autonomic dysfunction has been described in small cohorts after the 2002 SARS epidemic [4], and several other pathogens have been associated with autonomic dysfunction [5]. While an immune-mediated mechanism has been suggested, the pathophysiology remains to be elucidated. It is worth noting that our patient’s antibodies were initially positive on day 7 but were undetectable 2 months later, as reported in other patients with COVID-19. While our patient had no pre-existing symptoms of autonomic impairment, it is worth noting that her twin sister also developed similar symptoms after a similar infectious prodrome. This reinforces the importance of phenotyping to better understand vulnerability to both the severe acute manifestations and the chronic sequalae of COVID-19. Given the magnitude of the pandemic, COVID-19 represents a unique opportunity to study post-infectious autonomic syndromes, research which will hopefully lead to greater understanding of the pathogenic mechanisms of POTS. Electronic supplementary material Below is the link to the electronic supplementary material. Supplementary file1 (DOCX 16 kb)

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          The face of postural tachycardia syndrome – insights from a large cross‐sectional online community‐based survey

          Abstract Background Patients with postural tachycardia syndrome (POTS) experience chronic symptoms of orthostatic intolerance. There are minimal data detailing the demographics, clinical features and clinical course of this condition. This online, community‐based survey highlights patients’ experience with POTS. It consists of the largest sample of POTS patients reported to date. Objectives To describe the demographics, past medical history, medications, treatments and diagnostic journey for patients living with POTS. Methods Postural tachycardia syndrome patients completed an online, community‐based, cross‐sectional survey. Participants were excluded if they had not received a diagnosis of POTS from a physician. The questions focused on the patient experience and journey, rather than physiological responses. Results The final analysis included 4835 participants. POTS predominantly affects white (93%) females (94%) of childbearing age, with approximately half developing symptoms in adolescence (mode 14 years). POTS is a chronic multisystem disorder involving a broad array of symptoms, with many patients diagnosed with comorbidities in addition to POTS. POTS patients often experience lengthy delays [median (interquartile range) 24 (6–72) months] and misdiagnosis, but the diagnostic delay is improving. POTS patients can present with a myriad of symptoms most commonly including lightheadedness (99%), tachycardia (97%), presyncope (94%), headache (94%) and difficulty concentrating (94%). Conclusions These data provide important insights into the background, clinical features and diagnostic journey of patients suffering from POTS. These data should serve as an essential step for moving forward with future studies aimed at early and accurate diagnoses of these patients leading to appropriate treatments for their symptoms.
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            Postural orthostatic tachycardia syndrome: the Mayo clinic experience.

            To evaluate the prevalence and pathogenetic mechanisms of postural orthostatic tachycardia syndrome (POTS). We reviewed the medical records of patients with POTS seen at the Mayo Clinic in Rochester, Minn, from January 1, 1993, through December 31, 2003. All patients were required to have had a full autonomic reflex screen. The results of the following additional tests were evaluated: thermoregulatory sweat test, plasma catecholamine measurement, serum ganglionic (a3) acetylcholine receptor antibody detection, and 24-hour urinary sodium measurement. We identified 152 patients (86.8% female; mean +/- SD age, 30.2+/-10.3 years) with a mean duration of symptoms of 4.1 years. The mean orthostatic heart rate increment was 44 beats/min. Half the patients had sudomotor abnormalities (apparent on both the quantitative sudomotor axon reflex test and thermoregulatory sweat test), and 34.9% had significant adrenergic impairment, indicating that at least half of the patients had a neuropathic pattern of POTS. In 13.8% of patients, onset was subacute, and ganglionic acetylcholine receptor antibody was detected in 14.6%, suggesting an autoimmune origin in at least 1 in 7 patients. Hyperadrenergic status was documented in 29.0% of patients (standing plasma norepinephrine level 2600 pg/mL), and at least 28.9% were presumably hypovolemic (24-hour urinary sodium level <100 mEq/24h). The lack of correlation between urinary sodium and standing norepinephrine levels suggests that mechanisms other than hypovolemia accounted for the hyperadrenergic state. Our findings suggest a neuropathic basis for at least half the cases of POTS and that a substantial percentage of cases may be autoimmune. Hyperadrenergic and hypovolemic correlates are likely compensatory or exacerbating.
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              Infectious diseases causing autonomic dysfunction

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                Author and article information

                Contributors
                mmiglis@stanford.edu
                Journal
                Clin Auton Res
                Clin. Auton. Res
                Clinical Autonomic Research
                Springer Berlin Heidelberg (Berlin/Heidelberg )
                0959-9851
                1619-1560
                3 September 2020
                : 1-3
                Affiliations
                GRID grid.168010.e, ISNI 0000000419368956, Department of Neurology and Neurological Science, Autonomic Division, , Stanford University, ; 213 Quarry Road, Palo Alto, CA 94304 USA
                Article
                727
                10.1007/s10286-020-00727-9
                7471493
                32880754
                f2169573-6941-41ce-9fe4-d27b8c1fb004
                © Springer-Verlag GmbH Germany, part of Springer Nature 2020

                This article is made available via the PMC Open Access Subset for unrestricted research re-use and secondary analysis in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the World Health Organization (WHO) declaration of COVID-19 as a global pandemic.

                History
                : 4 August 2020
                : 28 August 2020
                Categories
                Letter to the Editor

                Medicine
                Medicine

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