new research on pots syndrome

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Large Cohort Study Finds Possible Association Between Postural Orthostatic Tachycardia Syndrome and COVID-19 Vaccination but Far Stronger Link With SARS-CoV-2 Infection

• Medical News & Perspectives As Their Numbers Grow, COVID-19 “Long Haulers” Stump Experts Rita Rubin, MA JAMA
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• JAMA Diagnostic Test Interpretation Tilt Table Testing William P. Cheshire, MD; Daniel V. Dudenkov, MD; Bala Munipalli, MD JAMA
• Original Investigation Use of Cardiopulmonary Exercise Testing to Evaluate Long COVID-19 Symptoms in Adults Matthew S. Durstenfeld, MD, MAS; Kaiwen Sun, MD; Peggy Tahir, MLIS, MA; Michael J. Peluso, MD, MHS, MPhil, DTMH; Steven G. Deeks, MD; Mandar A. Aras, MD, PhD; Donald J. Grandis, MD; Carlin S. Long, MD; Alexis Beatty, MD; Priscilla Y. Hsue, MD JAMA Network Open

Shortly after COVID-19 vaccines first became available, Tae Chung, MD, noticed something unusual at the Johns Hopkins Postural Orthostatic Tachycardia Syndrome (POTS) program, which he directs.

Seven patients newly diagnosed with POTS were either medical students or physicians. They had no recent history of SARS-CoV-2 infection, which, research has suggested, is associated with an increased risk of POTS. The autonomic disorder commonly occurs after a viral or bacterial infection and is characterized by brain fog, fatigue, and lightheadedness and increased heart rate upon standing— symptoms also seen in people with postacute sequela of COVID-19 (PASC).

Because the patients were health care workers, they were among the first to be vaccinated against the novel coronavirus, leading Chung to wonder whether POTS could be linked to COVID-19 vaccination in addition to SARS-CoV-2 infection.

Eventually, a few case reports appeared in the medical literature, from Japan , Korea , and the US , about new-onset POTS in previously healthy people who’d recently received a messenger RNA (mRNA) COVID-19 vaccine. But these were only 3 reported cases out of hundreds of millions of vaccine doses administered, far too few on which to base any conclusions.

This past December, however, a large cohort study identified a possible association between COVID-19 vaccination and POTS as well as a much stronger link between SARS-CoV-2 infection and POTS.

“I’m really excited this paper came out,” Chung, who wasn’t involved in the study, said in an interview. “It really confirms my long suspicion.”

The Need for Self Control(s)

The study, published in Nature Cardiovascular Research , analyzed electronic health records (EHR) data for outpatient encounters by nearly 285 000 individuals who’d received COVID-19 vaccines—93% of them an mRNA vaccine—at Cedars Sinai Medical Center in Los Angeles. “We were the vaccination center for a large portion of Los Angeles,” first author Alan Kwan, MD, explained in an interview.

In a summary of their study, Kwan and coauthor Susan Cheng, MD, both of the Cedars Sinai Smidt Heart Institute, acknowledged the challenges of trying to assess the relationship between COVID-19 vaccination and newly diagnosed POTS.

“This type of analysis is inherently difficult owing to the lack of ideal controls, multiple confounding factors related to the context of the pandemic and the effect of COVID-19 vaccination on patients’ engagement with the healthcare system,” they wrote.

So they took a page from pharmacoepidemiology studies in which patients serve as their own controls. Kwan and his collaborators compared patients’ odds of a POTS-related diagnosis—including POTS as well as fatigue, dysautonomia, mast cell disorders, and Ehlers-Danlos syndrome—for 90 days before vaccination with their odds during the 90 days after vaccination. And to account for the possibility of increased engagement with the health care system after vaccination, they compared the incidence of POTS-related diagnoses with the incidence of common primary care diagnoses that aren’t POTS related, such as urinary tract infections and gastroesophageal reflux disease.

The study design could be particularly useful for EHR-type cohorts in which limited data elements could impede controlling for confounders, Sean Coady, MA, a statistician in the National Heart, Lung, and Blood Institute (NHLBI) epidemiology branch, wrote in an email to JAMA . “The approach of using an individual as their own control has significant appeal” because it minimizes confounders that aren’t time-dependent, such as genetics, explained Coady, a program official for one of the study’s NHLBI grants.

A total of 4526 POTS-related diagnoses were made among the cohort members, with 2581 of them made after vaccination. This meant the odds of a POTS-related diagnosis were 33% higher after vaccination than before. In comparison, the odds of a diagnosis not related to POTS were 21% higher after vaccination than before.

After vaccination, the odds of a POTS-related diagnosis were 10% higher than the odds of a diagnosis not related to POTS. The authors noted that only 25 new cases of myocarditis, the best-characterized COVID-19 vaccine adverse event, occurred in the cohort, 7 before vaccination and 18 after.

The researchers also conducted a separate analysis of 12 460 patients with confirmed SARS-CoV-2 infection, none of whom had received a COVID-19 vaccine within 90 days before or after their diagnosis. A total of 1004 POTS-related diagnoses were made in this group, 605 of them after having COVID-19, making the odds of a POTS-related diagnosis after SARS-CoV-2 infection more than 5 times greater than after COVID-19 vaccination, the authors reported.

Given that POTS is known to be one of the PASC syndromes, it is biologically plausible “for a similar, even if attenuated, systemic response to vaccine,” Kwan and his coauthors wrote.

Interestingly, Kwan noted, although POTS in general is much more common among women, his study found the incidence to be similar in women and men. He said it’s unclear whether POTS associated with COVID-19 vaccination or SARS-CoV-2 infection is different from other POTS cases.

The study “is of major importance to POTS research and patient care,” neurologist Svetlana Blitshteyn, MD, a clinical associate professor at the University of Buffalo’s Jacobs School of Medicine and Biomedical Sciences, and Karolinska Institute cardiologist Artur Fedorowski, MD, PhD, wrote in an accompanying editorial . “[I]t undeniably establishes POTS and dysautonomia in general as adverse events after vaccination that should be recognized and investigated as other well-accepted post-vaccination syndromes.”

An Overestimation?

Kwan is the first to acknowledge that his study isn’t the final word on a possible relationship between COVID-19 vaccination and POTS. “I hope that this research spurs more research,” he emphasized.

In an email to JAMA , Jesse Goodman, MD, MPH, called Kwan’s article “provocative” but not conclusive. Using 90 days pre-vaccination as the control period, “while a valid approach, cannot, as the authors noted, eliminate confounding by unmeasured factors,” wrote Goodman, director of Georgetown University’s Center on Medical Product Access, Safety and Stewardship. “For example, if people tend to delay vaccination if they don’t feel well, that might make pre-vaccine period rates of any diagnoses, including POTS, artificially low, and, in comparison, make post-vaccine rates appear elevated.”

Goodman, an infectious disease specialist who formerly served as chief scientist at the US Food and Drug Administration, noted that the incidence of most diagnoses measured—not just those related to POTS—occurred more frequently after vaccination than before, further evidence, perhaps, that people who are unwell might postpone getting vaccinated until they feel better.

“Also, the overall rates of POTS seem high, even in the pre-vaccine or pre-COVID [infection] groups, when compared to what is in the literature,” Goodman noted. If the COVID-19 vaccines led to an excess of around 90 cases of POTS-related diagnoses per 100 000 individuals, as reported by Kwan’s team, “we might have expected to see a signal in the original controlled trials of [around] 15 000 to 20 000 or in post-authorization safety databases.” The evidence that SARS-CoV-2 infection causes POTS seems stronger, Goodman added.

Considering that the cohort’s average age was 52 years and that more than half its members were women, the overall rate of myocarditis also seemed high, Robert Bonow, MD, said in an interview. Myocarditis is seen most commonly in young men, explained Bonow, a cardiologist at the Northwestern Feinberg School of Medicine and editor of JAMA Cardiology .

Coady called the “fairly substantial” POTS-related incidence rate both before and after vaccination “somewhat surprising.” “[I]ndividuals may become more cognizant of certain symptoms of dysautonomia of the nervous system post-vaccination…given the relatively new vaccine, conflicting media reports, etc.,” he speculated. “Replication in other populations using a different study design, if possible, would be useful to confirm findings.”

A more precise approach to identify new POTS cases after vaccination would be to perform a diagnostic test for the condition before vaccination and then several weeks afterward, Coady said. One such test measures blood pressure and heart rate while lying down and then while standing for 10 minutes. A heart rate increase of at least 30 beats per minute, coupled with a drop in blood pressure of no more than 20 mm Hg, is characteristic of POTS.

The authors of the accompanying editorial pointed out that traditional POTS diagnostic criteria require that symptoms last at least 3 months—the same length of time assessed in Kwan’s study. That suggests that some of the people diagnosed with POTS or related diagnoses in the 90 days following vaccination might have been misdiagnosed and recovered later, leading to an overestimation of cases. However, Kwan explained, with a longer assessment period, the connection between vaccination and POTS would become hazier.

To assess the validity of their approach, he and his coauthors clinically adjudicated 50 sequentially encountered patients identified as having both unspecified cardiac arrythmia and unspecified disorder of the autonomic nervous system. They found that 40 of those patients (80%) either had been formally confirmed as having POTS through comprehensive diagnostic testing or had signs and symptoms consistent with guideline definitions of the condition but were still awaiting full diagnostic testing for confirmation. Notwithstanding those “acceptable results,” Kwan and his coauthors wrote, “we recognize that our analyses of EHR data are intrinsically subject to non-differential misclassification that generally tends to bias results toward the null.”

The editorialists noted that the reliability of POTS incidence data depends on awareness and diagnostic vigilance of the condition. Many patients with POTS experience lengthy delays in obtaining a diagnosis, research has found. “I think POTS is one of the conditions that’s been so misunderstood by a lot of doctors,” in part because it predominantly affects young women, Chung said. However, he added, “the COVID pandemic has definitely brought increased awareness” of POTS.

Responsible Messaging

Kwan said he worried that his findings might be exploited by people spreading vaccine disinformation. “I’d say we were concerned about responsible messaging,” he noted.

But the main feedback he’s received has been from patients who finally felt seen and heard, he said. They had developed POTS symptoms after COVID-19 vaccination but weren’t taken seriously when they suggested the 2 might be connected.

In medicine, “sometimes you make the correct choice, but bad things still happen,” Kwan said. “Good physicians have to be able to navigate that.”

As Chung pointed out, some people have developed Guillain-Barré syndrome (GBS), a rare neurological disorder, after receiving a flu shot, but research suggests that the odds of GBS are greater after an influenza infection.

Like flu vaccines, COVID-19 vaccines have protected countless individuals from sickness and death, so Chung said, “even if I thought there was maybe a causal relationship [with POTS], I’m not going to say don’t get the vaccine.”

Published Online: January 25, 2023. doi:10.1001/jama.2023.0050

Conflict of Interest Disclosures: None reported.

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Rubin R. Large Cohort Study Finds Possible Association Between Postural Orthostatic Tachycardia Syndrome and COVID-19 Vaccination but Far Stronger Link With SARS-CoV-2 Infection. JAMA. 2023;329(6):454–456. doi:10.1001/jama.2023.0050

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Mayo Clinic Study Identifies POTS Treatments

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A Mayo Clinic study  published this month in  Pacing and Electrophysiology  (PACE) , suggests that a class of medications more commonly prescribed for older adults is a strong first-line treatment for teenagers with a debilitating condition called postural orthostatic tachycardia syndrome, or POTS.

Phil Fischer, M.D., medical director of Mayo Clinic's children's hospital and a POTS specialist, led the retrospective study of teenagers diagnosed with POTS at Mayo Clinic. The patients were surveyed approximately a year after their diagnosis, and while over half of those taking midodrine reported improvement in symptoms, all of those taking β-blockers had felt improvement.

Dr. Fischer provides an overview of POTS, the study results and their implications for treatment of future patients with POTS:

"This is a small study, but it is an important step because POTS is not well understood even within the medical community," Dr. Fischer explains. "POTS is a real syndrome in which the patient's heart rate accelerates abnormally when moving from lying down to standing up, and it causes a whole cascade of symptoms from fatigue to stomach upset that are often mistaken for depression. This study points to the important role medications can play, in conjunction with other changes, to help these mostly high-achieving young people get their lives back."

A more extensive interview with Dr. Fischer providing more background on  POTS  is available on the  Mayo Clinic Podcast Blog .

As you can see from the  extensive comments  in response to the POTS podcast, there would be no shortage of patients to possibly include in a news story about this study. Another interesting angle is that the brother of the patient featured in the 2006  Mayo Clinic Medical Edge  TV story raised the funds to pay for the statistical analysis required for the study on medication effectiveness being reported this month in PACE.

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Research Summary: Postural orthostatic tachycardia syndrome (POTS) and migraine: A narrative review

Summarized by Nina Riggins, MD, PhD, FAHS

Patients with postural orthostatic tachycardia syndrome (POTS) commonly experience migraine as a comorbidity. By understanding the underlying mechanisms that may link POTS and migraine, primary care practitioners can find targeted treatments that significantly improve their patients’ quality of life. A recent study reveals three major subtypes of POTS and the pathophysiologic functions that are present in both POTS and migraine.

This month, the First Contact – Headache in Primary Care team summarized Postural orthostatic tachycardia syndrome and migraine: A narrative review .

Study Overview

• Postural orthostatic tachycardia syndrome (POTS) is the most common disorder of the autonomic nervous system.
• Narrative literature review was performed to summarize experimental and clinical evidence demonstrating mechanistic connections between POTS and migraine.
• POTS refers to a positional symptomatic tachycardia, defined by an increase in heart rate of at least 30 beats per minute on assuming an upright position, in the absence of orthostatic hypotension.
• Migraine is the most common comorbidity in patients with POTS.

Study Methods

• PubMed and Medline databases were utilized to perform a literature review and searched for the following keywords: “postural orthostatic tachycardia syndrome,” “POTS,” “autonomic nervous system,” “migraine,” “headache.”
• Articles in English, addressing pathophysiology, treatment, clinical trials, and observational studies, were included and analyzed.

Study Results

• The high prevalence of migraine in patients with POTS may be explained by common pathophysiologic mechanisms, with evidence of dysregulation of the sympathetic nervous system, hemodynamics, and central sensitization, in both POTS and migraine.
•  Three major POTS subtypes exist: 1) neuropathic (~ 50% of cases), 2) hypovolemic (~30 %), and 3) hyperadrenergic (~25-50 %).
• Data on neuropathic POTS suggests that partial sympathetic denervation, compensatory hypersensitivity of α-adrenergic receptors, and a vagal neuropathy may contribute to POTS.
• The loss of vagus nerve activity is associated with an increase in pro-inflammatory cytokines and could be reflected in increased prevalence of gastrointestinal symptoms and headache.
• There is evidence that the renin–angiotensin–aldosterone system is dysregulated in hypovolemic POTS. A reduction in intravascular volume leads to a reduction in blood pressure, which is sensed by baroreceptors and leads to an increase in heart rate and blood vessel constriction to maintain blood pressure.
• Hyperadrenergic POTS is characterized by an exaggerated sympathetic response to standing.
• Activation of brain regions involved in regulation of the autonomic nervous system, pain perception, and central sensitization has been demonstrated in patients with POTS and migraine.
• Treatments include cardiovascular exercise and hydration to increase plasma volume.
• Application of external compression and physical maneuvers (e.g., leg crossing, lower extremity muscle squeezing) can be useful.
• There are pharmacologic treatments such as midodrine, the role of which is not established in migraine. Treatments such as beta blockers could be helpful for patients living with migraine and POTS.
• Several small observational studies suggest non-invasive vagus nerve stimulation (nVNS) may decrease orthostatic tachycardia in patients with POTS.
• Migraine treatments that decrease peripheral and central sensitization, including onabotulinumtoxinA and calcitonin-gene-related peptide antagonists, may improve POTS symptoms, but this has not been studied.

Implications for Primary Care Clinicians

• This study shows that the high prevalence of migraine in patients with POTS may be explained by common pathologic mechanisms.

Understanding of shared pathophysiology may provide critical insight into the development of individualized treatment strategies for patients with POTS and migraine.

This summary is part of the First Contact — Headache in Primary Care initiative, an American Headache Society program that provides educational resources to empower healthcare professionals and improve headache and migraine care. We encourage providers in all stages of their careers to   visit our homepage to access educational tools to improve patient care .

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Clinic for Postural Orthostatic Tachycardia Syndrome Expands

March 8, 2019

Patients who have postural orthostatic tachycardia syndrome (POTS) face extraordinary challenges. Not only is their condition often misdiagnosed, but once individuals receive a POTS diagnosis, they often struggle to find follow-up care and treatment. The POTS clinic at Johns Hopkins — one of the few centers in the U.S. dedicated to POTS — is expanding to address these challenges. Pegah Dehghan , a physiatrist specializing in neuromuscular conditions including POTS and muscular dystrophy, joined the Johns Hopkins POTS clinic in 2018.

Dehghan brings a wealth of expertise to her role, in clinical medicine as well as clinical research. Currently, she says, a major stumbling block in the POTS field is that the biological basis of the condition is not well-characterized, slowing the search for new treatments. What is known is that POTS causes the heart rate to soar upon standing due to poorly understood defects in the autonomic nervous system. It is estimated that as many as 3 million people in the U.S. grapple with POTS.

But there are reasons for optimism for patients with POTS, says Dehghan.

Laboratory research is underway to uncover the root causes of POTS, which should propel translational studies that can suggest new treatment strategies. And as the POTS clinic at Johns Hopkins continues to move forward, Dehghan hopes to engage in clinical studies that will help evaluate potential new POTS treatments. “We have an extraordinary opportunity at Hopkins to help push the frontiers of clinical knowledge and treatment for POTS. I’m hopeful for what lies ahead.”

Neuromuscular medicine specialist  Tae Chung , who leads the POTS clinic, says that helping patients get the treatment they need is a top priority. “Not only are we highly focused on treatment, but we work across multiple clinical specialties, including GI, cardiology, neurology, as well as physical medicine and rehabilitation,” he says. “We have a very comprehensive and multidisciplinary program.”

While research pushes forward to identify the cause of POTS, Deghan and Chung continue to leverage state-of-the-art approaches to POTS treatment. That includes a variety of pharmacological approaches as well as physical therapy, which can be a vital tool for building strength and enabling patients to return to their daily routines. It also provides an objective metric to help monitor patients’ progress.

Dehghan says she finds caring for POTS patients incredibly fulfilling. “This is a group of patients who are often misdiagnosed or have been dealing with their condition for a long time without clear answers,” she says. “The fact that we can meet with these patients and help them is very rewarding.”

Published in Restore Spring 2019

Watch This:

Tae Chung of the Johns Hopkins Rehabilitation Network discusses  Postural Orthostatic Tachycardia Syndrome (POTS): Treatment and Rehabilitation Options .

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Postural Tachycardia Syndrome (POTS)

What is p ostural orthostatic tachycardia syndrome (pots) .

Postural orthostatic tachycardia syndrome (POTS) is one of a group of disorders that have orthostatic intolerance (OI) as their primary symptom.  OI is a condition in which an excessively reduced volume of blood returns to the heart after an individual stands up from a lying down position. The primary symptom of OI is lightheadedness or fainting.

In POTS, the lightheadedness or fainting is also accompanied by a rapid increase in heartbeat of more than 30 beats per minute, or a heart rate that exceeds 120 beats per minute, within 10 minutes of rising. The faintness or lightheadedness of POTS is relieved by lying down again.

Anyone at any age can develop POTS, but it mainly affects women between the ages of 15 to 50 years of age. Some women report an increase in episodes of POTS right before their menstrual periods. POTS often begins after a pregnancy, major surgery, trauma, or a viral illness. It may make individuals unable to exercise because the activity brings on fainting spells or dizziness.

Some people with Ehler-Danlos syndrome type III (also called hypermobile Ehlers–Danlos syndrome, or hEDS), an inherited connective tissue disorder that is caused by defects in a protein called collagen, may also be diagnosed with POTS.

The cause of the disorder is unknown. Treatment is targeted at relieving low blood volume or regulating circulatory problems that may cause the disorder. A number of drugs seem to be effective in the short term. Whether they help in long term is uncertain.

Simple interventions such as adding extra salt to the diet and attention to adequate fluid intake are often effective.

The drugs fludrocortisone (for those on a high salt diet) and midodrine in low doses are often used to increase blood volume and narrow blood vessels. Drinking 16 ounces of water (two glasses) before getting up can also help raise blood pressure. Some individuals are helped by beta receptor blocking agents. There is some evidence that an exercise program can gradually improve orthostatic tolerance.

POTS may follow a relapsing-remitting course, in which symptoms come and go, for years. In most cases, an individual with POTS improves to some degree and becomes functional, although some residual symptoms are common.

How can I or my loved one help improve care for people with postural tachycardia syndrome (POTS)?

Consider participating in a clinical trial so clinicians and scientists can learn more about POTS and related disorders. Clinical research uses human volunteers to help researchers learn more about a disorder and perhaps find better ways to safely detect, treat, or prevent disease.

All types of volunteers are needed— those who are healthy or may have an illness or disease— of all different ages, sexes, races, and ethnicities to ensure that study results apply to as many people as possible, and that treatments will be safe and effective for everyone who will use them.

For information about participating in clinical research visit NIH Clinical Research Trials and You . Learn about clinical trials currently looking for people with POTS at Clinicaltrials.gov .

Where can I find more information about postural tachycardia syndrome (POTS)? Information may be available from the following resources: Dysautonomia International Dysautonomia Youth Network of America, Inc. Phone: 301-705-6995 National Dysautonomia Research Foundation Phone: 651-327-0367  

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Recognizing POTS

Learn to Spot This Mysterious Condition

A condition called POTS can have a huge impact on a person’s life. People with POTS often feel lightheaded or dizzy when standing up from a lying position. Their heart tends to race. They may even faint. Other symptoms can include extreme fatigue, shortness of breath, and trouble thinking.

“POTS can be quite debilitating. It can make it hard to do everyday activities, like attending work or school,” says Dr. Cheryl L. McDonald, who helps oversee NIH’s POTS research programs. “Some people even require the use of a wheelchair because they can’t stand or walk for long periods.”

POTS is an abbreviation for Postural Orthostatic Tachycardia Syndrome. Postural means it’s linked to your body’s position. Orthostatic is related to standing. Tachycardia means rapid heart rate. And syndrome means it’s a group of symptoms. (See the Wise Choices box.)

Normally, when a person stands up, gravity pulls blood down toward the legs and feet. This briefly reduces blood flow to the upper body, including the heart and brain. So the brain immediately sends signals that tighten the body’s lower blood vessels and make the heart pump faster. This pushes blood upward, so it can travel throughout the body.

But for people with POTS, these signals break down. The lower blood vessels don’t tighten enough upon standing, and the heart beats much faster than it should. The brain and other organs may not get enough blood, which can lead to fainting and other symptoms.

POTS can affect anyone at any age. It is most common among women, ages 15 to 50. Its causes are unknown. Researchers suspect there can be different causes, and each might require different treatments. Some data suggest that POTS may arise after major surgery, head injury, pregnancy, or viral illness.

POTS can be diagnosed by looking at your symptoms, heart rate, and blood pressure when you go from lying down to standing. Adults might have POTS if their heart rate rises by more than 30 beats a minute within 10 minutes of standing, without a big blood pressure change. For those under age 20, an increase of at least 40 beats a minute without a major blood pressure change could signal POTS. Symptoms may quickly improve by lying down.

Treatment often involves increasing salt intake and drinking plenty of water, which can boost blood volume. Blood volume is the total amount of fluid circulating around your body. Some patients benefit from medications that help to raise blood pressure or reduce heart rate. Compression socks can help keep blood from pooling in the legs. Exercise training and maintaining a regular sleep schedule may also help.

Many people—even some health care providers—have never heard of POTS. “But awareness has increased in recent years, particularly since POTS has been seen in patients who have had COVID-19,” McDonald says. The links between POTS and COVID-19 are still unclear, and researchers are working to learn more.

Despite increased awareness of POTS, it can be hard for some patients to get a diagnosis. “If you have symptoms that look like they could fit with POTS, it’s a good idea to discuss the possibility with your doctor,” McDonald says. “It’s perfectly acceptable to be your own advocate. You can show an article to your doctor and ask: Do you think I might have POTS?”

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Clinical Trials

Postural orthostatic tachycardia syndrome.

Displaying 15 studies

The aims of this study will be to measure changes in postural orthostatic tachycardia syndrome (POTS) symptoms, functional disability and catastrophizing subsequent to patients’ participating in the 2-day Pediatric Pain Rehabilitation Program.

The purpose of this research study is to better understand what causes POTS. We believe that a number of different causes of POTS exist and that detailed testing can demonstrate the different causes. Knowing what causes POTS in a particular patient will be helpful in choosing the right treatment strategy for that particular patient in the future.

This study is designed to investigate whether the treatment of non-anemic iron deficiency with intervenous iron sucrose will result in decreased symptom reporting and improved cardiovascular indices in adolescents (age 12-18) with Postural Orthostatic Tachycardia Syndrome (POTS).

The purpose of this study is to test the feasibility of using a novel wearable biosensor and mobile health monitoring platform to capture patients’ physiology, functional capacity and assessment of symptoms, thereby building a profile of Positional Orthostatic Tachycardia Syndrome (POTS) while excluding more serious cardiac, neurological and endocrine causes for their symptomatology. We hypothesize that as a non-fatal condition, a complete physiological profile of the POTS patients can be built entirely remotely therefore avoiding the need for these patients to visit the hospital and clinic.

The study aims to evaluate if a hybrid semi-supervised remote monitoring three month strength and aerobic exercise training program can be as efficacious as in-person exercise training has previously demonstrated. 

The purpose of this study is to evaluate if the patient/participant will self-enter clinical survey information into an iPad or choose to enter the same information by paper and pen for use in clinical research.

The goal of this study is to gain a better understanding of the sleep and fatigue complaints of adolescent POTS patients by objectively measuring sleep with actigraphy prior to and after attending the Pain Rehabilitation Center (PRC) 3 week program. A questionnaire will be administered to assess subjective sleep complaints and correlate them with objective findings.

The purpose of this study is to assess the hydration status via body impedance of patients suffering from postural orthostatic tachycardia syndrome.

This is a 3-day study comparing pyridostigmine versus placebo in the treatment of postural tachycardia syndrome (POTS). The researchers expect pyridostigmine to improve tachycardia and stabilize blood pressure.

This study aims to investigate whether the treatment of non-anemic iron deficiency with intravenous iron sucrose will result in decreased symptom reporting and improved cardiovascular indices in patients with Postural Orthostatic Tachycardia syndrome (POTS).

The purpose of this study is to gather information about symptoms of autonomic dysfunction, depressive and anxiety symptoms, health behaviors, social support, and ability to do everyday tasks.

If the efficacy of 3,4-diaminopyridine (3,4-DAP) can be demonstrated in this study, the use of 3,4-DAP alone and in combination with other agents such as pyridostigmine and L-DOPS would be further evaluated in a double-blind randomized placebo-controlled cross-over study

The purpose of this study is to gain a better understanding of the sleep quality and fatigue complaints of adolescent orthostatic intolerance (OI) and postural orthostatic tachycardia syndrome (POTS) patients by objectively measuring sleep duration and timing with actigraphy. Sleep questionnaire will be administered to assess subjective sleep complaints and correlate them with objective findings.

The purposes of this study are to compare the functional connectivity in adolescent patients with Postural Orthostatic Tachycardia Syndrome (POTS) both with and without chronic pain, to those with chronic pain alone, to that of healthy controls; to evaluate whether there is a change in functional connectivity following participation in an intensive rehabilitation-oriented program previously demonstrated to have excellent outcomes with regard to functional recovery and symptom control; and to correlate outcomes using standardized symptom and function rating scales to imaging findings.

The aim of this study is to examine the role of mast cell mediators in children with allergic disorders in a two part study. Part 1 of the study will prospectively obtain the values of mast cell mediators, including 2,3 dinor 11β-PGF2α, n-MH, and LTE4 in the urine of a healthy pediatric reference population. Part 2 of the study will prospectively evaluate the urine concentrations of mast cell mediators in a cohort of pediatric allergic disorder patients including asthma, allergic rhinoconjunctivitis, eczema, urticaria, systemic anaphylaxis, and mast cell disorders, as well as POTS (postural orthostatic tachycardia syndrome). Comparisons of these ...

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• News & Views
• Published: 12 December 2022

The risks of POTS after COVID-19 vaccination and SARS-CoV-2 infection: more studies are needed

• Svetlana Blitshteyn   ORCID: orcid.org/0000-0002-3982-2031 1 , 2 &
• Artur Fedorowski 3  

Nature Cardiovascular Research volume  1 ,  pages 1119–1120 ( 2022 ) Cite this article

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This article has been updated

Postural orthostatic tachycardia syndrome (POTS) can follow COVID-19 as part of the post-acute sequelae of SARS-CoV-2 infection, but it can also develop after COVID-19 vaccination, although at a lower frequency.

Vaccines represent one of the most groundbreaking scientific advances that substantially reduced the mortality and morbidity associated with various infectious pathogens. Since the introduction of COVID-19 vaccines in the USA in December 2020, vaccination against SARS-CoV-2 has remained the most effective and influential global public health strategy to mitigate the pandemic. However, reports of post-vaccination adverse events involving various cardiovascular and neurological manifestations, including POTS, have been mounting in the Vaccine Adverse Event Reporting System 1 .

POTS, a common disorder of the autonomic nervous system, is characterized by an increase in heart rate of at least 30 beats per minute within 10 minutes of standing and symptoms of orthostatic intolerance, such as pre-syncope, palpitations, light-headedness, generalized weakness, headache and nausea, with symptom duration exceeding three months 2 . In the USA, the pre-pandemic prevalence of POTS has been estimated to be in the range of 500,000–3,000,000 people, affecting predominantly women of reproductive age and roughly 1 in 100 teenagers 3 . However, current prevalence is likely significantly higher owing to post-COVID-19 POTS, which can develop as part of the post-acute sequelae of SARS-CoV-2 infection (PASC) 4 , 5 .

New-onset POTS can also follow vaccination (Fig. 1 ) and was reported in the literature after immunization with Gardasil, a human papillomavirus (HPV) vaccine, in 2010 and, more recently, after the administration of COVID-19 vaccines 6 , 7 , 8 . However, a causative relationship between HPV vaccines and increased incidence of POTS has not been thoroughly investigated. This is despite several case series reported from different countries and two studies that demonstrated an increased signal for POTS and its associated symptom clusters following HPV vaccination, based on data from the World Health Organization’s pharmacovigilance database and a meta-analysis of clinical study reports from 24 clinical trials 9 , 10 , 11 .

Data taken from Kwan et al. 12 and Shaw et al. 6 .

In a study published in this issue of Nature Cardiovascular Research , Kwan et al. examined the frequency of new POTS-associated diagnoses — POTS, dysautonomia, fatigue, mast cell disorders and Ehlers–Danlos syndrome — before and after COVID-19-vaccination 12 . They found that the odds of POTS and associated diagnoses were higher in the 90 days after vaccine exposure than the 90 days before exposure, with a relative risk increase of 33% 12 . Furthermore, the authors showed that the odds of new POTS-associated diagnoses following natural SARS-CoV-2 infection were higher than pre-infection with an increased risk rate of 52%.

The study is based on a large series of approximately 300,000 vaccinated individuals from one geographic territory in the USA (Los Angeles County), with 0.27% new post-vaccination POTS diagnoses compared with 0.18% in the pre-vaccination period, giving an odds ratio of 1.52 for post-vaccination POTS diagnoses 12 . Accumulating all POTS-associated diagnoses in one group gave slightly lower odds. Interestingly, among 12,460 individuals with confirmed SARS-CoV-2 infection, the pre-infection incidence of POTS was 1.73%, compared with 3.42% after infection. This suggests that those with symptomatic COVID-19 infection were more likely to develop POTS in general, and that the risk of post-infection POTS is higher than post-vaccination POTS in this cohort 12 .

The study has some limitations. First, the accuracy of POTS and POTS-associated diagnoses is crucial for study validity. Second, the general awareness and diagnostic vigilance of POTS and access to adequate diagnostic modalities are decisive for POTS incidence reliability. Third, the generalizability of this report is limited to a specific population. Moreover, the traditional POTS diagnostic criteria require symptoms to occur over a duration of at least 3 months — that is, at least 90 days — which is the assessed period. As such, some of the affected individuals may have recovered later. We therefore cannot exclude the possibility that the incidence of POTS and POTS-associated diagnoses was overestimated.

Despite these limitations, the study by Kwan et al. 12 is of major importance to POTS research and patient care for several reasons. First, it undeniably establishes POTS and dysautonomia in general as adverse events after vaccination that should be recognized and investigated as other well-accepted post-vaccination syndromes, such as Guillain–Barre syndrome and acute disseminated encephalomyelitis. Second, it clearly demonstrates that POTS and POTS-associated comorbidities occur more frequently after COVID vaccination than before, and much more frequently than myocarditis, which, despite increasing at a higher rate after vaccination, remains a rare post-vaccination complication. Consequently, POTS and POTS-associated conditions may be among the most common adverse events after COVID-19 vaccination. Third, it reaffirms that POTS occurs at a high rate after SARS-CoV-2 infection and is likely one of the major phenotypes of PASC. Fourth, the rate of new POTS diagnoses made after natural SARS-CoV-2 infection was higher than after COVID-19 vaccination, although a direct comparison is not possible at this stage, given the intrinsic differences in POTS incidence at baseline in the two cohorts. The last point is particularly poignant and clinically relevant, as it provides compelling evidence that can be referenced during physician–patient encounters in support of vaccination and against vaccine hesitancy.

We hope that large prospective studies utilizing the new ICD-10 diagnostic code specific for POTS, which has been implemented by the US Center for Disease Control and Prevention committee as of October 1, 2022, can be conducted in the future. Similarly, mechanistic studies investigating POTS following SARS-CoV-2 infection and COVID-19 vaccination are needed to determine causation and delineate the underlying immune-mediated mechanism, possibly involving the spike protein and/or formation of autoantibodies to G-protein-coupled receptors and other targets in the cardiovascular system and beyond 13 . Furthermore, developing a screening pathway with genetic testing to identify at-risk individuals with a genetic predisposition toward post-vaccination adverse events is necessary, and would lead to a reduction in serious post-vaccination adverse events and promote public trust and vaccination compliance.

As we continue to navigate and mitigate the SARS-CoV-2 pandemic and long-term post-COVID-19 complications with the help of COVID-19 vaccines, the need to invest in POTS research to advance our understanding, diagnosis and management of POTS — a common sequela of both SARS-CoV-2 infection and COVID-19 vaccination — has never been more pressing.

Change history

11 september 2023.

Since publication of this News & Views, the source article it discusses (Kwan et al., https://doi.org/10.1038/s44161-022-00177-8 (2022)) has been updated to clarify that a fully-adjusted comparison of odds of POTS attributable to vaccination versus infection is not possible within the study design, given the two mutually exclusive populations, leading to changes in this article’s title, and descriptions of POTS risk in the abstract, fourth and seventh paragraphs. The changes are made in the HTML and PDF versions of the article.

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Blitshteyn, S., Fedorowski, A. The risks of POTS after COVID-19 vaccination and SARS-CoV-2 infection: more studies are needed. Nat Cardiovasc Res 1 , 1119–1120 (2022). https://doi.org/10.1038/s44161-022-00180-z

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Cardiovascular autonomic dysfunction in post-covid-19 syndrome: a major health-care burden.

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Author Correction: Apparent risks of postural orthostatic tachycardia syndrome diagnoses after COVID-19 vaccination and SARS-Cov-2 Infection

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Nature Cardiovascular Research (2023)

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People have been searching for POTS diagnoses and treatment for decades. The COVID-19 pandemic is bringing them hope

Postural Orthostatic Tachycardia Syndrome, or POTS, is a chronic illness impacting the nervous system that debilitates many around the Northwoods.

Research and interest in the condition has expanded as a result of the COVID-19 pandemic.

WXPR spoke with a resident of Minocqua about her experiences trying to find the right care.

Jody's Story:

Jody Bognar and her daughter both love tennis.

Her daughter is 24 now, but back in high school, she qualified for state.

“I used to try and play with her. And I got to the point where, you know, I couldn't even play for 10 minutes, and I was done. You know, I spent my daughter's whole, well, basically her whole life, I've been sick, she has never known me as a healthy person, I've never known myself, as a healthy mom,” said Bognar.

Bognar was diagnosed with POTS, Postural Orthostatic Tachycardia Syndrome, back in 2001.

She’s been dealing with debilitating symptoms from POTS and Chronic Fatigue Syndrome for over 20 years.

Bognar regularly experiences an exaggerated increase in heart rate when standing, lightheadedness, difficulty thinking, exercise intolerance, headaches, a tremor, nausea, and more.

Her daughter, Allison, said that it took years for her to start to fully understand her mom’s illness.

“When I was, like, a lot younger, she kind of tried to hide it and stuff just trying to keep up with me as a kid,” she remembered.

Within the past few years, Bognar and her daughter have had more open and honest conversations about how she’s impacted day to day.

“It's a very, I guess, invisible illness, I'd say. Like, just anybody walking on the street necessarily wouldn't be able to tell how debilitating it is for her,” said Allison.

Rural Healthcare:

On top of dealing with debilitating symptoms, people with POTS report significant difficulty locating knowledgeable providers, particularly in rural areas.

Dr. Satish Raj is a Canadian Heart Rhythm Specialist and Professor at the University of Calgary, as well as Director of Education at the Libin Cardiovascular Institute.

“The bigger fundamental problem is that we don't have great treatments. We need more research into it. We need a better understanding of what's going on. We need to develop better treatments. And then we need to make sure that those can be accessed by patients equitably in rural areas,” said Dr. Raj.

Shannon Koplitz is the Treasurer of Dysautonomia International, an advocacy organization.

She says that more than half of POTS patients travel more than 100 miles from home to receive ongoing care.

“Dysautonomia symptoms can be completely debilitating to the point where the patients are homebound and or bedridden. And so traveling 100+ miles is not only physically exhausting, it's mentally exhausting on them as well,” said Koplitz.

Patients are often reliant on their caregivers and families for support.

“My mom would drive me four and a half hours each way to Mayo Clinic with me laying down in the backseat, I was so sick,” said Koplitz.

At some point, Koplitz said that many patients stop seeking treatment because the obstacles are just too great.

“Why should I go travel 600 miles to a facility I've never been to? How do I know that they're going to be able to help me? You know, that may be a huge waste of my time and energy and money and resources,” she explained.

The Impacts of the Pandemic:

There is some hope that this may be changing- in part due to the COVID-19 pandemic.

“For the Dysautonomia community, it actually was in some ways a blessing because it raised awareness. And it's helping millions around the country obtain the diagnosis that they've been searching for,” explained Koplitz.

A 2023 study found that a significant percentage of COVID-19 survivors develop POTS within six to eight months of infection.

“I'm not glad that there's people having these problems. But I'm glad that at least now, if it takes COVID and takes long COVID illnesses and people to bring about more awareness, you know, I'm glad for that, because it'll help us all hopefully,” said Bognar.

She hopes that research into POTS in long COVID patients will benefit the larger community.

“There's always the chance of in the next years or decades or some kind of, you know, cure or even better management maybe through more awareness,” she said.

Bognar struggles to imagine her future with POTS, but she holds on for her family and loved ones.

“There's times that I think I don't think I can live with this for another 30 years, if I live as long as my mother was 89, 90, that'll be 30 more years. And sometimes I don't know, if I'm gonna make it through the night, I had such a bad night or whatever. But there's times I'm like, you just have to hang on, because who knows what's on the horizon?” she said.

Most of the time, she’s in survival mode, just existing, but on those rare days when she feels like she’s really living, she’s reminded of why she fights.

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POTS, a debilitating heart condition, is linked to Covid and, to a lesser degree, vaccines

Research published Monday has confirmed a link between a Covid infection and a debilitating heart condition called POTS, or postural orthostatic tachycardia syndrome, that has been diagnosed in some patients with long Covid.

The findings, published in the journal Nature Cardiovascular Research , are in line with earlier reports from physicians that Covid may trigger POTS, a disorder of the autonomic nervous system often characterized by a rapid heart rate, low blood pressure, fainting and lightheadedness.

Physicians often fail to recognize the condition, experts say, because it can be confused with a myriad of other health problems, including anxiety and dehydration. Many patients spend years trying to get properly diagnosed.

One of the earlier discoveries with long Covid was that it could be associated with POTS and this new research builds on that, said lead study author Dr. Alan Kwan, a cardiologist at Cedars-Sinai Medical Center.

POTS was also linked, to a lesser degree, to Covid vaccination with an mRNA vaccine, according to the new study.

Researchers analyzed data on nearly 300,000 patients from the Cedars-Sinai Health System in Los Angeles County from 2020 to 2022 who had either received at least one dose of a Covid vaccine or had a confirmed case of Covid. The vast majority of the vaccinated people in the study got an mRNA vaccine — either from Pfizer-BioNTech or Moderna. People with a confirmed case of Covid had not been vaccinated.

While the researchers found a small but increased risk of POTS following Covid vaccination and, in particular, the first dose, the risk was greater following a Covid infection itself: Getting Covid was linked to a five times greater risk of POTS than vaccination.

“The main message here is that while we see a potential link between Covid-19 vaccination and POTS, preventing Covid-19 through vaccination is still the best way to reduce your risk of developing POTS,” Kwan said.

He added the study has limitations, including that the results were based on patient data from a single health system. He also said that the link between POTS and Covid vaccination needs to be confirmed with further studies.

It’s unclear why the Covid vaccines would trigger the condition, Kwan said, but added that it could be related to the immune response generated by the shots.

Dr. Ofer Levy, the director of the Precision Vaccines Program at Boston Children’s Hospital, agreed.

He noted that Pfizer’s and Moderna’s vaccines have been linked to a small risk of myocarditis. That condition, he said, may also be related to the immune response generated by the shots. Still, the myocarditis risk is significantly higher after a Covid infection than after vaccination.

Researchers should further explore the immune response to shots, because “the better we understand how the adverse events work, the smarter we can become in designing better vaccines in the future,” Levy said.

Other vaccines have also been linked to POTS in early accounts, but further research did not establish a causal link.

The HPV vaccine Gardasil, for example, was thought to cause POTS based on early reports, but subsequent reviews found that not to be the case, said Dr. William Schaffner, an infectious diseases expert at Vanderbilt University Medical Center, who was not involved with the new research.

The link between an infection — including Covid — and POTS, however, is more well-established.

"Many conditions can trigger POTS, including viral infections such as SARS-CoV-2, the virus that causes Covid-19," Dr. Bala Munipalli, a physician who heads the Post-Acute Sequelae of Covid Clinic at the Mayo Clinic in Jacksonville, Florida, said in an email.

POTS following other types of infection is not uncommon, Schaffner said. The condition has been linked to a number of viral or bacterial infections, including influenza, mononucleosis and Lyme disease.

Dr. Daniel Dudenkov, a physician at the Mayo Clinic, said that although Covid vaccines may be associated with POTS, it is important to keep in mind that Covid infection itself is much more likely to lead to POTS.

"Vaccines continue to be an important strategy to fight against Covid and its effects," he said.

Schaffner agreed, saying the event following vaccination is "rare."

"The risk of this happening is much greater with Covid than it is with the vaccine. So please get vaccinated," he said.

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Berkeley Lovelace Jr. is a health and medical reporter for NBC News. He covers the Food and Drug Administration, with a special focus on Covid vaccines, prescription drug pricing and health care. He previously covered the biotech and pharmaceutical industry with CNBC.

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Postural orthostatic tachycardia syndrome.

Sean Zhao ; Vu H. Tran .

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Last Update: August 7, 2023 .

• Continuing Education Activity

Postural orthostatic tachycardia syndrome is a condition where an unusually significant increase in heart rate accompanies the action of an individual going from lying to standing. This activity reviews the evaluation and management of postural orthostatic tachycardia and highlights the role of the interprofessional team in caring for patients with this condition.

• Describe the epidemiology of orthostatic tachycardia syndrome.
• Explain the pathophysiology of postural orthostatic tachycardia syndrome.
• Describe the treatment modalities indicated for postural orthostatic tachycardia syndrome.
• Describe interprofessional team strategies for effective care coordination and provision of patient education to successfully manage postural orthostatic tachycardia syndrome.
• Introduction

Postural orthostatic tachycardia syndrome (POTS) is a common form of autonomic dysregulation characterized as an excessive tachycardia upon standing in the presence of orthostatic intolerance. [1] [2] [3] Current adult diagnostic criterion requires a heart rate increase of greater than or equal to 30 bpm within the initial 10 minutes of standing or head-up tilt (HUT) in the absence of orthostatic hypotension. [4] [5] POTS predominantly affects premenopausal females (5 to 1) between 15 and 50 years of age, manifesting with symptoms of fatigue, headache, palpitations, sleep disturbance, nausea, bloating, among others. [2] [6] [3] A multitude of pathophysiologic mechanisms including but not limited to disproportionate sympathoexcitation, volume depletion, autoimmune dysfunction, cardiac and physical deconditioning point to a heterogeneously complex etiology. [3] [5] [7] Most significantly, the debilitating nature of POTS predisposes patients to a high degree of functional impairment and decreased quality of life, [8] emphasizing the need for further investigation into the understanding and management of this increasingly prevalent clinical syndrome.

A variety of proposed etiologies have led to the characterization of specific postural orthostatic tachycardia syndrome subtypes as described below, with a general consensus of excessive tachycardia in the setting of cardiovascular deconditioning as the final common pathway. [7]

Neuropathic

Neuropathic postural orthostatic tachycardia syndrome is a length-dependent autonomic neuropathy characterized by predominantly lower limb sympathetic denervation leading to reduced venoconstriction and venous pooling. [2] [5] One study observed 50% of POTS patients exhibited peripheral sudomotor denervation correlated with a distal pattern of anhidrosis demonstrated by thermoregulatory sweat testing. [9] POTS patients have been observed to have decreased norepinephrine spillover in the lower extremities despite normal systemic norepinephrine spillover implicating dysfunctional norepinephrine reuptake due to injured terminal nerves. [10] Peripheral venous pooling evidenced by dependent acrocyanosis has also been observed. [11] Thus, an excessive cardiovascular response is necessary to maintain adequate mean arterial pressures.

Hyperadrenergic

An estimated 30 to 60% of postural orthostatic tachycardia syndrome patients fall under the hyperadrenergic subtype, characterized by elevated standing plasma norepinephrine levels of greater than or equal to 600 pg/mL with predominant symptoms of increased sympathetic tone including palpitations, tremors, hypertension, anxiety, and tachycardia. [4] [5] A norepinephrine transporter (NET) loss of function gene mutation (SLC6A2) resulting in deficient norepinephrine transport contributing to an increased mean supine heart rate was a feature in one case. [12] NET block is more frequently seen in the setting of pharmacologic inhibition by medications including tricyclic antidepressants, sympathomimetics (i.e., methylphenidate), and norepinephrine reuptake inhibitors (i.e., bupropion). [4] [5] These medications are often useful in treating the associated cognitive effects of POTS such as depression, anxiety, and concentration difficulties. Therefore it is prudent to ensure patients are systemically clear of possible pharmacologic causes of elevated catecholamine levels and tachycardia throughout diagnostic evaluations.

Hypovolemic

Up to 70% of patients with postural orthostatic tachycardia syndrome exhibit decreased plasma, red blood cell, and total blood volumes, although the degree of hypovolemia varies between studies. [13] [5] [14] In POTS patients, this physiologic low volume state persists in association with a paradoxically low level of renin and aldosterone levels, suggesting a possible impairment of the renin-angiotensin-aldosterone axis that is crucial to maintaining adequate plasma volume [15] . Secondary hypovolemic states present in patients with co-existing gastrointestinal conditions culminating in excessive fluid loss and poor volume intake (nausea, vomiting, diarrhea). [4]

An autoimmunity hypothesis is one proposal for postural orthostatic tachycardia syndrome given the significant overlapping commonalities (female predominance, post-viral onset, elevated autoimmune markers) seen in other systemic autoimmune disorders such as rheumatoid arthritis, lupus, and Sjogren’s syndrome. [4] [6] Previous studies have demonstrated increased autoantibodies in POTS. Positive antinuclear antibodies were present in up to 25% of patients, with Hashimoto thyroiditis being the most prevalent. [1] [16] One study demonstrated increased proinflammatory IL-6 levels in POTS patients associated with increased sympathetic drive, perhaps driven by chronic systemic immune activation. [17] Additionally, other autoimmune markers including ganglionic AChR, G-protein coupled receptor, and various nonspecific autoantibodies have presented in the POTS population. [1] [3] [18]

Deconditioning

Physical and cardiovascular deconditioning is often evident in patients with postural orthostatic tachycardia syndrome, although its presence as either a cause or effect is unclear. [11] [13] Moreover, it appears the severity of deconditioning does not necessarily correlate with objective laboratory or autonomic findings. [19] Similar POTS-like symptoms have been observed in otherwise healthy individuals placed in microgravity environments such as space flight, further implicating the physical and gravity dependent roles underlying POTS. [7] Decreased cardiac size and mass have been demonstrated in POTS patients compared to healthy controls, with an average decreased left ventricular mass of 16% and reduced plasma volume of 20%. [20] [21] The well documented chronic fatigue, autonomic instability, and overall functional impairment give way to reduced physical activity and prolonged bed rest states, resulting in an unfavorable feedback cycle that exacerbates already prominent existing symptoms.

• Epidemiology

As one of the most common forms of orthostatic intolerance globally, postural orthostatic tachycardia syndrome is estimated to affect over 500000 patients in the United States alone. [4] [20] [22] Worldwide prevalence has not been well-established, although previous study populations have estimated ranges between 0.2 to 1% in developed countries. [1] [11] The overwhelmingly demographic of POTS patients are young, premenopausal Caucasian females (4.5 to 1) between the ages of 15 and 45 years old, [1] [2] [6] with the majority presenting between the ages of 15 and 25 years. [5] [6] [11] [13] There is a significant overlap between POTS, chronic fatigue syndrome and across a spectrum of autoimmune disorders. [3] [16]

• Pathophysiology

The pathophysiology underlying postural orthostatic tachycardia syndrome is heterogeneous, encompassing excess sympathetic tone, impaired peripheral autonomic function, volume dysregulation, cardiovascular deconditioning, and autoimmune dysfunction. [4] [5] [7] [11] In normal healthy subjects, a shift of the intravascular volume to the interstitial space reduces the total effective circulating blood volume, reflecting the gravity-dependent physiology seen in orthostatic-related pathologies. As expected, a subsequent reduction in stroke volume results in a compensatory increased sympathetic drive augmenting cardiac contractility, heart rate, and systemic vascular resistance. POTS patients exhibit persistent decreased stroke volume despite an exaggerated sympathetic response with postural changes such as standing, culminating in a final common pathway of tachycardia in the presence of orthostatic intolerance on standing. [4] [7]

The mechanisms as mentioned earlier are not mutually exclusive but instead overlap in a complex interaction of cause and effect. Affected physiologic systems include neuropathic, cardiovascular, renal, immune, and hematologic; this widespread implication of complex systems have added a certain degree of difficulty in constructing a comprehensive framework in the understanding of POTS. Common symptoms include chronic fatigue, dizziness, sleep disturbance, headache, tremors, tachycardia, anxiety, depression, gastrointestinal disturbances, syncope, and vision changes. [1] [6] [13] [22]

• History and Physical

The typical POTS patient is a young female between 15  and 25 years old presenting with multiple often chronic symptoms such as fatigue, lightheadedness, palpitations, cognitive impairment, and less commonly syncope. [1] [5] [13] Autonomic dysfunction often manifests as gastrointestinal symptoms (nausea, abdominal pain) and bladder complaints (suprapubic pain, frequency). [11] Additionally, stressors including viral infections, trauma, surgery, and pregnancy have been noted to precipitate symptom onset. [5] [11] Family history is not well correlated due to the generalized and chronic nature of the syndrome. It is important to elucidate possible contributing factors such as physical fitness level, sleep hygiene, fluid intake, and current medication or supplement usage.

The physical exam may reveal peripheral edema, acrocyanosis, clammy skin, joint hypermobility, and changes in peripheral sensation. [1] [5] [6] [22] The absence of discrete findings on the physical exam does not preclude the presence of POTS.

The initial evaluation of suspected postural orthostatic tachycardia syndrome should focus on excluding primary cardiovascular etiologies such as structural heart defects or tachyarrhythmias, underlying systemic causes including endocrine dysfunction, establishing chronicity of autonomic complaints, medication review, and assessing associated co-morbidities including gastrointestinal, neurological, and psychiatric signs and symptoms. [5]

In addition to a complete history and physical, basic labs and a thorough cardiac evaluation (electrocardiogram, echocardiogram, Holter monitor) should be initiated. The predominance of specific states such as physical deconditioning, gastrointestinal, urologic, and hyperadrenergic symptoms may necessitate additional testing including VO2 max exercise testing, thyroid function panel and autoimmune studies, plasma, and urinary metanephrines, and specialist consultation. [1] [4]

An active stand test consists of having the patient lying supine for 10 minutes with measurement of supine baseline blood pressure and heart rate; the patient then stands and with re-measurement of BP and HR at timed intervals (1, 3, 5, and 10 minutes). [4] The head-up tilt table (HUT) with non-invasive hemodynamic monitoring is the accepted gold standard for assessing orthostatic intolerance in POTS. [1] Current adult diagnostic criterion requires a heart rate increment greater than or equal to 30 bpm within the first 10 minutes of standing or HUT in the absence of orthostatic hypotension. [4] [5]

• Treatment / Management

The management of postural orthostatic tachycardia syndrome divides into non-pharmacologic and pharmacologic approaches and contingent on accurate diagnosis, patient education, and therapy adherence.

Patient education and management of expectations are crucial to the overall successful management of POTS given its often non-specific and chronic debilitating nature. It is important to assess the patient’s understanding, answer and follow-up on questions and concerns, and emphasize the need for a multi-pronged therapeutic approach to treatment to improve quality of life. There is no current class I recommendations for POTS management. [1] [11] Regardless of treatment, each approach should be tailored individually to predominating subtypes (e.g., hyperadrenergic, hypovolemic).

Exercise conditioning is a fundamental aspect of postural orthostatic tachycardia syndrome treatment (class IIA), [1] [11] and it is a recommendation for all patients to start on a gradual physical exercise regimen. [22] Given the high probability of symptom exacerbation with activity, beginning with a supervised low-intensity program focused on avoiding upright positioning (rowing, swimming) with incremental progression over 3 months has been demonstrated to improve symptoms. [4] [6] [11] A previous progressive 3-month exercise regimen was found to increase maximal oxygen intake 11%, left ventricular mass 12%, end-diastolic volume 8%; at the conclusion, 53% (10/19 patients) no longer met POTS criteria. [20] Other conservative non-pharmacologic interventions include physical counter maneuvers (muscle contraction, leg crossing, forward bending), [5] compression garments, increased fluid (2-3 liters) and salt (slowly up to 10 grams) intake, [7] and avoidance of symptom exacerbation (caffeine, alcohol, prolonged heat exposure).

Pharmacologic therapies (class IIb) are not considered first-line treatment for POTS and enter the clinical picture in severe or refractory cases with the goal of stabilization for continued physical reconditioning. [11] POTS medications are not proven to be more effective than non-pharmacologic approaches and should be utilized with caution given potential adverse interactions and side effects. The US Food and Drug Administration has not approved any drug for POTS treatment. The following medications are used off label. [4] [22] Some common medications are described here and summarized in table 1.

Fludrocortisone, a synthetic mineralocorticoid aldosterone analog, increases salt retention and plasma volume. Adverse hypertension, hypokalemia, and headaches may be present.

The alpha-1-adrenergic agonist midodrine causes systemic vasoconstriction leading to an increase in venous return that may be effective in hypotensive phenotypes. Limitations include frequent dosing, urinary retention, and supine hypertension. [13]

Clonidine and alpha-methyldopa are central-acting alpha-2 agonist sympatholytics that may be beneficial in hyperadrenergic subtypes with hypertension as a predominant symptom. May cause adverse sedation, cognitive clouding, and fatigue.

Beta-blockers (propranolol, metoprolol) may reduce upright tachycardia without significant hemodynamic changes. However, worsening fatigue is a concern.

Pyridostigmine is an acetylcholinesterase inhibitor that increases acetylcholine levels in the autonomic ganglia. [11] In turn, this may reduce tachycardia with minimal hemodynamic effects; however worsening cramps, vomiting, and urinary symptoms often limit continued use.

Generally medications exacerbating specific symptoms such as tachycardia (sympathomimetics including amphetamines, selective serotonin and/or norepinephrine reuptake inhibitors, droxidopa) or worsening orthostatic intolerance (diuretics, calcium channel blockers, nitrates, opiates, tricyclic antidepressants) should be avoided; in specific cases it may be beneficial in accordance with the patient’s history and presentation. [4] [22]

• Differential Diagnosis

The broad and often non-specific signs and symptoms observed in postural orthostatic tachycardia syndrome can mimic numerous other disease processes, especially given the systemic nature of the syndrome. It is therefore imperative to obtain a complete history and physical to establish onset, chronicity, family history, medication use in the context of at-risk demographic (young White female), in addition to the above mentioned diagnostic tests.

Significant differential and diagnostic exclusions include but are not limited to: structural heart defects, cardiac arrhythmias, pulmonary embolism, myocardial infarction, chronic fatigue syndrome, fibromyalgia, anemia, adrenal insufficiency, systemic lupus erythematosus, Sjogren’s syndrome, rheumatoid arthritis, vasculitis, diabetes mellitus, diabetes insipidus, infectious etiologies, thyroid disease, renal insufficiency, peripheral neuropathies, central dysautonomia, pheochromocytoma, malignancy, epilepsy, anxiety, depression, and adverse medication reactions.

The prognostic outcome for postural orthostatic tachycardia syndrome is favorable, although long-term data is limited. Over half of patients do not meet criteria for POTS within 5 years, most within the first 1 to 2 years, characterized as the absence of orthostatic symptoms with minimal functional impairment. [1] [22] Younger patients generally experience more favorable outcomes, [22] with only a sporadic few cases of POTS developing in those over 50 years old. [13] There have no deaths attributed directly to POTS. [6] [13]

• Complications

There is limited data regarding specific complications arising from postural orthostatic tachycardia syndrome; however, the impact on the quality of life and daily function may be quite significant. Worsening physical and cardiovascular deconditioning may predispose some individuals to increased rates of infection, thromboembolism in addition to detrimental maladaptive psychological and cognitive processes. Anxiety, depression, and fatigue often persist despite treatment, perhaps revealing a therapeutic avenue for cognitive and behavioral approaches.

• Deterrence and Patient Education

As described above, patient education remains a cornerstone in postural orthostatic tachycardia syndrome management. Information regarding differentiation and attribution of symptoms, alleviating and exacerbating factors, combination treatment modalities, and focus on daily functional improvement must be presented in a clear manner. As with many chronic conditions, establishing a favorable physician-patient rapport via timely follow up, close monitoring, and if needed specialty consultation is key to therapeutic adherence and overall recovery.

• Pearls and Other Issues
• Postural orthostatic tachycardia syndrome (POTS) is a common form of autonomic dysregulation predominantly affecting young White females characterized by excessive tachycardia upon standing in the presence of orthostatic intolerance.
• Adult diagnostic criteria require a heart rate increase of greater than or equal to 30 bpm within the first 10 minutes of standing or head-up tilt (HUT) in the absence of orthostatic hypotension.
• The complex heterogeneous etiologies of POTS generally classify as neuropathic, hyperadrenergic, hypovolemic, autoimmune, and physical deconditioning with significant overlap between the various etiologies.
• Symptoms are often chronic and non-specific and may include chronic fatigue, dizziness, sleep disturbance, headache, tremors, tachycardia, anxiety, depression, gastrointestinal disturbances, syncope, and vision changes.
• Management and treatment require an emphasis on patient education, and a progressive monitored exercise regimen with second-line pharmacologic approaches aimed at increasing fluid volume and controlling excessive sympathetic drive (fludrocortisone, midodrine, clonidine, propranolol).
• Prognosis is favorable especially with younger age at onset, with more than half of patients no longer meeting POTS criteria within 5 years.
• Enhancing Healthcare Team Outcomes

Postural orthostatic tachycardia syndrome is a complex, heterogeneous disease that requires a multimodal, interprofessional approach to effective management. The presentation of nonspecific and often chronic symptoms that overlap neurological, cardiovascular, and autoimmune domains makes diagnosis itself a significant challenge; therefore, initiating appropriate treatment designed to address pertinent subtypes may at times be more burdensome. Patient education is essential for establishing expectations and treatment compliance.

A recent 2016 study evaluating 33 adolescents with confirmed POTS who underwent a 3-week an interprofessional rehabilitation program consisting of physicians, physical and occupational therapists, psychologists, and nurses saw significant reductions in psychological stress and functional impairment (class IIb). [23]

As noted above, no current class I recommendations exists for the management of POTS, although exercise rehabilitation is considered an integral aspect of treatment (class IIa). Physical rehabilitation therapists play a crucial role in this regard, and dieticians may alleviate a significant burden of creating and maintaining a cardiovascularly healthy nutritional plan. The ongoing cognitive and psychological disruption experienced by many POTS patients often necessitates establishing a trusting, long-term rapport between the patient and healthcare team, and continuous psychological evaluation and therapy have been demonstrated to improve overall outcomes. Also, pharmacist-directed medication management would impart a significant benefit especially in more serious, refractory cases.

More investigation is still necessary into the complex pathophysiology and treatment of POTS. A collaborative an interprofessional approach should be encouraged and personalized for all patients to alleviate the significant physical, psychological, and functional impairment of POTS.

Diagnosis and management of POTS require a collaborative effort from an interprofessional team, including physicians, specialists, specialty-trained nursing staff, and pharmacists, communicating effectively to bring about optimal patient outcomes. [Level V]

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POTS Table 01 Contributed by Sean Zhao, MD

Disclosure: Sean Zhao declares no relevant financial relationships with ineligible companies.

Disclosure: Vu Tran declares no relevant financial relationships with ineligible companies.

This book is distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) ( http://creativecommons.org/licenses/by-nc-nd/4.0/ ), which permits others to distribute the work, provided that the article is not altered or used commercially. You are not required to obtain permission to distribute this article, provided that you credit the author and journal.

• Cite this Page Zhao S, Tran VH. Postural Orthostatic Tachycardia Syndrome. [Updated 2023 Aug 7]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-.

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• Review Postural tachycardia syndrome: a heterogeneous and multifactorial disorder. [Mayo Clin Proc. 2012] Review Postural tachycardia syndrome: a heterogeneous and multifactorial disorder. Benarroch EE. Mayo Clin Proc. 2012 Dec; 87(12):1214-25. Epub 2012 Nov 1.
• [Clinical analysis and follow-up study of postural orthostatic tachycardia syndrome in 28 pediatric cases]. [Zhonghua Er Ke Za Zhi. 2005] [Clinical analysis and follow-up study of postural orthostatic tachycardia syndrome in 28 pediatric cases]. Zhang QY, Du JB, Li WZ. Zhonghua Er Ke Za Zhi. 2005 Mar; 43(3):165-9.
• Dysautonomia: A Forgotten Condition - Part 1. [Arq Bras Cardiol. 2021] Dysautonomia: A Forgotten Condition - Part 1. Rocha EA, Mehta N, Távora-Mehta MZP, Roncari CF, Cidrão AAL, Elias Neto J. Arq Bras Cardiol. 2021 Apr; 116(4):814-835.
• Autonomic dysfunction presenting as postural orthostatic tachycardia syndrome in patients with multiple sclerosis. [Int J Med Sci. 2010] Autonomic dysfunction presenting as postural orthostatic tachycardia syndrome in patients with multiple sclerosis. Kanjwal K, Karabin B, Kanjwal Y, Grubb BP. Int J Med Sci. 2010 Mar 11; 7(2):62-7. Epub 2010 Mar 11.
• Review Postural orthostatic tachycardia syndrome: clinical presentation, aetiology and management. [J Intern Med. 2019] Review Postural orthostatic tachycardia syndrome: clinical presentation, aetiology and management. Fedorowski A. J Intern Med. 2019 Apr; 285(4):352-366. Epub 2018 Nov 23.

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What is eldest daughter syndrome? Is it a real condition?

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Eldest daughter syndrome describes the responsibility eldest daughters are often given in a family and how that shapes them. But this Northeastern professor says birth order and gender aren’t “a horoscope.”

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Who plans the agenda for vacations in your family? Who’s the first to step up to care for mom and dad or grandma and grandpa? Who’s the one organizing family holidays? Chances are if you have an older sister, it’s her. And if she’s the only one in your family doing this, she may have “eldest daughter syndrome.”

In a viral video on TikTok, licensed family and marriage therapist Kati Morton broke down the eight “symptoms” of “eldest daughter syndrome.” They include feeling an intense sense of responsibility for others, having an inclination toward overachieving, struggles with anxiety, people-pleasing, and placing boundaries, feelings of guilt, having a difficult time with adult relationships and having feelings of resentment toward your siblings and parents.

Eldest daughter syndrome is not a real diagnosable condition, says Laurie Kramer , a professor of applied psychology at Northeastern University. Nor does one’s birth order and gender mean they will automatically have certain traits or roles within the family. But Kramer, whose research focuses on sibling relationships , said that many eldest daughters do end up taking on duties without recognition due to societal norms.

“(Eldest daughter syndrome) does feel real and for good reason,” Kramer said. “When I hear eldest daughter syndrome, I’m thinking about families where we have just been unintentionally putting burdens on particular individuals. This happens across the world, but we haven’t really been paying attention to the cost of that. When a sibling provides a lot of caregiving to other siblings or parents, it comes at a cost.”

Kramer said research shows that first born/older girls are often asked to take on a caretaking role with their younger siblings, sometimes as young as 5 years old. In doing so, it creates a family dynamic where the older girls are socialized to take on more responsibilities and learn to be more conscientious of others’ needs, Kramer said. 

Putting responsibility on the oldest daughter is a common dynamic that often continues as the children become adults and end up caring for elderly parents, Kramer added. It can end up creating resentment not just between parent and children, but between siblings as well . For many eldest daughters, this ends up shaping their personality and relationships outside the family.

When I hear eldest daughter syndrome, I’m thinking about families where we have just been unintentionally putting burdens on particular individuals. Laurie Kramer , professor of applied psychology at Northeastern

Eldest sons aren’t exempt from also taking on more responsibility within the family, Kramer said. But often they’re expected to take on financial responsibilities instead of responsibilities around the house or involving caregiving. The former tends to get more recognition while housework and caregiving tend to be more overlooked, she said.

“For example, when there’s a family business, those sorts of things have traditionally been handed down to eldest sons,” Kramer said. “Eldest daughters in some families are expected to be the ones to bring people together, to be that emotional source of support and … we don’t tend to explicitly value a lot of what they’re doing. It’s invisible.”

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But this type of dynamic between an older sister and her siblings and parents is not a given. Kramer said other factors play a role in establishing a family dynamic. These include the age gap between siblings, how well the siblings get along with each other and how they treat each other, and whether there’s a family member with a medical condition that requires them to receive more attention. 

“It’s really important that we not look at this as a horoscope,” Kramer said. “Families are really, really different and sometimes parents are very well aware of the impact of assigning roles like that to their children. … What’s deeper is really looking at the roles of individuals and siblings within the family and understanding we can’t just assign a role to someone based simply on birth order.”

This type of awareness can help parents avoid falling into the eldest daughter trap when raising their own family. Kramer said parents looking to avoid placing too much burden on their eldest daughter should embrace balance and create an environment where children can speak openly if they feel something is unfair.

“We are not destined to play these roles in our lives,” Kramer said. “We have choice and that’s one of the reasons why I stay away from emphasizing the importance of birth order and gender. There is nothing we can do about those sorts of things. … But (parents) have choices every single day when parenting their kids.”

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80% recovery with early diagnosis and best practice treatment.

Complex Regional Pain Syndrome (CRPS) is a chronic and debilitating pain disorder, typically considered lifelong with limited treatment options. Now, groundbreaking research finds that early detection and effective treatment can lead to significant recovery within 18 months, offering hope to millions of people worldwide.

Led by NeuRA's Centre for Pain IMPACT and conducted in partnership with the University of South Australia, the findings could deliver life-changing outcomes for people with CRPS, with up to 80% of patients recovering within the first 18 months of being diagnosed with the disorder.

CRPS is a multi-system disorder triggered by trauma such as surgery or fracture. It manifests with severe pain localised to a single limb, but often persists beyond typical recovery periods. Sufferers can experience issues with sweating, temperature regulation, and mobility. Women are disproportionately affected, with up to four times as many diagnosed with the condition as men.

The new study reviewed the latest advances in CRPS epidemiology, pathophysiology, diagnosis, and treatment. It found that the best approach to treatment includes education about CRPS, medicines to control pain, physical rehabilitation, and psychological support, if needed.

Lead researcher, NeuRA's Michael Ferraro says this is a paradigm shift for understanding CRPS.

"Complex regional pain syndrome is a rare pain disorder. It's characterised by intense pain and changes in muscle, sensation, skin, bone, and nerves, and often severely limits a person's ability to work or engage in social activities," Ferraro says.

"Because the disorder is so rare, there is little evidence to inform effective treatment.

"In this research we challenge the prevailing notion that CRPS is a lifelong burden.

"By reviewing and consolidating the latest developments in understanding CRPS, we've found that unlike previous theories, recovery is likely for most people with CRPS, and may be more likely with early diagnosis and a comprehensive treatment approach to match the multi-system nature of the disorder.

"By combining education on the condition, pain medication, rehabilitation and psychology, we can tackle CRPS from all angles, giving patients the best chance of recovery within the first 12-18 months of symptoms."

Co-researcher and pain expert, UniSA's Professor Lorimer Moseley says the research marks a significant milestone for understanding and treating CRPS, offering hope and new avenues for patients and healthcare professionals alike.

"This is a major step towards better understanding CPRS," Prof Moseley says.

"While more research is needed, our review highlights that biological and psychosocial factors are involved, and successful management of the disorder should target these factors.

"The next steps will require national and international networks of researchers to test the most promising treatments in clinical trials."

Among these intiatives is the ongoing MEMOIR study conducted by NeuRA and UniSA, an Australian Government-funded trial evaluating a medication and a newly developed rehabilitation program, with recruitment and treatment facilitated through telehealth to enable nationwide participation.

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• Michael C Ferraro, Neil E O’Connell, Claudia Sommer, Andreas Goebel, Janet H Bultitude, Aidan G Cashin, G Lorimer Moseley, James H McAuley. Complex regional pain syndrome: advances in epidemiology, pathophysiology, diagnosis, and treatment . The Lancet Neurology , 2024; 23 (5): 522 DOI: 10.1016/S1474-4422(24)00076-0

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New findings activate a better understanding of Rett syndrome's causes

by Greta Friar, Whitehead Institute for Biomedical Research

Rett syndrome is a rare neurodevelopmental disorder for which there is currently no cure or good therapy. It causes severe physical and cognitive symptoms, including many that overlap with autism spectrum disorder.

Rett syndrome is caused by mutations to the gene MECP2, which is highly expressed in the brain and appears to play important roles in maintaining healthy neurons. The gene is located on the X chromosome and the syndrome mainly affects girls. In order to develop therapies for Rett syndrome, researchers want to understand more about MECP2 and its functions in the brain.

Researchers including Whitehead Institute Founding Member Rudolf Jaenisch have been studying MECP2 for decades, and yet many basic facts about the gene remained unknown. The MECP2 protein encoded by the gene is involved in gene regulation ; it binds to DNA and affects the expression level of various other genes—meaning the amount of protein produced from them.

However, researchers did not have a complete list of the genes that MECP2 affects, nor was there a consensus on the effect that MECP2 has on those genes.

Early research into MECP2 suggested that it was a repressor, decreasing the expression of its target genes, but research by Jaenisch and others previously found that MECP2 also acts as an activator, increasing its targets' expression—and that it might primarily be an activator. Also unknown was MECP2's mechanism of action, or what the protein actually does that leads to changes in gene expression.

Limitations in technology had prevented researchers from gaining clarity on these questions. However, Jaenisch, postdoc in his lab Yi Liu, and Jaenisch lab alumnus Anthony Flamier, now an assistant professor at the CHU Sainte-Justine Research Center at the Université de Montréal, have used cutting-edge techniques to answer these outstanding questions about MECP2 and gain new insights into its role in brain health and disease.

Their findings were published in the journal Neuron on May 1, and the researchers have also created an online repository of their MECP2 data, the MECP2-NeuroAtlas portal , as a resource for other researchers.

"I think this paper will drastically change how people think about MECP2 causing Rett syndrome. We have a completely new understanding of the mechanism, and that could provide new ways to approach developing treatments for the disorder," says Jaenisch, who is also a professor of biology at the Massachusetts Institute of Technology.

Fleshing out the picture of MECP2 in the brain

First, the researchers created a comprehensive map of where in the sequence of human neuronal genes MECP2 binds, either within genes or in the regulatory regions of DNA near them. They used an approach called CUT&Tag that can identify protein interactions with DNA with high resolution.

The researchers found more than four thousand genes bound by MECP2. The researchers repeated their mapping in neurons with common Rett-linked MECP2 mutations, to determine where MECP2 is depleted in a disease state.

Knowing which genes MECP2 binds allowed Liu and Flamier to begin drawing connections between MECP2's targets and brain health. They found that many of its targets are involved in the development and functioning of neuronal axons and synapses.

They also compared their list of MECP2 targets to the Simons Foundation Autism Research Initiative (SFARI) database of autism-linked genes, and found that 381 genes in that database are targeted by MECP2.

These findings may help to narrow in on the mechanisms underlying Rett syndrome's autism-like symptoms, and they provide a good starting point for investigating a possible role of MECP2 in autism.

"We established the first integrated epigenome map of MECP2 in a health and disease state, and this map can guide future research," Liu says. "Knowing which genes MECP2 target, and which genes are directly dysregulated in disease, provides a strong foundation for understanding Rett syndrome and asking questions about neuronal gene regulation."

The researchers also examined whether MECP2 appears to increase or decrease the expression of its target genes. Consistent with a history of MECP2 being identified by some as an activator and others as a repressor, Liu and Flamier found instances of MECP2 playing both roles.

However, whereas MECP2 is more commonly thought of as a repressor, Liu and Flamier found that it is mostly an activator—confirming earlier findings by Jaenisch and Liu. One new experiment indicated that MECP2 activates at least 80% of its targets, and another indicated that it activates as many as 88% of its targets.

The researchers' map of target genes provided further insight into MECP2's activator role. They found that for the genes that MECP2 activates, it typically binds a region of DNA upstream of the gene called the transcription start site.

This site is where cellular machinery initiates the process of the gene being transcribed or read into RNA, after which the RNA is translated into a functional protein that is the product of gene expression. MECP2's presence at the transcription start site, where gene expression begins, is consistent with its role as a gene activator.

Next, the researchers set out to determine what MECP2's role is in gene activation. They investigated what molecules MECP2 binds to at this site, in addition to the DNA, and found that MECP2 interacts directly with a protein complex called RNA polymerase II (RNA Pol II). RNA Pol II is the key cellular machine that transcribes DNA into RNA. RNA Pol II cannot locate genes on its own, so it requires a plethora of cofactors or collaborator proteins that help it to carry out its job.

The researchers propose that MECP2 serves as one such cofactor, helping RNA Pol II to initiate transcription at the genes where MECP2 binds. Structural analysis of MECP2 identified the parts of the molecule that bind RNA Pol II, and other experiments confirmed that loss of MECP2 decreases the presence of RNA Pol II at relevant transcription start sites as well as expression levels of the target genes.

This suggests that Rett syndrome may be caused by a decrease in transcription of the genes targeted by MECP2, due to MECP2 mutations that prevent it from binding RNA Pol II or binding DNA. Consistent with this idea, most of the common disease-linked MECP2 mutations are truncations: mutations in which part of the protein is missing, which may alter the interaction between MECP2 and RNA Pol II.

The researchers hope that not only will their findings reshape our understanding of MECP2, but that a deeper and broader understanding of how MECP2 impacts brain development and function may lead to new insights that can help people with Rett syndrome and related disorders, including autism.

"This project is a great example of the collaborative nature of the Jaenisch lab," Flamier says. "Rudolf and Yi had a specific problem to solve about Rett syndrome, and I had familiarity with a technology, CUT&Tag, that could solve the problem. Through discussion we realized we could merge our efforts and now we've got a great repository of information on MECP2 and its connections to disease."

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UCL Queen Square Institute of Neurology

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Study finds half of people living with Dravet Syndrome experience feeding problems

30 April 2024

We are pleased to share the results of our research partnership with Dravet Syndrome UK, exploring an aspect of living with Dravet Syndrome which is rarely talked about but has a huge impact on family life.

A study to explore the impact of feeding difficulties in children and adults living with Dravet Syndrome, found that over half (52%) reported that they had experienced some form of feeding difficulty and some experienced many different problems with feeding.  The findings also showed that around 1 in 5 people with Dravet Syndrome may require a feeding tube (called a gastrostomy) at some point during their life to help address the feeding issues.

The research conducted with Dravet Syndrome UK revealed that 88% of carers of someone with Dravet Syndrome had a high level of concern and fear about having a feeding tube fitted and that there was a lack of information available. However, once the gastrostomy was inserted, the opinions of caregivers completely changed with 88% happy that their child had the gastrostomy, and more than 90% agreed that they had a better-quality life, better nutrition, got their medication on time and that caregivers found that it was easy to use.

Lisa Clayton, Clinical Research Fellow, Department of Clinical and Experimental Epilepsy, UCL Queen Square Institute of Neurology and Neurology Registrar, who led this research said: “We found that feeding problems were common in people living with Dravet Syndrome and can emerge at any age. Severe problems with eating can be particularly worrying for caregivers as it can affect both nutrition, hydration and giving medicines to the person they care for. It is vital that health professionals have early discussions with caregivers about feeding issues to avoid unnecessary delays in intervention if needed.”

Galia Wilson, Chair of Trustees, Dravet Syndrome UK, said: This important research highlights one of the many challenges faced by children and adults living with Dravet Syndrome and their families on a daily basis. Our strategy is to create a better understanding of the realities of caring for people with Dravet Syndrome, and to empower families to access the support they need by providing an evidence base through studies like this.

Underlying causes and risk factors for feeding issues in people living with Dravet Syndrome are currently unknown and are likely to be complex. More research is needed to explore the causes and find ways to try and address them.

Taliah's story

Edwina Williams, mother of Taliah who lives with Dravet Syndrome, contributed to this research as her daughter had feeding problems for a number of years and then had a gastrostomy fitted. She said: “As a parent you always want to do the best for your child, but sometimes it is difficult to figure out what the best thing is. As time went on, Taliah’s feeding issues worsened, and I was watching my daughter wither away in front of my eyes. This is when I contacted her medical team to arrange for her to have a feeding tube fitted as I knew that we needed help. It has been a long journey, but I can honestly say that the feeding tube has been the absolute best thing for Taliah, and our family. She is no longer dehydrated, she no longer sleeps for most of the day as her body has the correct nutrients, her hair is glossy, and she is a chatterbox now too!”

About the research

The anonymous, cross-sectional survey regarding feeding difficulties and gastrostomy was developed by adult neurologists working with individuals with Dravet Syndrome, alongside representatives, and caregivers, from Dravet Syndrome UK (DSUK). The survey was shared through email and private Facebook group to DSUK-registered families, and open for responses between 7th and 28th January 2022. Survey questions were multiple choice, including Likert scale responses, with opportunities for open-ended responses. 124 families took part in the survey.

Clayton et al. Feeding Difficulties and Gastrostomy in Dravet Syndrome : A UK-Wide Survey and 2-Center Experience . Neurology: Clinical Practice 2024;14:e200288. doi:10.1212/CPJ.0000000000200288

• Dravet Syndrome UK (DSUK)
• Dr Lisa Clayton's academic profile
• Dr Lisa Clayton explains the results of her study looking at feeding issues in Dravet Syndrome

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