Five months post-covid, Nicole Murphy’s heart rate is still doing strange things

Authors: Ariana Eunjung Cha February 21, 2022

The Washington Post
The Washington Post

Five months after being infected with the coronavirus, Nicole Murphy’s pulse rate is going berserk. Normally in the 70s, which is ideal, it has been jumping to 160, 170 and sometimes 210 beats per minute even when she is at rest — putting her at risk of a heart attack, heart failure or stroke.

No one seems to be able to pinpoint why. She’s only 44, never had heart issues, and when a cardiologist near her hometown of Wellsville, Ohio, ran all of the standard tests, “he literally threw up his hands when he saw the results,” she recalled. Her blood pressure was perfect, there were no signs of clogged arteries, and her heart was expanding and contracting well.

Murphy’s boomeranging heart rate is one of a number of mysterious conditions afflicting Americans weeks or months after coronavirus infections that suggest the potential of a looming cardiac crisis.

A pivotal study that looked at health records of more than 153,000 U.S. veterans published this month in Nature Medicine found that their risk of cardiovascular disease of all types increased substantially in the year following infection, even when they had mild cases. The population studied was mostly White and male, but the patterns held even when the researchers analyzed women and people of color separately. When experts factor in the heart damage probably suffered by people who put off medical care, more sedentary lifestyles and eating changes, not to mention the stress of the pandemic, they estimate there may be millions of new onset cardiac cases related to the virus, plus a worsening of disease for many already affected.

“We are expecting a tidal wave of cardiovascular events in the coming years from direct and indirect causes of covid,” said Donald M. Lloyd-Jones, president of the American Heart Association.

In February 2021, the National Institutes of Health launched an initiative to look at the causes and possible treatments for long covid, the constellation of symptoms from brain fog and exercise fatigue to heart-related issues that some people experience well past their initial infections. In addition, the American College of Cardiology has recognized the serious, longer-term effects of the coronavirus by preparing new guidelines, scheduled out in March, for monitoring and returning to exercise after infection. But many experts and patient advocacy groups say more is needed, and are calling on President Biden and other leaders for comprehensive changes in the health care system that would provide more funding for research and treatment, financial support for people who can no longer work and address the social and emotional consequences of illness in the decades to come.

Zaza Soriano, 32, a software engineer from Millersville, Md., who works for a NASA subcontractor, got covid right before Christmas despite being fully vaccinated and boosted, and since then, her blood pressure has remained very high with the bottom number, or diastolic pressure when the heart rests between beats sometimes as high as 110 when it should be lower than 80. She also has brain fog and her joints ache.

“It’s so frustrating we still know so little about why this is happening,” she said.

Ziyad Al-Aly, an assistant professor of medicine at Washington University and a Veterans Affairs physician who co-authored the Nature Medicine study, describes the pandemic as an earthquake. “When the earth stops shaking and the dust settles, we will have to be able to deal with the aftermath on heart and other organ systems,” he said.

“Governments around the world need to pay attention,” Al-Aly emphasized. “We are not sufficiently prepared.”

Heart disease is the planet’s No. 1 killer, responsible for 17.9 million deaths, or a third of the total each year before the pandemic, and there’s already growing evidence of the outsize impact the coronavirus is having on our long-term health.

Multiple studies suggest that Americans’ collective blood pressures has jumped since the crisis began. According to a December study in the journal Circulation, for example, the average blood pressure among a half-million U.S. adults studied from April to December 2020 went up each month for both of the numbers measured by monitors.

The Centers for Disease Control and Prevention as of this month had logged more than 1 million excess deaths or deaths since the start of the pandemic that are beyond what we would have expected in normal times. While most of those were directly caused by the virus, there were also an additional 30,000 deaths due to ischemic heart disease and nearly 62,000 additional deaths due to hypertensive disease.

When the coronavirus first hit the United States in 2020, doctors were surprised by the heart involvement in cases they saw: professional athletes with signs of myocarditis or hardening of the heart walls; patients dying from their illness with hundreds of tiny clots in major organs; children rushed to emergency rooms with an inflammatory reaction involving cardiac complications.

Many of those presentations turned out to be rare or rarely serious. But they led researchers to an important discovery: that SARS-CoV-2 could directly attack the heart and blood vessels, in addition to the lungs.

Myocarditis has mostly been a transient issue, impacting activity or becoming life-threatening in only a small minority of cases; the clotting is more widespread but something that usually can be controlled with blood thinners; and the pediatric inflammatory syndrome has affected only about 6,400 children out of millions of cases, as of January.

The idea that infections increase cardiovascular risk is not new. It has been documented in cases of influenza and other viruses as well. But in coronavirus, that impact seems “enhanced,” said Antonio Abbate, a professor of cardiology at the VCU Pauley Heart Center. And the early and obvious cases, he said, should serve “as a kind of warning” for the type of longer-term cases we may see into the future.

Indeed, as the months since their infections have turned into years, people who initially had mild or even some asymptomatic coronavirus cases are pouring into cardiology practices across the country.

At Memorial Hermann-Texas Medical Center in Houston, Abhijeet Dhoble, an associate professor of cardiovascular medicine, said they are seeing an increase in arrhythmia, an abnormality in the timing of the heartbeat, and cardiomyopathy, a heart muscle disease. The patients, who previously had covid, range in age from their 30s to 70s and many had no previous heart disease.

“We are seeing the same patterns at university clinics and the hospital,” he said.

Two different processes may be at play, according to David Goff, director of the National Heart, Lung and Blood Institute’s division of cardiovascular sciences. The virus may inflict direct damage to the heart muscle cells, some of which could die, resulting in a weaker heart that does not pump as well. Another possibility is that after causing damage to blood vessels through clots and inflammation, the healing process involves scarring that stiffens vessels throughout the body, increasing the work of the heart.

“It could lead over time to failure of the heart to be able to keep up with extra work,” he explained.

Blood vessels and fatigue

David Systrom, a pulmonary and critical care doctor at Brigham and Women’s Hospital in Boston, said he believes blood vessel damage may be responsible for one of the most common and frustrating symptoms of long covid — fatigue.

Systrom and his colleagues recruited 20 people who were having trouble exercising. Ten had long covid. The other half had not been infected with the virus. He inserted catheters into their veins to provide test information before putting them on stationary bikes and took a number of detailed measurements. The study was published in the journal Chest in January.

In the long covid group, he found that they had normal lung function and at peak exercise, their oxygen levels were normal even as they were short of breath. What was abnormal was that some veins and arteries did not appear to be delivering oxygen efficiently to the muscles.

He theorized this could be due to a malfunction in the body’s autonomic nervous system, which controls involuntary actions such as the rate at which the heart beats, or the widening or narrowing of blood vessels.

“When exercising, it acts like a traffic cop that distributes blood flow to muscles away from organ systems like the kidney and gut that don’t need it. But when that is dysfunctional, what results is inadequate oxygen extraction,” he said. That may lead to the feeling of overwhelming exhaustion that covid long haulers are experiencing.

The overall the message from providers is that “covid by itself is a risk factor for heart disease” like obesity, diabetes, or high blood pressure, according to Saurabh Rajpal, a cardiologist at Ohio State University Wexner Medical Center.

“This is a virus that really knocks people down,” agreed Nicole Bhave, a cardiologist with Michigan Medicine and member of the American College of Cardiology’s science committee. “Even young, healthy people don’t often feel very normal for weeks to months, and it’s a real challenge to distinguish what’s just your body slowly healing versus a new pathological problem.”

“People experiencing what appear to be heart issues should have a “a low threshold for seeing their primary care doctor,” she said.

Heart beats

Unexplained high blood pressure has been a common symptom after covid infection.

Lindsay Polega, 28, an attorney from St. Petersburg, Fla., had never had any medical issues before covid. She had been an all-state swimmer in high school and ran, swam or otherwise exercised an hour or more every day since. But after two bouts with covid, the first in early 2020 and the second in spring 2021, she’s been having what doctors call “hypertensive spikes” that result in shooting pains in her chest that make her shaky and weak. During those incidents, which sometimes occur a few times a day, her blood pressure has gone as high as 210/153 — far above the 120/80, that is considered normal.

One incident happened during a light Pilates class and she had to go to the emergency room. Other times, it has happened while walking. “Sometimes I’ll just be on the couch,” she said.

Each specialist she saw referred her to another — endocrinology, immunology, cardiology, neurology. Finally, she found herself at a long-covid clinic where the doctor theorized the issue may be with her adrenal gland. Scientists have documented that the virus can target the adrenal glands, which produce hormones that help regulate blood pressure among other essential functions. Polega was put on a heavy-duty blood pressure drug called eplerenone that’s typically used in patients after a heart attack, and it has helped to reduce but not eliminate the episodes.

The scariest part for Polega is that women taking eplerenone are cautioned against pregnancy due to research in animals showing low birth weights and other potential dangers. Polega and her boyfriend of six years had recently purchased a house together, and were talking about starting a family soon.

“That’s a big thing to have taken away at my age — my future,” she said.

Of all the symptoms of long covid, among the most baffling have been erratic heart rates and skipped heartbeats with no clear cause.

Tiffany Brakefield, a 36-year-old pharmacy tech from Bonita Springs, Fla., who had covid in June 2020, said the spikes are so unpredictable that she found herself having to sit down on the floor at Walmart during a recent shopping excursion.

“I felt like I was going to fall down, and all I could do was wait for it to calm down on its own,” she said. Her doctors had put her on a heart medication, metoprolol, but it has not helped.

Rick Templeton, a 52-year-old community college instructor in Lynchburg, Va., felt chest tightness along with a racing heart rate, but in his case it disappeared five to six months after his infection in September 2020, and doctors never knew why it happened because his test results were normal.

Rajpal, the cardiologist in Ohio, said a large majority of his post-covid cases are similarly vexing.

“The most common type of long haulers we are seeing have shortness of breath, chest discomfort, and fast heart rate. But when we investigate them for heart disease they come back as normal,” he said.

Goff, the NIH scientist, said the presentation looks similar to a condition known as POTS, or postural orthostatic tachycardia syndrome, in which symptoms such as lightheadedness and heart rate changes are related to reduced blood volume, typically worsened by changing positions. A body of emerging evidence suggests that for many people, it could be a post-viral syndrome.

He said the unstable heart rate for many post-covid patients “can be quite serious and debilitating, and can really interfere with ordinary day-to-day activities.” Doctors can use blood pressure medications to try to stabilize heart rates but because they depress blood pressures at the same time, they can be tricky to use.

Murphy, the Ohio long covid patient, said that when her heart rate soars, which happens several times an hour, she said “it feels like a hamster in my chest.”

Her troubles began on Sept. 5, when she and her teenage daughter tested positive for the virus. Her daughter got over her illness in a few days. Murphy was acutely ill for about three weeks, and many of her symptoms never went away.

The 44-year-old single mom says she’s extraordinarily weak and has trouble with her memory sometimes. Before she was infected, she worked 12-hour days as a day care provider, a waitress and a cashier. Now she’s lucky if she can last three to four hours at her job as a DoorDash driver.

She’s tried to stay active by taking walks but sometimes “when I take steps, it’ll be like stars.” When she saw the cardiologist, she passed out during the stress test on the treadmill.

“I constantly live in fear I’m going to have a heart attack or stroke,” she said.

After all her heart tests came back fine except for her EKG, which showed the jumping heart rate, her doctors referred her to the Cleveland Clinic’s long covid group. She hopes they will help her find answers.

Long COVID Could Be Linked to the Effects of SARS-CoV-2 on the Vagus Nerve



New research to be presented at this year’s European Congress of Clinical Microbiology and Infectious Diseases (ECCMID 2022, Lisbon, April 23-26) suggests that many of the symptoms connected to post-COVID syndrome (PCC, also known as long COVID) could be linked to the effect of the virus on the vagus nerve – one of the most important multi-functional nerves in the body. The study is by Dr. Gemma Lladós and Dr. Lourdes Mateu, University Hospital Germans Trias i Pujol, Badalona, Spain, and colleagues.

The vagus nerve extends from the brain down into the torso and into the heart, lungs, and intestines, as well as several muscles including those involved in swallowing. As such, this nerve is responsible for a wide variety of bodily functions including controlling heart rate, speech, the gag reflex, transferring food from the mouth to the stomach, moving food through the intestines, sweating, and many others.

Long COVID is a potentially disabling syndrome affecting an estimated 10-15% of subjects who survive COVID-19. The authors propose that SARS-CoV-2-mediated vagus nerve dysfunction (VND) could explain some long COVID symptoms, including dysphonia (persistent voice problems), dysphagia (difficulty in swallowing), dizziness, tachycardia (abnormally high heart rate), orthostatic hypotension (low blood pressure) and diarrhea.

The authors performed a pilot, extensive morphological and functional evaluation of the vagus nerve, using imaging and functional tests in a prospective observational cohort of long COVID subjects with symptoms suggestive of VND. In their total cohort of 348 patients, 228 (66%) had at least one symptom suggestive of VND. The current evaluation was performed in the first 22 subjects with VND symptoms (10% of the total) seen in the Long COVID Clinic of University Hospital Germans Trias i Pujol between March and June 2021. The study is ongoing and continues to recruit patients.

Of the 22 subjects analyzed, 20 (91%) were women with a median age of 44 years. The most frequent VND-related symptoms were: diarrhea (73%), tachycardia (59%), dizziness, dysphagia and dysphonia (45% each), and orthostatic hypotension (14%). Almost all (19 subjects, 86%) had at least 3 VND-related symptoms. The median prior duration of symptoms was 14 months. Six of 22 patients (27%) displayed alteration of the vagus nerve in the neck shown by ultrasound – including both thickening of the nerve and increased ‘echogenicity’ which indicates mild inflammatory reactive changes.

A thoracic ultrasound showed flattened ‘diaphragmatic curves’ in 10 out of 22 (46%) subjects (which translates a decrease in diaphragmatic mobility during breathing, or more simply abnormal breathing). A total of 10 of 16 (63%) assessed individuals showed reduced maximum inspiration pressures, showing weakness of breathing muscles.

Eating and digestive function was also affected in some patients, with 13 of 18 assessed (72%) having a positive screen for self-perceived oropharyngeal dysphagia (trouble swallowing). An assessment of gastric and bowel function performed in 19 patients revealed 8 (42%) had their ability to deliver food to the stomach (via the esophagus) impaired, with 2 of these 8 (25%) reporting difficulty in swallowing. Gastroesophageal reflux (acid reflux) was observed in 9 of 19 (47%) individuals; with 4 of these 9 (44%) again having difficulty delivering food to the stomach and 3 of these 9 (33%) with hiatal hernia – which occurs when the upper part of the stomach bulges through the diaphragm into the chest cavity.

A Voice Handicap Index 30 test (a standard way to measure voice function) was abnormal in 8/17 (47%) cases, with 7 of these 8 cases (88%) suffering dysphonia.

The authors say: “In this pilot evaluation, most long COVID subjects with vagus nerve dysfunction symptoms had a range of significant, clinically-relevant, structural and/or functional alterations in their vagus nerve, including nerve thickening, trouble swallowing, and symptoms of impaired breathing. Our findings so far thus point at vagus nerve dysfunction as a central pathophysiological feature of long COVID.”

Meeting: The European Congress of Clinical Microbiology & Infectious Diseases (ECCMID 2022)

Post-COVID-19 Tachycardia Syndrome: A Distinct Phenotype of Post-Acute COVID-19 Syndrome

Authors: Marcus Ståhlberg, MD, PhD,a,⁎ Ulrika Reistam, MD,a Artur Fedorowski, MD, PhD,b,c Humberto Villacorta, MD,d Yu Horiuchi, MD,e Jeroen Bax, MD,f Bertram Pitt, MD,g Simon Matskeplishvili, MD,h Thomas F. Lüscher, MD, PhD,i,j Immo Weichert, MD,k Khalid Bin Thani, MD,l and Alan Maisel, MDm

Am J Med. 2021 Dec; 134(12): 1451–1456.Published online 2021 Aug. doi: 10.1016/j.amjmed.2021.07.004


In this paper we highlight the presence of tachycardia in post-acute COVID-19 syndrome by introducing a new label for this phenomenon—post-COVID-19 tachycardia syndrome—and argue that this constitutes a phenotype or sub-syndrome in post-acute COVID-19 syndrome. We also discuss epidemiology, putative mechanisms, treatment options, and future research directions in this novel clinical syndrome.

Clinical Significance

  • • Post-acute COVID-19 syndrome is a novel clinical syndrome with symptoms beyond 4-12 weeks after a SARS-CoV-2 infection
  • • Tachycardia is commonly reported in these patients and may be considered a distinct phenotype
  • • Putative mechanism for tachycardia in this setting include dysautonomia
  • • Post-acute COVID-19 syndrome patients reporting palpitations should be subjected to basic cardiovascular evaluation (including head-up tilt testing if concomitant orthostatic intolerance)
  • • Treatment options include cardiovascular drugs and structured rehabilitation program


The novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) virus has triggered a pandemic of coronavirus disease 2019 (COVID-19) lasting for more than 1 year, with over 130,000,000 reported cases globally as of April 2021.1 Due to its novelty and lack of historical data, several aspects of COVID-19 remain unclear. So far, COVID-19 research mostly focused on epidemiology, risk factors for disease severity, description of the clinical course, and identification of optimal management strategies in hospitalized COVID-19 patients.

However, there is growing evidence that COVID-19 may cause persistent symptoms and organ damage that stretch beyond the 3-month period after the infection, usually regarded as the normal convalescence phase. This is now considered to constitute a novel clinical long-term condition: post-acute COVID-19 syndrome.2 The clinical characteristics, pathophysiology, and appropriate management strategies for post-acute COVID-19 syndrome remain largely unknown.

Patients with post-acute COVID-19 syndrome have a wide range of symptoms including fatigue, chest pain, reduced exercise tolerance, cognitive impairment, dyspnea, fever, headache, and loss of smell and taste, but rapid heartbeats and palpitations are typical and frequent complaints.3 We have recently reported that a sub-group of patients with post-acute COVID-19 syndrome develop postural orthostatic tachycardia syndrome, a cardiovascular dysautonomia associated with sinus tachycardia and intolerance following orthostatic challenge.4 However, postural orthostatic tachycardia syndrome is likely not the sole explanation for elevated heart rate; several other conditions may explain tachycardia in post-acute COVID-19 syndrome, for example, inappropriate sinus tachycardia, deconditioning, hypoxia, anxiety, sinus node dysfunction, myocarditis/heart failure, and persistent fever.

In this paper we highlight the presence of tachycardia in post-COVID-19 patients with persisting symptoms by introducing a new label for this phenomenon: post-COVID-19 tachycardia syndrome, and argue that this should be considered a phenotype or sub-syndrome in post-acute COVID-19 syndrome. Furthermore, we discuss the epidemiology, putative mechanisms, treatment options, and future directions for clinical and basic research in this novel clinical syndrome.Go to:

Post-Acute COVID-19 Syndrome

Post-acute COVID-19 syndrome is defined as symptoms after COVID-19 infection persisting for 4-12 or >12 weeks.2 The prevalence of post-acute COVID-19 syndrome remains difficult to establish and varies by definition and methodology used. A recently published structural follow-up of Swedish health care workers with mild COVID-19 documented a post-acute COVID-19 syndrome prevalence of 10%.5 The longest follow-up study to date of hospitalized patients reports that >60% suffer fatigue or muscle weakness at 6 months follow-up.3 Given the extremely high number of reported cases and the uncertain long-term prognosis, post-acute COVID-19 syndrome is likely to become a major clinical problem for the foreseeable future.

Unfortunately, post-acute COVID-19 syndrome remains a poorly defined clinical syndrome. Typical symptoms include headache, fatigue, dyspnea, and mental blurring, but a very extensive list of symptoms reflecting involvement of multiple organs have been reported. Moreover, the type of symptoms reported may differ vastly among individuals with post-acute COVID-19 syndrome. In addition, symptoms are likely to be caused by several different mechanisms. All of this taken together suggests that post-acute COVID-19 syndrome should not be considered a single clinical syndrome but rather a uniting term characterized by different sub-syndromes and phenotypes.6Go to:

Post-COVID-19 Tachycardia Syndrome as a Sub-Syndrome or Phenotype of Post-Acute COVID-19 Syndrome

In our experience, approximately 25%-50% of patients at a tertiary post-COVID multidisciplinary clinic report tachycardia or palpitations persisting 12 weeks or longer. Systematic investigations suggest that 9% of post-acute COVID-19 syndrome patients report palpitations at 6 months.3

We and others have recently presented case reports describing patients with postural orthostatic tachycardia syndrome associated with post-acute COVID-19 syndrome.4 , 7 This syndrome is characterized by sinus tachycardia and symptoms of orthostatic intolerance. Inappropriate sinus tachycardia can also be triggered by infections (and associated conditions) and shares some clinical features with postural orthostatic tachycardia syndrome.8 Importantly, apart from the evident tachycardia, both these conditions are characterized by other non-specific symptoms such as headache, fatigue, and cognitive impairment, resembling symptoms reported in post-acute COVID-19 syndrome.

Moreover, Holter electrocardiogram (ECG) monitoring and measures of heart rate during different physiological challenges may not correlate to reported symptoms in post-acute COVID-19 syndrome, that is, patients with and without abnormally elevated heart rate may share several symptoms and there is no typical symptom strongly linked to the presence or absence of tachycardia in post-acute COVID-19 syndrome.

Together, this suggests that tachycardia is a common feature in post-acute COVID-19 syndrome and it may clinically present as postural orthostatic tachycardia syndrome or inappropriate sinus tachycardia. We suggest that persistent symptomatic tachycardia may be a sub-syndrome or specific phenotype of post-acute COVID-19 syndrome, and propose to label it “post-COVID-19 tachycardia syndrome.”

Potential distinctions and overlaps among post-acute COVID-19 syndrome, other sub-syndromes and post-acute COVID-19 syndrome, as well as postural orthostatic tachycardia syndrome, inappropriate sinus tachycardia, and sinus tachycardia in post-COVID-19 tachycardia syndrome are displayed in Figures 1 A and B, respectively.

Figure 1

Figure 1

Potential distinctions and overlaps between post-COVID tachycardia syndrome and other sub-syndromes in post-acute COVID-19 syndrome. COVID = coronavirus disease.

Moreover, tachycardia can be considered a universal and easily obtainable quantitative marker of post-acute COVID-19 syndrome and its severity rather than patient-reported symptoms, blood testing, and thoracic computed tomography scans. Not only does it reflect autonomic dysfunction, chronic inflammation, possible myocardial injury, or neurophysiological distress, but may reveal the general status of the patient being unhealthy. Holter ECG monitoring and the plethora of mobile personal heart rhythm tracking devices may facilitate diagnosis and treatment monitoring in outpatient settings.Go to:

Putative Mechanisms for Symptomatic Tachycardia in Post-COVID-19 Tachycardia Syndrome

Postural orthostatic tachycardia syndrome is characterized by autonomic dysfunction causing a variety of symptoms, including tachycardia following postural change.9 It has previously been documented that viral infections can trigger postural orthostatic tachycardia syndrome.10 The pathophysiological mechanism in postural orthostatic tachycardia syndrome remains elusive but there is evidence of autoimmunity, that is, autoantibodies activating adrenergic and muscarinic receptors;11 a hyper-adrenergic state;12 peripheral denervation, similar to taste and smell loss, causing blood pooling in the lower extremities; and reflex tachycardia13 and deconditioning.9 In addition, magnetic resonance imaging studies revealed lesions in the midbrain, suggesting that central sympathetic activation may be involved as well.14 All these mechanisms may contribute to tachycardia in postural orthostatic tachycardia syndrome. Whether the same mechanisms are responsible for post-acute COVID-19 syndrome-associated postural orthostatic tachycardia syndrome and to what extent they contribute to post-COVID-19 tachycardia syndrome remain to be established.

Inappropriate sinus tachycardia is defined as an average heart rate exceeding 90 beats per minute on 24-hour ECG monitoring or a resting heart rate >100 beats per minute, and may have several causes, such as gain-of-function mutation in the cardiac pacemaker HCN4 channel,15 cardiac intrinsic sinus node abnormality, autoimmunity, excess sympathetic activation, or vagal withdrawal.8 Clearly, several pathophysiological mechanisms are shared between postural orthostatic tachycardia syndrome and inappropriate sinus tachycardia, but the mechanism for inappropriate sinus tachycardia in the context of post-acute COVID-19 syndrome needs to be established.

Regarding tachycardia in post-acute COVID-19 syndrome, there may be several other factors contributing to the observed heart rate elevation. SARS-CoV-2 enters cells by attaching its spike protein to the angiotensin-converting enzyme 2 receptor, which is abundant in several different cell types and tissues, and the virus therefore can cause injury in several organs.16 Structural injury to the lungs, kidneys, pancreas, and heart have been reported in COVID-19, acutely as well as months after the occurrence of first symptoms, also in low-risk non-hospitalized patients.17 , 18 In addition, COVID-19 may damage the cardiovascular system by other mechanisms such as hyperinflammation, hypercoagulability with thrombosis, and dysfunction of the renin-angiotensin-aldosterone system.19 , 20 These factors may contribute to the observed and reported tachycardia in post-acute COVID-19 syndrome.

In addition to direct and indirect damage caused by the viral infection, there may be several other mechanisms contributing to post-COVID-19 tachycardia syndrome, for example: 1) Persistent pulmonary injury or exacerbation of underlying lung disease causing desaturation and reflex tachycardia;21 2) persistent or intermittent fever, which may increase heart rate;3 3) pain; 4) anxiety and depression;3 5) neuroinflammation; and 6) hypovolemia. Given the novelty of the disease and the lack of basic and clinical data, several unknown mechanisms may also play a role in post-COVID-19 tachycardia syndrome.Go to:

Proposed Cardiovascular Assessment in Patients with Post-COVID-19 Tachycardia Syndrome

We suggest liberal use of at least basic cardiovascular assessment in patients with post-acute COVID-19 syndrome to identify patients with post-COVID-19 tachycardia syndrome (and associated postural orthostatic tachycardia syndrome and inappropriate sinus tachycardia). A 24-hour ambulatory ECG is recommended to detect arrhythmias, assess average heart rate, detect abnormal pulse reactions, and link symptoms to heart rate abnormalities. Figure 2 displays 2 ECGs from patients who meet the criteria of post-acute COVID-19 syndrome. The first ECG (Figure 2A) shows short runs of symptomatic sinus tachycardia (marked with orange arrows) and a typical excessive increase in heart rate in the morning when shifting from bedrest to upright body position (green arrow). These are 24-hour ECG patterns raising suspicion of postural orthostatic tachycardia syndrome. The second ECG shows an elevated average sinus rate of 93 beats per minute, which is consistent with inappropriate sinus tachycardia.

Figure 2

Figure 2

Examples of 24-hour Holter electrocardiogram monitoring from patients with post-COVID tachycardia syndrome due to (A) postural orthostatic tachycardia syndrome and (B) inappropriate sinus tachycardia. COVID = coronavirus disease.

Patients with Holter ECG findings suggestive of postural orthostatic tachycardia syndrome or presenting with symptoms of orthostatic intolerance should optimally perform a head-up tilt test or, at least, an active standing test to confirm the diagnosis.9 A 30-beat-per-minute increase in heart rate within the first 10 minutes of head-up tilt or active standing test without concomitant blood pressure decrease and with reproduction of symptoms is diagnostic of postural orthostatic tachycardia syndrome.9

A transthoracic echocardiogram should be performed to exclude cardiac abnormalities.

Cardiovascular magnetic resonance (CMR) studies have reported a prevalence of myocarditis ranging from 27%-60% in patients recovering from COVID-19.17 , 22 Because perimyocarditis may cause tachycardia, we argue that CMR should be considered in the setting of typical or atypical chest pain, elevated cardiac biomarkers, or typical ECG changes. Moreover, CMR should be performed when cardiovascular autonomic testing did not lead to a diagnosis of cardiac autonomic disturbance (postural orthostatic tachycardia syndrome or inappropriate sinus tachycardia), and the patient reports abnormal or rapid heartbeats.

Blood tests are recommended also, to evaluate extracardiac causes of tachycardia (autoimmune biomarkers, endocrine tests, inflammation biomarkers, autoimmune biomarkers, and hemoglobin levels). Pulmonary pathology is a common source of tachycardia, and basic evaluation should also include peripheral oxygen saturation (at rest and during physiological stress, such as a 6-minute walk test), thoracic computed tomography scan, and spirometry.Go to:

Possible Treatment for Post-COVID Tachycardia Syndrome

Current treatment of postural orthostatic tachycardia syndrome includes the selective sinus node inhibitor ivabradine,23 beta-blockers,9 and compression garments24 to stabilize cardiovascular regulation. Other pharmacological options to reduce associated symptoms are midodrine (symptoms of low blood pressure or cerebral hypoperfusion; peripheral blood pooling), pyridostigmine (muscle weakness; associated gastrointestinal dysfunction) and modafinil (brain fog).25 A structured, regular, and supervised rehabilitation program is also recommended.25 Immunomodulation and drugs targeting possible associated mast cell activation syndrome have not been systematically evaluated in postural orthostatic tachycardia syndrome, but might be considered ex iuvantibus if the typical clinical manifestation is present.26

Although postural orthostatic tachycardia syndrome in the context of COVID-19 may be different from the “traditional” postural orthostatic tachycardia syndrome (pre-COVID-19), we suggest starting patients with post-acute COVID-19 syndrome and postural orthostatic tachycardia syndrome on heart rate-lowering drugs and a rehabilitation program. Other pharmacological interventions may also be considered but should be carefully monitored.

Whether patients with post-COVID-19 tachycardia syndrome are responsive to heart rate-lowering drugs and other symptomatic treatment previously used in postural orthostatic tachycardia syndrome remains to be established.Go to:

Future Endeavors

Basic and clinical research programs to characterize post-COVID-19 tachycardia syndrome and determine similarities and disparities with other sub-syndromes of post-acute COVID-19 syndrome are highly warranted. A clear aim should be to improve our understanding of the pathophysiology of long-term post-COVID-19 complications and to find novel targets for interventions that may provide disease-modifying effects rather than focusing on pure symptom control.

We therefore call for large registries containing both clinical data and biomarkers, and interventional studies testing the efficacy of drugs used previously in traditional postural orthostatic tachycardia syndrome, alone or in combination with experimental drugs targeting putative mechanism in post-COVID-19 tachycardia syndrome.Go to:


We highlight the phenomenon of abnormal sinus tachycardia in patients with post-acute COVID-19 syndrome. We propose that post-COVID-19 tachycardia syndrome should be considered a phenotype or sub-syndrome of post-acute COVID-19 syndrome. This provides a safety net for those who have multiple symptoms besides the tachycardia and who subsequently may not even mention this to their health care provider.

Post-COVID-19 tachycardia syndrome may present as postural orthostatic tachycardia syndrome or inappropriate sinus tachycardia, and likely contributes to several symptoms and the physical and mental disabilities in post-acute COVID-19 syndrome. Future studies should focus on biological and clinical characterization of this novel clinical syndrome and interventional studies, testing established and novel pharmacological approaches.Go to:


Funding: None.

Conflicts of Interest: None.

Authorship: All authors had access to the data and have read and approved the final version of the manuscript.Go to:


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COVID-19: A Mitochondrial Perspective

Authors: Pankaj Prasun 1

Coronavirus disease 2019 (COVID-19) is the worst public health crisis of the century. Although we have made tremendous progress in understanding the pathogenesis of this disease, a lot more remains to be learned. Mitochondria appear to be important in COVID-19 pathogenesis because of its role in innate antiviral immunity, as well as inflammation. This article examines pathogenesis of COVID-19 from a mitochondrial perspective and tries to answer some perplexing questions such as why the prognosis is so poor in those with obesity, metabolic syndrome, or type 2 diabetes. Although effective vaccines and antiviral drugs will be the ultimate solution to this crisis, a better understanding of disease mechanisms will open novel avenues for treatment and prevention.

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Covid-19 Story Tip: Brain Fog, Fatigue, Dizziness … Post-COVID POTS Is Real

Authors: Tae Chung, M.D., assistant professor of physical medicine and rehabilitation and neurology at the Johns Hopkins University School of Medicine and director of the Johns Hopkins POTS Program

For almost one year, COVID-19 has impacted the world and taken the lives of many people. While some survivors have fully recovered from this illness, others are still experiencing lingering effects, such as chronic fatigue, brain fog, dizziness and increased heart rate. These survivors have been called “long-haulers,” and experts say some of the symptoms they are experiencing are thought to be caused by postural orthostatic tachycardia syndrome (POTS), a blood circulation disorder.

Some patients may, at first, believe their symptoms are “all in their head,” but Tae Chung, M.D., assistant professor of physical medicine and rehabilitation and neurology at the Johns Hopkins University School of Medicine and director of the Johns Hopkins POTS Program, says “POTS is very real.”

While experts are still researching the long-term side effects of COVID-19, it is clear to experts that some survivors are experiencing the classic signs of POTS as a result of their COVID-19 diagnosis.

Chung says POTS is related to autonomic nerve dysfunction. He explains that the autonomic nervous system is responsible for involuntary control of many of our body functions, such as sweating, pupil movement, bowel movement and blood flow. Many POTS symptoms are thought to be related to inadequate control of blood flow, causing brain fog and dizziness. Chung suspects that COVID-19 may be associated with chronic inflammation in the autonomic nervous system, causing POTS.

For More Information:–post-covid-pots-is-real