Stories about patients with persistent symptoms following infection with the coronavirus started surfacing in the news during the summer of 2020. “When I heard people describe what they were feeling, they sounded very much like my patients with POTS,” says Tae Chung, a Johns Hopkins physiatrist with a joint appointment in the Johns Hopkins Department of Neurology and Neurosurgery, and director of the Johns Hopkins Postural Orthostatic Tachycardia Syndrome (POTS) Program.

By December 2020, the program had received a flood of referrals for patients exhibiting symptoms similar to those of POTS, after Chung’s colleagues from comparable programs across the country were reporting that they, too, were receiving a large number of patient referrals dealing with POTS-like symptoms.

In October 2020, Chung launched a clinic specifically for patients who were once infected with SARS-CoV-2 — the virus that causes COVID-19 — and who now experience severe fatigue; orthostatic tachycardia, dizziness or intolerance to standing; chronic muscle pain; headache; and nausea, vomiting or irritable bowel syndrome. 

Every flu season, Chung expects to meet new patients — as many as half of all patients with POTS previously had a viral or bacterial infection — but he’s never seen an influx of patients like the one he is seeing now.  

“The virus clearly seems to be affecting the autonomic nervous system,” says Chung, “and we are seeing it manifest in two scenarios.”

These scenarios include patients who begin having POTS symptoms during the acute phase of COVID-19, and patients who don’t present with POTS symptoms until weeks after the acute phase. 

The current proposed pathology for POTS is an inability to regulate blood volume. Researchers suspect that vasomotor denervation causes dilation of the blood vessels, leading to reduced preload to the heart, which triggers an increase in the central sympathetic nervous system response. Resulting symptoms are likely related to inadequate blood circulation and overcompensation by the sympathetic nervous system. 

In collaboration with the Johns Hopkins Post-Acute COVID-19 Team (PACT) service, the Johns Hopkins Division of Infectious Disease and other domestic and international partners, Chung is coordinating research to understand the incidence of POTS after COVID-19 and whether the incidence is the same as after other infections. He also aims to uncover if there is something about the condition that makes people more susceptible to developing POTS, including with regard to the disease’s effect on autoantibodies or on the sympathetic nervous system.  

“The majority of patients in the Post-COVID-19 POTS clinic seem to have had very mild cases of COVID-19, and some were asymptomatic cases,” he says. “If we can understand the relationship between COVID-19 and POTS, it will also help us understand the cause of POTS.”

Chung is concerned about the link between the disease and POTS, but he’s glad that patients are getting a diagnosis, so they can pursue treatment.

“Despite the good research around POTS and the evidence around autonomic nerve damage,” says Chung, “symptoms may be diagnosed as psychological. A lot of people with chronic fatigue and heart palpitations end up in physiatry clinics because they are debilitated. But there are various treatments for POTS that have been effective for many patients.”