Beyond its scientific backing, the notion that a COVID-19 patient might wind up with long-term lung scarring or breathing issues has the ring of truth. After all, we hear the stories, right? The virus can leave survivors explaining how they struggled to breathe, or how it can feel, in the words of actress Alyssa Milano, “like an elephant is sitting on my chest.”
We’ve also known for a while that some COVID-19 patients’ hearts are taking a beating, too—but over the past few weeks, the evidence has strengthened that cardiac damage can happen even among people who have never displayed symptoms of coronavirus infection. And these frightening findings help explain why college and professional sports leagues are proceeding with special caution as they make decisions about whether or not to play.
From an offensive lineman at Indiana University dealing with possible heart issues to a University of Houston player opting out of the season because of “complications with my heart,” the news has been coming fast and furiously. More than a dozen athletes at Power Five conference schools have been identified as having myocardial injury following coronavirus infection, according to ESPN; two of the conferences—the Big Ten and the Pac-12—already have announced they are postponing all competitive sports until 2021. And in Major League Baseball, Boston Red Sox ace pitcher Eduardo Rodriguez told reporters that he felt “100 years old” as a result of his bout with COVID, and of MLB’s shortened season because of myocarditis—an inflammation of the heart muscle, often triggered by a virus. Said Rodriguez: “That’s [the heart is] the most important part of your body, so when you hear that … I was kind of scared a little. Now that I know what it is, it’s still scary.”
Why are these athletes (and their leagues and conferences) taking such extreme precautions? It’s because of the stakes. Though it often resolves without incident, myocarditis can lead to severe complications such as abnormal heart rhythms, chronic heart failure and even sudden death. Just a few weeks ago, a former Florida State basketball player, Michael Ojo, died of suspected heart complications just after recovering from a bout of COVID-19 in Serbia, where he was playing pro ball.
Here’s the background: Myocarditis appears to result from the direct infection of the virus attacking the heart, or possibly as a consequence of the inflammation triggered by the body’s overly aggressive immune response. And it is not age-specific: In The Lancet, doctors recently reported on an 11-year-old child with multisystem inflammatory syndrome (MIS-C)—a rare illness—who died of myocarditis and heart failure. At autopsy, pathologists were able to identify coronavirus particles present in the child’s cardiac tissue, helping to explain the virus’ direct involvement in her death. In fact, researchers ((HAS NO LINK)) are reporting the presence of viral protein in the actual heart muscle, of six deceased patients. Of note is the fact that these patients were documented to have died of lung failure, having had neither clinical signs of heart involvement, nor a prior history of cardiac disease.
Ossama Samuel, associate chief of cardiology at Mount Sinai Beth Israel in New York, told me about a cluster of younger adults developing myocarditis, some of them a month or so after they had recovered from COVID-19. One patient, who developed myocarditis four weeks after believing he had recovered from the virus, responded to a course of steroid treatment only to develop a recurrence in the form of pericarditis (an inflammation of the sac surrounding the heart). A second patient, in her 40s, now has reduced heart function from myocarditis, and a third—an athletic man in his 40s—is experiencing recurring and dangerous ventricular heart rhythms, necessitating that he wear a LifeVest defibrillator for protection. His MRI also demonstrates fibrosis and scarring of his heart muscle, which may be permanent, and he may ultimately require placement of a permanent defibrillator.
This is an incredibly tricky diagnosis. Patients with myocarditis often experience symptoms like shortness of breath, chest pain, fever and fatigue—while some have no symptoms at all. J.N., a health care provider who asked that his full name not be used, told me that COVID-19 symptoms first appeared in his case in late March. He ultimately was hospitalized at Mount Sinai Medical Center after developing unrelenting fevers spiking to 104 degrees, chest tightness, nausea, vomiting and diarrhea.
“Even the Advil and acetaminophen wouldn’t help my fevers,” said J.N. Just 34 years old, he was diagnosed with COVID-induced myocarditis and severe heart failure. Doctors admitted him to the intensive care unit and placed him on a lifesaving intra-aortic balloon pump due to the very poor function of his heart. He spent two weeks in the hospital, has suffered recurrences since his discharge, and now says, “I’m very careful. I’m very concerned about the length of time I’ve been feeling sick, and if these symptoms are lifelong or will go away anytime soon.” J.N. said that everyday activities, like carrying his one-year-old daughter up a flight of stairs, leave him feeling winded and fatigued. He has been unable to work since March.
According to some reports, as many as 7 percent of deaths from COVID-19 may result from myocarditis. (Others feel that estimate is too high.) The arrhythmia that sometimes accompanies it is also worrisome, and researchers have found that to be fairly common among COVID-19 patients. In J.N.’s case, he noticed his heart racing on several occasions into the 130 beats per minute range. And while the prevalence of this in virus patients is not known exactly, a study found that ventricular arrhythmias occurred in 78 percent of patients without COVID-19, with up to 30 percent of them experiencing serious arrhythmias 27 months later.
Experts estimate that half of myocarditis cases resolve without a chronic complication, but several studies suggest that COVID-19 patients show signs of the condition months after contracting the virus. One non–peer reviewed study, involving 139 health care workers who developed coronavirus infection and recovered, found that about 10 weeks after their initial symptoms, 37 percent of them were diagnosed with myocarditis or myopericarditis—and fewer than half of those had showed symptoms at the time of their scans.
Any such cardiac sequelae lingering weeks to months after the fact is clearly concerning, and we’re seeing more evidence of it. A German study found that 78 percent of recovered COVID-19 patients, the majority of whom had only mild to moderate symptoms, demonstrated cardiac involvement more than two months after their initial diagnoses. Six in 10 were found to have persistent myocardial inflammation. While emphasizing that individual patients need not be nervous, lead investigator Elike Nagel added in an e-mail, “My personal take is that COVID will increase the incidence of heart failure over the next decades.”
Taking on myocarditis is a chore. Thankfully, some acute cases resolve on their own, requiring only hospital monitoring and possibly some heart medications. We’ve learned that steroids and immunoglobulins—useful elsewhere—aren’t effective in acute viral myocarditis, although Samuel said there may be a role for steroids in younger COVID-19 patients who seem to present with more of an autoimmune type of the condition. And, of course, an effective vaccine could help prevent cases in the first place.
Samuel called it “extremely dangerous” for athletes diagnosed with myocarditis to play competitive sports for at least three to six months, because of the risk of serious arrhythmia or sudden death, and several athletes already have made the decision to heed those dire warnings. We’ll likely see more such decisions in the very near future, as each sport enters its peak season.
And for the rest of us? Wear a mask, social distance, avoid large gatherings, and spend more time in the great outdoors. I would echo the advice of J.N.: “Be careful. Just don’t get the virus in the beginning.” As of today, it’s still the best defense we’ve got.