Brady Feeney hadn’t even taken any classes at Indiana University when he fell ill with Covid-19. Three weeks after he moved to Bloomington, the incoming freshman was in the emergency room, struggling to breathe. Before his illness, Feeney had been a perfectly healthy teenager, with no preexisting conditions. In high school, he was a three-time all-state football player and won two state titles in Missouri. But after two weeks of “hell” fighting the virus, his mother said, his bloodwork indicated possible heart problems.
When SARS-CoV-2 first struck the United States, the medical community had two working assumptions: First, this was primarily a respiratory disease, and second, it seemed to hit older people much harder than younger people, with eight out of 10 confirmed Covid-19 deaths in the U.S. happening in adults 65 or older. But now, new research is challenging both of these assumptions.
Growing evidence suggests that SARS-CoV-2 doesn’t only infect the lungs. It also affects the brain, kidneys, and heart. At first, doctors and researchers wondered if these issues beyond the lungs came just from the stress of having Covid-19 and being on a ventilator or life support. But increasingly, research indicates that the virus may be attacking other organs in the body directly—and this may be more common than previously thought, even among those who aren’t sick enough to be hospitalized. Some have suggested that Covid-19 is actually a blood vessel disease; the lungs are merely the way the virus enters the body, but from there it gets into the bloodstream and takes up residence in major organs, leaving patients with complex, long-lasting symptoms. Moreover, experts now believe, healthy young people can get mild cases of the coronavirus—even not knowing they were sick—that could leave them with lasting cardiovascular damage. Even those who seem to have recovered from the deadly respiratory illness are not free of its complications.
Heart failure could be “the next chapter” of the coronavirus illness, Dr. Gregg C. Fonarow, interim chief of UCLA’s Division of Cardiology, recently argued in a co-authored editorial in the journal JAMA Cardiology. “Even if in younger adults Covid-19 may not be fatal, there still may be important health consequences,” he told me.
Myocarditis, or inflammation of the heart, is usually a rare condition that can occur with viral infections, including the flu. But from the start of the pandemic, doctors were seeing heart inflammation among patients hospitalized with serious cases of Covid-19, Fonarow said: Early research showed that 20 to 30 percent of those hospitalized had heart issues. Left untreated, myocarditis can damage the heart and lead to heart attacks and arrhythmias, among other complications.
In one preliminary study from Europe, presented at an online respiratory conference in early September, nearly 50 percent of Covid-19 patients discharged from the hospital had heart dysfunction six weeks later. Another study of 100 people in Germany found that 78 percent of recovered Covid-19 patients had heart issues two to three months later, and most—60 percent—of those issues involved myocardial inflammation. Perhaps most troubling, these conditions weren’t related to the severity of the respiratory illness or preexisting conditions.
One of the first indications of how widespread coronavirus-related heart issues may be came from athletes, whose health is monitored even when there isn’t a pandemic. The preliminary results of one study revealed that nearly 15 percent of college athletes who recovered from Covid-19 had myocarditis—and nearly all of them had mild or no symptoms. This news is surprising not just because athletes tend to be very physically active. It could signal that many people—even healthy young people with no preexisting conditions—are vulnerable to coronavirus-induced heart issues, and they may not even know they have had it.
While myocarditis goes away in some people, in others it can leave permanent damage and lead to a rise in arrhythmias, heart attacks, blood clots, and strokes. These conditions may greatly affect quality of life for months or years, and they’re potentially fatal even among young people.
On August 7, Michael Ojo, a 27-year-old professional basketball player in Europe, died of a heart attack during practice after a monthlong case of Covid-19. A few days later, the Big Ten and Pac-12 football conferences canceled their fall season in large part because of rising concerns about myocarditis, which already causes 2 to 5 percent of sudden deaths among American athletes.
Yet other divisions have played on. Lincoln Riley, the head coach of the University of Oklahoma’s football team, told reporters on Tuesday that the team would stop publicly releasing Covid-19 results, citing the “competitive advantage” of others not knowing how many players are sick. Also on Tuesday, Jamain Stephens Jr., a 20-year-old defensive tackle at the California University of Pennsylvania and the son of an NFL offensive tackle, died suddenly. A week before his death, he told friends he had tested positive for Covid-19.
Findings on the long-term effects of the coronavirus upon athletes may serve as a barometer for how common these conditions are among other young people. “What’s not known is what percentage of individuals this will impact,” Fonarow told me. “But even if it’s a very small percentage, with millions of individuals coming down with Covid-19, it really raised the concerns even in younger individuals without preexisting conditions that they could develop heart damage related to Covid-19.” Further research is needed to determine how serious and long-lasting the damage may be.
Other research on Covid-19 and hearts, some of it preliminary, is even more troubling. It’s possible that some of the cardiovascular change is actually cell death, similar to what happens in a heart attack. One study from Germany published in July, for instance, found that 24 of 39 autopsied patients who died from Covid-19 had heart cells heavily infected with the coronavirus.
That result made sense, said Todd McDevitt, when he saw what happened to heart cells ravaged by SARS-CoV-2 in a petri dish. McDevitt was part of a team of researchers at the University of California, San Francisco’s Gladstone Institute of Cardiovascular Disease that in late August posted a preprint study, which has not been peer-reviewed or published by a journal, to further the discussion of the ways the coronavirus affects heart cells and to see what other researchers were finding. “We started to see some very odd behaviors,” he told me. “It’s not that all the cells are gone right away. They’re undergoing this process where their insides are being chewed up.” From the outside, the cells looked mostly fine. But inside, they were shredded—“chopped up,” McDevitt said.
A petri dish of heart stem cells is not the same as a real organ in a real human body, so there are limitations to their study. But the consistent damage to the cells in the lab, McDevitt said, aligns with the research on patients and suggests that if the coronavirus finds its way to your heart, it doesn’t seem to let go easily. “This could explain why someone who maybe initially didn’t have signs of heart damage recovers, but then months later is complaining of either chest pains, racing heart, some of the things that are starting to become noticed,” McDevitt said.
What researchers would like to know next is how the virus enters the heart, how much it damages it, and how permanent the damage is. Typically, heart muscle cannot heal itself: Once it’s damaged, the damage is permanent. But, McDevitt said, the way the coronavirus enters the heart muscle is something researchers haven’t seen before. “This is a different injury. Maybe the heart can recover from this. Because if the cell isn’t just dying right away, and if the virus passes, then maybe there is some ability to restore those muscle fibers,” he said. But it’s too soon, and there’s too little data, to know now if that’s the case.
What they’re seeing so far alarms McDevitt. “I am way more scared of this virus now than I was four months ago,” he said. If the virus does indeed damage cells in real life the way it does in the lab, precautions against the virus need to be taken even more seriously—even or especially among younger, healthier people who previously thought the virus wouldn’t harm them.
“If people think that it’s a respiratory [virus] and I can recover from this and get over it, it’s a little different message than if you tell someone that there’s a chance that you could suffer some permanent damage,” McDevitt said. So far, his research has looked at the heart. “But what if it is in your brain; what if it is in other tissues that have a tougher time for regenerating?”
Brady Feeney, the incoming freshman at Indiana now facing heart complications, is eager to get healthy and get back to the football field. But first, he wants to recover fully—and he wants other people his age to understand the wide-ranging toll the coronavirus can take on anyone. “Covid-19 is serious,” he said on Monday on Twitter. “We need to listen to our medical experts.’’