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Last Monday, when I called the cardiologist Amy Kontorovich in the late morning, she apologized for sounding tired. “I’ve been in my lab infecting heart cells with SARS-CoV-2 since 6 a.m. this morning,” she said.
That might seem like an odd experiment for a virus that spreads through the air, and primarily infects the lungs and airways. But SARS-CoV-2, the new coronavirus behind the COVID-19 pandemic, can also damage the heart. That much was clear in the early months of the pandemic, when some COVID-19 patients would be hospitalized with respiratory problems and die from heart failure. “Cardiologists have been thinking about this since March,” said Kontorovich, who is based at Mount Sinai. “Data have been trickling in.”
Autopsies have found traces of the coronavirus’s genetic material in the heart, and actual viral particles within the heart’s muscle cells. Experiments have found that SARS-CoV-2 can destroy lab-grown versions of those cells. Several studies have now shown that roughly 10 to 30 percent of hospitalized COVID-19 patients had high levels of troponin—a protein released into the blood when the heart’s muscle cells are damaged. Such patients are more likely to die than others with no signs of heart injury.
This is worrying for people with severe symptoms, but more recently, a few studies suggested that COVID-19 can cause heart inflammation, or myocarditis, even in people who showed mild symptoms, or had recovered. These results were controversial but concerning. Myocarditis is frequently caused by viruses, and resolves on its own in many cases. But it can progress to more severe heart problems, and is one of the leading causes of sudden death in young adults. These studies contributed to decisions by two college football conferences—the Big Ten and the Pac-12—to cancel their fall season. (The Big Ten has since reversed its call, and the Pac-12 is considering doing the same)
These developments have only added to COVID-19’s mystique. News stories and scientific articles have spun a narrative about a bizarre virus that behaves like no other, and a supposedly respiratory illness that should perhaps be reconsidered as a vascular disease. But several cardiologists and virologists I’ve talked with say such claims are overblown. COVID-19 is a severe disease that should be taken seriously, but it’s not all that strange. It seems that way in part because it is new and extremely widespread, and so commands our full attention in the way that most viral illnesses don’t. Hundreds of researchers are studying it. Millions of people have been infected by it. And every study, every news story, and every unusual detail quickens the pulse.
From a virus’s point of view, the heart is both an easy target and a terrible one. It is easy to reach and invade because it collects blood from all over the body and, unlike the brain, has no protective barrier. But infecting the heart also risks killing the host without triggering symptoms that would allow a virus to easily spread—coughing, sneezing, diarrhea, or vomiting. For that reason, viruses that affect only the heart “do not exist,” says Efraín Rivera-Serrano, a virologist at the University of North Carolina at Chapel Hill.
But viruses can incidentally affect the heart. They do so often enough that in the Western world, they are the most common cause of myocarditis. At least 20 known viruses can trigger this condition, including those that cause influenza, Zika, dengue, and measles.
The list also includes the original SARS virus: One Toronto-based study found its genetic material in seven of 20 autopsied hearts. These hearts also had myocarditis. By contrast, autopsied hearts with traces of the new coronavirus typically don’t (with some exceptions). The virus was there, but whether it was actually doing anything is unclear.
But a virus doesn’t need to be in the heart to wreak havoc. It can cause indirect damage by attacking the lungs and starving the heart of oxygen, or by triggering an inflammatory immune response that affects the entire body. Even viruses that primarily affect the gut (like enteroviruses) or the respiratory system (like adenoviruses) can cause myocarditis in this way, when molecules produced at the site of infection travel through the bloodstream and inflame the heart. Coxsackie B, for example, is the most widely studied cause of viral myocarditis, but is primarily a gut virus that spreads through fecal contamination; it can infect the heart, but it does much of its damage via the immune system.
“To say a virus is cardiac or vascular or respiratory simplifies things too much,” says Paul Checchia, a cardiologist at Texas Children’s Hospital. “Anytime a pathogen invades the body, the whole body reacts.” SARS-CoV-2 is no exception. The immune system’s response to this coronavirus can be slow to kick off, but then prolonged and severe. These immune overreactions are similar in kind to those triggered by other respiratory viruses, like influenza, but greater in degree. The heart could potentially be caught in this stronger crossfire.
But how often does that happen? In the early months of the pandemic, it seemed clear that the risk of heart injuries was “directly proportional to the severity of the illness,” says Neel Chokshi, a sports cardiologist at the University of Pennsylvania. But in July, a team led by Valentina Puntmann at University Hospital Frankfurt, in Germany, complicated that picture. The researchers showed that 78 percent of people who had recovered from COVID-19 (including many who had never been hospitalized) still had some kind of heart abnormality that was detectable on MRI scans two months later. About 60 percent still had signs of myocarditis.
The study was explosive. It spawned a wave of articles and papers about the possibility that COVID-19 could inflict stealthy and prolonged harm upon the hearts of people who aren’t outwardly sick, and reportedly influenced decisions about whether college athletes should be allowed to play. These intense discussions sparked intense criticism. Other scientists slammed the study for several errors, including data that were missing, reported incorrectly, or analyzed with the wrong statistical tests. The Frankfurt team corrected its paper, and says the main conclusions still stand.
“I think the data are good,” says Tiffany Chen of Penn Medicine, who specializes in cardiac imaging and was not involved in the study. “These were relatively healthy, mild cases of COVID-19, and they had a lot of abnormalities. It’s unsettling.” But the clinical implications of these findings—what they mean for COVID-19 patients whose symptoms have abated, but whose MRI scans are abnormal—aren’t yet understood, she says.
Viral myocarditis isn’t always a problem. It’s entirely possible that you have had the condition at some point in your life without ever realizing it. Some people recover but have persistent scarring that weakens their heart and increases the risk of problems years down the line. And in a third group, the inflammation rapidly worsens, leading to faulty heartbeats, heart failure, or even death.
The latter two outcomes are rare, but “it’s really hard to give accurate percentages,” says Chokshi. Doctors typically see cases of viral myocarditis only when they fall into the third group, and severe symptoms warrant MRIs and other diagnostic tests. “We don’t do MRIs on everyone who has the flu, so we don’t know how many have inflammation or what their long-term outcomes are,” says Martha Gulati, the cardiology chief at the University of Arizona. For example, in two small pilot studies, Checchia found signs of heart damage in 40 and 55 percent of children who were hospitalized with RSV—a common respiratory virus. “On discharge, they seemed perfectly fine,” he says. “But we couldn’t get funding to look at them months or years down the line.”
Without that information, it’s hard to know what to make of the Frankfurt COVID-19 study or others like it. Yes, some patients have myocarditis—but what does that mean? How do the numbers compare to other respiratory viruses? Will COVID-19 patients with myocarditis recover fully, or will some have long-term problems? Is this virus doing something strange, or are researchers just studying it more intensely than other viral infections? For now, it’s difficult to say.
The worry is that COVID-19 is doing whatever it’s doing at scale. The original SARS epidemic of 2003 infected only 8,000 people, killed slightly fewer than 800, and was over in three months; its impact on the heart was “lost in the historical bin of the scientific literature,” says Checchia. SARS-CoV-2, by contrast, has infected at least 31 million people and killed at least 960,000. Its effects are thousands of times more obvious than its predecessor’s. Even if it’s no worse than any other viral illness, its sheer scope means that a tiny risk of severe long-term problems would still translate to a lot of failing hearts.
Reassuringly, “there hasn’t been an obvious influx of patients being admitted to the hospital with unexplained myocarditis, despite the huge numbers who have had COVID-19,” says Venkatesh Murthy, a cardiologist at the University of Michigan. “I don’t find it convincing that there is a major amount of serious clinically relevant myocarditis in people who are feeling well.”
Still, he and others say that long-term studies are important. “We’re still early,” says Chen. “I don’t think there’s a defined time point when we’d expect to see heart failure, so we have to follow these patients for months or years down the road.”
That can be unnerving for people who are currently sick. Long-haulers, who are struggling with months of debilitating COVID-19 symptoms, are “responding to the media’s interpretation of these studies and, to put it bluntly, are rightfully freaking out,” said Kontorovich, who is part of a team that provides care for long-haulers. But for now, she sees the myocarditis issue and the long-hauler phenomenon as separate matters.
Some long-haulers have been diagnosed with dysautonomia—a group of disorders that disrupt involuntary bodily functions, including heartbeats (which can become inexplicably fast) and blood pressure (which can suddenly crash). But people who have lingering heart problems after viral myocarditis don’t usually experience the chronic symptoms that long-haulers do, and they typically have measurable changes to their hearts that long-haulers don’t. “There may be a connection, but it hasn’t been proved,” Kontorovich said.
College athletes are also facing immediate decisions. In just the past two months, the 27-year-old basketball player Michael Ojo died from a heart attack during a practice, while the 20-year-old football player Jamain Stephens Jr. died from a blood clot in his heart. Both had previously contracted COVID-19.
In a recent study, a research team at the Ohio State University scanned the hearts of 26 college athletes who tested positive for COVID-19 and had mild or absent symptoms. Four of them—15 percent—had signs of myocarditis. But the Ohio study didn’t examine a control group of similar athletes who didn’t have COVID-19, and even healthy athletes experience changes in their heart as they train, including features that are “similar to what you might see with infections or scarring,” says Gulati, the cardiologist at the University of Arizona.
If athletes come down with clinical myocarditis—that is, with obvious signs of heart problems—they’re taken out of play for at least three months to let the infection run its course and to give the heart a chance to bounce back. The question now is: What to do about the people who have subclinical myocarditis after COVID-19, which presents with no symptoms and can be seen only on a medical scanner? Chokshi, the sports cardiologist, says the risk that these abnormalities will lead to heart failure “is very, very low,” but “the outcome is catastrophic.” The American College of Cardiology published guidance advising that all athletes who test positive for COVID-19 rest for at least two weeks, even if they show no symptoms.
Setting myocarditis aside, it still makes sense to stop players from spreading the virus to one another, especially when so many colleges are facing large outbreaks. “There are plenty of reasons to not play football independent of this issue,” Murthy says. “We already have plenty of evidence to take COVID-19 seriously.”
As pandemics get wider, they feel weirder. Ebola was identified in 1976, but its ability to affect eyes, linger in semen, and afflict survivors with long-term complications wasn’t fully appreciated until it infected 28,000 people in West Africa, from 2014 to 2016. Zika was identified in 1947, but its ability to cause microcephaly—a condition where babies are born with small heads—wasn’t noted until the explosive epidemic of 2015.
When millions of people become infected, rare events become commonplace, and phenomena that might typically have gone unnoticed suddenly become prominent. This creates a deceptive sense that the disease in question is stranger than most, and has uprooted the world because there’s something inherently odd about it.
COVID-19 is different only in that everyone is encountering it for the first time during a pandemic. The world has gone from complete ignorance to an onslaught of detail in a matter of months, and those details can seem jarring. The virus affects the heart. Also, the brain. Odd symptoms. A multisystem inflammatory syndrome in children. Cases of reinfection. Some of these phenomena will be particular to SARS-CoV-2. Others would also show up if any new virus infected millions within months.
This is not to downplay the severity of the pandemic. Some claims about COVID-19’s effect on the heart may be overwrought, but that doesn’t mean the virus is harmless. Conversely, the claims that COVID-19 is equivalent to the flu are clearly wrong, but that doesn’t mean anything goes. The reality lies between this false dichotomy and is still grim, as evidenced by the sheer number of infections, deaths, and lingering disabilities. “It’s hard to find a balance,” says Rivera-Serrano. “It’s not an apocalyptic zombie virus that’s so different from everything else and can suddenly do all these things to the body. But you also don’t want to trivialize what is happening.”
Indeed, by bringing underappreciated aspects of viral infections to light, COVID-19 might help to change our understanding of diseases in general. The long-term consequences of viral myocarditis, for example, are still unclear, because “it can be really hard to identify hundreds of people who have all been exposed to the same virus in a relatively short amount of time,” Murthy says. That’s no longer true. And beyond making studies possible, the pandemic also clarifies that such studies are worthwhile. “We have a mindset that this is a problem we need to work on,” Murthy adds.
The heightened focus on COVID-19 allows hype and sensationalism to flourish, but also shines a spotlight on phenomena that have long been consigned to the shadows. For example, many of the lingering symptoms that long-haulers are facing are similar to known chronic conditions such as dysautonomia and myalgic encephalomyelitis, which can be triggered by other viral infections. These illnesses have been dismissed and trivialized for decades. Few doctors know how to deal with them. Few scientists study them. That might change as thousands of people with similar problems are emerging all at once, and are pushing for recognition and research. In a pandemic, experiences that might once have been dismissed grab attention. Perhaps that tells us they should never have been dismissed at all.
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