British science journalist Ed Yong in the material for The Atlantic writes about how COVID-19 will change our understanding of disease in general
Last Monday, when I called cardiologist Amy Kontorovich in the late afternoon, she apologized for her tired voice. “I’ve been in my laboratory, infecting heart cells with SARS-CoV-2 since six in the morning,” she explained.
This may seem like a strange experiment for a virus that spreads through the air and primarily affects the lungs and respiratory tract. But SARS-CoV-2, the new coronavirus behind the COVID-19 pandemic, could also harm the heart. This was clear back in the early months of the pandemic, when some COVID-19 patients were hospitalized with respiratory problems, and they were dying of heart failure. “Cardiologists have been thinking about this since March,” Kontorovich said. “The data is coming in.”
Autopsies found traces of coronavirus genetic material in the heart and real viral particles in the cells of the heart muscle. Experiments have shown that SARS-CoV-2 can destroy laboratory-grown versions of these cells. Several studies have shown that approximately 10% to 30% of hospitalized COVID-19 patients had high levels of troponin, a protein that enters the bloodstream when heart muscle cells are damaged. These patients are more likely to die than those without signs of heart damage.
In terms of a virus, the heart is both an easy target and a terrible target
This is alarming information for people with severe symptoms, but more recently, several studies have shown that COVID-19 can cause heart inflammation or myocarditis, even in people who have had mild symptoms or have recovered. Myocarditis is often caused by viruses and in many cases goes away on its own. But it can progress to more serious heart problems and is one of the main causes of sudden death in young people. These studies contributed to the decision by two college football associations – Big Ten and Pac-12 – to cancel the fall season. (…)
From a virus perspective, the heart is both an easy target and a terrible target. 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 infection of the heart also risks killing the host without causing symptoms that would allow the virus to spread easily – through coughing, sneezing, diarrhea, or vomiting. For this reason, viruses that infect only the heart “do not exist,” says Efrain Rivera-Serrano, a virologist at the University of North Carolina at Chapel Hill.
But the virus doesn’t have to be in the heart to create chaos. It can cause indirect damage by affecting the lungs and putting the heart under oxygen starvation conditions, or by triggering an inflammatory immune response that affects the entire body. (…) “To say that the virus is cardiac, vascular or respiratory is oversimplifying,” says Paul Chekchia, a cardiologist at Texas Children’s Hospital. “Every time 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, but then prolonged and severe. These immune overreactions are similar to those caused by other respiratory viruses such as influenza, but to a greater extent. The heart could potentially get caught in this stronger crossfire.
But how often does this happen? In the early months of the pandemic, it seemed clear that the risk of heart damage «is directly proportional to the severity of the disease, ”says Neil Chokshi, a sports cardiologist at the University of Pennsylvania. But in July, a group led by Valentina Puntmann of the University Hospital Frankfurt in Germany complicated the picture. Researchers have shown that 78% of people who recovered from COVID-19 (including many who had never been hospitalized), there were still cardiac abnormalities that could be detected on an MRI two months later. About 60% still had signs of myocarditis.
The study had the effect of a bomb exploding. It spawned a wave of articles about the possibility that COVID-19 could cause latent and long-term harm to the hearts of people who are not externally ill, and reportedly influenced decisions about whether college athletes should be allowed to compete. These intense discussions drew strong criticism. Other scholars criticized the study for several errors, including missing data that were incorrectly presented or analyzed using incorrect statistical tests. The Frankfurt team revised their article and states that the key findings remain valid.
«I think the data is okay, says Tiffany Chen of the Pennsylvania Medical Center, which specializes in cardiac imaging and was not involved in the study. – These were relatively healthy, mild cases of COVID-19, and they had many anomalies. It worries. ” But the clinical implications of these results – what they mean for COVID-19 patients, whose symptoms have all but disappeared but MRI results show abnormalities – have not yet been studied, she says.
Viral myocarditis is not always a problem. It is possible that at some point in your life you had this condition, but you did not even notice it. Some people recover but they end up with permanent scars that weaken their heart and increase their risk of problems for years to come. In other cases, inflammation quickly worsens, leading to abnormal heart rhythms, heart failure, or even death (…).
Doctors usually see cases of viral myocarditis only when severe symptoms warrant MRI and other diagnostic tests. “We don’t do MRIs for everyone with the flu, so we don’t know how many of them have inflammation and what the long-term consequences are,” says Martha Gulati, head of cardiology at the University of Arizona. For example, in two small pilot studies, Chekchia found signs of heart disease in 40 percent and 55 percent of children hospitalized with RSV, a common respiratory virus. “When they were discharged, they seemed completely normal,” he says. “But we couldn’t get funding to diagnose them in months or years.”
Without this information, it is difficult to know what to do with the Frankfurt COVID-19 study or the like. Yes, some patients have myocarditis, but what does that mean? How do these numbers compare with other respiratory viruses? Will COVID-19 patients with myocarditis recover completely, or will some have long-term problems? Is this virus doing something weird, or are researchers just studying it more intensively than other viral infections? It’s hard to say yet.
The worry is that COVID-19 is doing everything it does on a large scale. The original 2003 SARS epidemic only infected 8,000 people, killed just under 800, and ended three months later; its effect on the heart was «lost in the historical basket of scientific literature, ”says Cekchia. SARS-CoV-2, on the other hand, has infected at least 31 million people and killed at least 960,000. Its impact is thousands of times more evident than that of its predecessor. Even if the disease is as good as any other viral disease, given its magnitude, the tiny risk of serious long-term problems will still show a large number of people with heart problems.
It is encouraging that «there was no apparent influx of patients admitted to the hospital with myocarditis of unclear etymology, despite the huge number of patients with COVID-19, ”says Venkatesh Murthy, a cardiologist at the University of Michigan.
However, he and others say long-term research is important. “We’re still in the early stages,” says Chen. “I don’t think there is a certain point in time when we should see heart failure, so we should watch these patients for months or years.” (…)
In a recent study, a team of researchers from Ohio State University scanned the hearts of 26 college athletes who tested positive for COVID-19 and had mild or no symptoms. Four of them – 15% – had signs of myocarditis. But the Ohio study did not look at a control group of similar athletes who did not have COVID-19, and even healthy athletes experience heart changes during exercise, including those similar to those that «you can see with infections or scarring, ”says Gulati, a cardiologist at the University of Arizona.
If athletes have clinical myocarditis, that is, with clear signs of heart problems, they are taken out of the game for at least three months to allow the infection to go away and give the heart a chance to bounce back. Now the question arises: what to do with people who, after COVID-19, have subclinical myocarditis, which is asymptomatic and can only be detected on a medical scanner? The American College of Cardiology has published a guideline advising all athletes who test positive for COVID-19 to rest for at least two weeks, even if they have no symptoms.
When millions of people become infected, the deceptive feeling arises that the disease in question is stranger than most others, and has turned everything upside down. COVID-19 differs only in that everyone encounters it for the first time. In a matter of months, the world went from complete ignorance to detail. The virus attacks the heart. Also the brain. Strange symptoms. Multisystem Inflammatory Syndrome in Children. Reinfection cases. Some of these phenomena will be specific to SARS-CoV-2. Others will also appear if a new virus infects millions within a few months.
This is not to downplay the severity of the pandemic. Some claims about the impact of COVID-19 on the heart may be exaggerated, but this does not mean that the virus is harmless. Conversely, claims that COVID-19 is equivalent to influenza are clearly wrong. The reality lies between this false dichotomy and is still grim, as evidenced by the sheer number of infections, deaths and chronic diseases. “It’s hard to find a balance,” says Rivera-Serrano. “This is not an apocalyptic zombivirus that is so different from everything else and can suddenly do it all to the body. But you also shouldn’t underestimate what’s going on. “ (…)
Indeed, by highlighting the underrated aspects of viral infections, COVID-19 could help change our understanding of disease in general.
Read the full version at The Atlantic
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