After a year of frightening headlines, widespread concern, and countless retweets that the virus that causes Covid-19 may attack the heart more aggressively than any other viral illness, the verdict is in: It doesn’t.
A report published last week in the journal JACC: Cardiovascular Imaging made that verdict blatantly clear.
It’s time to set the record straight on Covid-19 and the heart, and to consider the lessons for how science is communicated to the public.
The concern emerges
An early report that set in motion fears of a Covid-heart disease connection was published in JAMA Cardiology on July 27, 2020. German researchers claimed that 78% of recently recovered Covid-19 patients had “abnormal” signs on their cardiac magnetic resonance scans and 60% showed signs of inflamed heart muscle, a condition known as myocarditis. Those astonishing numbers were covered in nearly 400 news outlets. The report has so far received been viewed more than 900,000 times — a rarity for academic papers.
Soon after its publication, however, the paper was criticized for statistical and methodologic errors. It eventually underwent a long but much quieter correction that indicated that many of the abnormalities were only marginally more common among those recovering from Covid-19 than among similar control individuals who had not had Covid-19.
A few weeks later, on Sept. 11, 2020, a study out of Ohio State University showed that 15% of competitive athletes who had recovered from Covid-19 had abnormalities on cardiac magnetic resonance scans. This study, of just 26 athletes, was entirely lacking in controls. What’s more, earlier and contemporary studies had found similar abnormalities among elite athletes without Covid-19. But the news coverage and social media posts continued at a frenzied pace. College sports nearly stopped. And people with mild or even asymptomatic disease sought out cardiac magnetic resonance scans, and some physicians even recommended having them.
The outsized attention spurred a group of concerned medical professionals, led by University of Michigan cardiologist Venkatesh Murthy, to issue a letter of concern to medical organizations asking that these scans be performed only as part of careful research studies with appropriate control groups. All three of us signed this letter because of our concern about overdiagnosis.
The signal of cardiac harm isn’t replicated
The question raised by the two reports wasn’t whether SARS-CoV-2 could cause myocarditis. Doctors have long known that viruses can cause heart inflammation and sometimes even lead to congestive heart failure and sudden cardiac death. The concern was that SARS-CoV-2 had some special proclivity to harm the heart.
Over the ensuing months, numerous research groups published studies that refuted the early concerns and provided reassuring evidence that SARS-CoV-2 had no extra toxicity to the heart — though they did little to dispel the public idea that it did.
In January 2021, University of Wisconsin researchers studied 145 student athletes who had Covid-19 and found myocarditis in only 1.4% of them, none of whom required hospitalization. In March, a group of sports cardiologists reported on nearly 800 professional athletes who had tested positive for Covid-19. Less than 1% of these athletes had abnormal findings on cardiac magnetic resonance scans or stress echocardiography. None of these athletes had cardiovascular trouble when they returned to play.
In April, another group of authors published a series of 19,000 athletes who were tested for Covid-19. About 3,000 tested positive for SARS-CoV-2, most of whom then underwent basic cardiac testing. Reassuringly, less than 1% of these work-ups yielded abnormal findings. And just 21 of the 3,000 had definite, probable, or possible cardiac involvement based on lab testing and cardiac imaging. Five (0.2%) of the athletes required hospitalization for non-cardiac complications of Covid-19 and one (0.03%) had a successfully resuscitated cardiac arrest that was deemed not related to Covid-19 because a heart scan done as part of the evaluation showed no evidence of myocarditis.
In a stronger study published last week, an international team compared two groups of health care workers: one with Covid-19 and the other without it. There were absolutely no differences in biomarkers of heart function or heart scans using echocardiography or magnetic resonance.
These three studies enrolled young people with mild symptoms. But even in the sickest of the sick, Covid-19’s effect on the heart appears to be modest. A London-based team reported on a series of 148 patients who had recovered from severe Covid-19. Cardiac magnetic resonance scans done during convalescence showed that nearly half of the individuals had no major heart abnormalities, and 9 out of 10 had normal heart function. These researchers coined a new phrase for myocarditis seen on cardiac magnetic resonance scans: they called it a myocarditis-like pattern because “we do not know what is causing this.”
To sum up: The issue of Covid-19 induced cardiac problems was massively overblown.
The broader lessons — science messaging
The flawed German report that sparked the hyperbolic messaging was tweeted by more than 19,000 accounts and covered by nearly 400 news outlets. An opinion piece in the New York Times by cardiologist Haider Warraich, titled “Covid-19 Is Creating a Wave of Heart Disease,” was published shortly after the paper. If not for public critical appraisal from Mayo Clinic cardiologist Michael Ackerman, the 2020 college football season might not have happened.
We can only speculate on the reasons for this failure of science communication. Fear is likely a contributor. As doctors who care for people with serious illness, the three of us have witnessed firsthand the way fear shreds rational decision-making.
The pandemic injected fear in big doses. It stems from more than the virus’s high death rate in older people or its ability to spread rapidly and collapse health care systems. The most fear-inducing aspect of Covid-19 is its unpredictability. Many of us wonder: could I fall ill tomorrow?
Lax scientific review might also have played a role. Two of us (J.M. and A.F.) tried to shed light on this issue. Our first study, conducted with several colleagues, showed that the timeline from receipt to publication of studies was eight times faster during the pandemic than the year before. Of course, speedier publication isn’t a problem in and of itself: normal peer review may simply be too slow. But in our systematic follow-up study comparing top-cited papers during the pandemic with those published before it, Covid-19 related articles were of significantly lower scientific rigor. Scientific publication moved faster during the pandemic, but the quality of the work was poorer.
We take away two lessons from the Covid-19 myocarditis story. One is that SARS-CoV-2 can sometimes, though rarely, cause heart inflammation — just as many other viruses do. Clinicians, therefore, can appeal to sound medicine; further testing can be decided on an individual basis. Screening low-risk patients with MRI and other fancy tests is neither necessary nor wise.
The broader lesson is that science communication in times of crisis must keep a level head. The public, and decision-makers, need properly controlled studies instead of early sensational reports. In a world where success is measured by clicks, the idea that even mild cases of Covid-19 could pose a new and unprecedented threat to the heart took off. That fear has largely been unsubstantiated, though news of it won’t spread nearly as quickly.
The story of “Covid heart” is not over. Future studies will undoubtedly provide more information. But people who have recovered from Covid-19 have no special reason to worry about their hearts. Instead, we should all worry about the incentives in the modern media world, and why we got so far ahead of ourselves.
John Mandrola is a Kentucky-based cardiologist and electrophysiologist. Andrew Foy is a cardiologist and assistant professor of medicine at Penn State University. Vinay Prasad is a hematologist-oncologist and associate professor of epidemiology and biostatistics at the University of California, San Francisco.
What about the impact of Covid-19 on the cellular level, as indicated here: https://www.statnews.com/2020/09/04/carnage-in-lab-dish-shows-how-coronavirus-may-damage-heart/
El sars cov 2 expresa su sintomatología clínica y su severidad según el grado de compromiso endotelial e inflamatorio del órgano en cuestión es por eso que lo he llamado el síndrome de las mil caras, presentándose manifestaciones iniciales que van desde las vías respiratorias hasta la piel como primer órgano afectado
This article omits observations of profound and fatal left ventricular failure, hypokinesis, inability to contract forcefully enough to pump blood, developing without much warning in otherwise healthy young adults as they recover from covid pneumonia.
I am not interested in the 99% who do not have covid cardiomyopathy, but in the 1% (or fewer) who do. This tiny fraction in whom the heart is severely damaged has precedence in other viral cardiomyopathies such as with Coxsackie virus, an infection which is usually survived without cardiac injury but can rarely require heart transplantation.
Cardiac magnetic resonance scans done during convalescence showed that nearly half of the individuals had no major heart abnormalities, and 9 out of 10 had normal heart function….
Inverting the sentence…So more than half had major heart abnormalities… is this not clinically relevant??
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