It's not often that myocarditis , but cardiac MRI findings after recovery from acute COVID-19 symptoms have rocketed to public attention for their impact on decisions being made about sports.
One (as yet unpublished) study found who tested positive, largely after mild or no symptoms. A more alarming statement by Penn State football's team doctor put that rate at , but that claim has since been .
Before that was a German cardiac MRI study in non-athletes that turned up lingering myocardial inflammation and other cardiac abnormalities in 78 of 100 people. While the study was subsequently corrected, the message remained the same: even a mild course of COVID-19 in relatively healthy people could leave a mark on the heart.
That study, too, received an enormous amount of attention due, in part, to its use by colleges and sports programs to determine the future of the fall athletics season.
"We did expect high uptake, but we didn't expect that much of a focus," said Eike Nagel, MD, PhD, of University Hospital Frankfurt in Germany, who was the senior author on the German MRI paper. "A lot of papers get downloaded 10 times, maybe 20 times; this paper got downloaded 550,000 times."
Myocarditis is the top concern around COVID-19 for college athletics, due to the risk it poses for cardiac arrhythmia and sudden cardiac death.
Darrel Francis, MD, of the National Heart and Lung Institute of Imperial College London, saw reason for reassurance in Nagel's corrected data rather than reason to stop sports.
The troponin and C-reactive protein (CRP) measurements were elevated but still within the normal range, he told Ƶ. "These are much more reassuring, that there isn't a huge amount of myocarditis going on unnoticed in COVID survivors."
However, focusing on sports not only politicizes the findings but misses the point, Nagel argued in an interview with Ƶ.
There are no long-term data to indicate whether this inflammation is clinically relevant for an individual, whether it will lead to heart failure, arrhythmias, or other chronic complications, Nagel said.
Nor is it clear how long it might take to disappear in those who suffer no long-term consequences. That process took around 2 years for the lingering pulmonary function issues seen with the prior SARS coronavirus outbreak.
But Nagel's study suggested that for some subset of patients there really will be clinical consequences for the heart long-term.
Significantly abnormal native T2 indicating edema -- more than four standard deviations above normal -- was found in 22% of the COVID survivors tested versus none of the risk factor-matched people, Nagel noted. Also, nonischemic scar tissue by late enhancement was found in 20% of the COVID patients and 7% of the risk factor-matched group.
"We know that the presence of scar tissue, late enhancement by MRI, is prognostically relevant in almost any disease that has been looked at," he said. "The same for inflammation."
Even so, while that "will change their outcome statistically, again that doesn't mean on an individual level," Nagel said. "The person who has that doesn't need to worry that they are now going to die sooner. But on a population level, if you have a million people with COVID and 22% of them develop more scar...there is a relevant risk that we'll have a larger incidence of heart failure and chain of outcome in 10 years' time."
Even small but measureable elevations in troponin and CRP chronically, while of no pathologic value, can be relevant for cardiovascular outcome, he added.
"In the long term, we need to change our attitude toward these things, because we are trained to look at these enzymes or ejection fraction or whatever in patients where there's severe damage -- like myocarditis," Nagel argued. "They say the others heal with no damage at all. This is too binary for me. For me, myocarditis is a spectrum. ... There are loads of people who have some cardiac damage; it doesn't have to be massive, it can be just minimal."
There might not be any guideline-directed therapy to offer those without overt heart failure, but these post-COVID cases need to be studied to check for functional changes at 6 months and beyond, he said.
"We've seen with other viruses where there is inflammation of the heart, there are individuals for whom there is spontaneous recovery," Gregg Fonarow, MD, of the University of California Los Angeles, said in a from the American Heart Association. "And in some people, we can treat this effectively with medication. The question becomes specifically with COVID-19, what is that frequency and does it differ from other viruses that infect the heart."
Newly released European Society of Cardiology guidelines suggested that people with myocarditis should hold off on vigorous exercise likely for 3 to 6 months. And based on "pretty much no data," it makes sense to that to COVID-related cardiac inflammation and fibrosis too, Nagel said.