LSU autopsy findings point to endothelium as target in heart

Create PDF

The decedent’s family granted permission for an autopsy. While her heart appeared grossly normal, microscopically endotheliitis and vasculitis were present, “diffusely involving the small cardiac vessels and extending into the surrounding epicardial fat and interstitial spaces,” Dr. Vander Heide and colleagues wrote in the report.

He calls those findings “similar to what we saw with the initial COVID infections, but much worse. There’s many more cells involved.”

“This might have something to do with the MSIS [multisystem inflammatory syndrome] that people are talking about, which is usually seen in children and young adults, but we think might also be present in this particular young woman of 31,” he continues. “What people think at this point with MSIS is that it may be a secondary hyperinflammatory response to the initial SARS-CoV-2 infection. And so we think, with the heart being a more severe vascular response, it fits with that.”

Moreover, the case study leads him to speculate that this vascular response is a mimicker of myocarditis in imaging studies. If true, that would explain the recent reports from cardiologists in the clinical literature of something “they think is consistent with myocarditis,” he says.

One example: a study conducted in Germany, reported online July 27, that examined 100 patients recently recovered from COVID-19. Of the 78 patients found with cardiac MRI to have some type of cardiac involvement, 60 percent of them “showed some kind of cardiac involvement and what they called ‘myocardial inflammation,’” Dr. Vander Heide says (Puntmann VO, et al. JAMA Cardiol. 2020. doi:10.1001/jamacardio.2020.3557).

“Some of those studies are very convinced that there’s actually myocarditis in these patients,” he says. “Because it’s centered on the vascular system, and maybe associated with some edema in the heart, which is what they’re looking for with their imaging studies, this might be what they’re finding—not so much a myocarditis, but this vasculitis, endotheliitis.”

In the MSIS-like patient, there is a pattern of brisk endotheliitis/vasculitis involving the small blood vessels and expanding the interstitial spaces.

He hypothesizes further that the alteration of the endothelial structure and function secondary to the SARS-CoV-2 infection of the endothelial space is causing alterations in blood clotting function such that there are small blood vessel clots in the heart that lead to very small amounts of myocyte damage.

“A lot of these patients, if you look at them clinically, have small elevations in troponin T,” he says. “The fact that troponin is elevated in these patients to a small degree was always supportive of myocarditis, but it wasn’t a large increase in troponin, which always bothered me. And so we think there is small vessel ischemia that’s causing these small amounts of myocytes to die and lead to that small elevation in troponin in most of these patients.”

Dr. Vander Heide hopes that reports in the literature like those of his team will help call more attention to the role of the heart in COVID-19.

“This stuff that we’re starting to describe in the heart is relatively new,” he says. “It’s interesting, and has been relatively back seat compared to the hypoxia, which is obviously most important for most patients who are in the hospital.” He points out that after the 2002–2004 SARS epidemic, “years later, people would show up with heart changes, heart failure, and fibrosis, which indicated there was some damage at some point, but it was not severe enough to cause someone to go to the hospital.”

He hopes that in the current pandemic, patients who recover from SARS-CoV-2 infection will be followed, not just those who are very sick and end up on ventilators but also the large number of people who don’t become ill enough to be admitted to the hospital. “That population that might get mild or moderate illness and recover—I don’t think we know anything about the long-term consequences.”

Given how many people have been, are, or will be infected with SARS-CoV-2, that’s a sobering thought. As Dr. Vander Heide puts it: “If you’ve got five or six million people infected, it doesn’t take a big percentage of those to cause a sudden, pretty significant increase in long-term cardiac complications. So I think it’s important going forward, for clinicians especially, to try to develop lab testing protocols and imaging protocols to follow up some of these patients, because we’re going to find out a lot of new information as time goes by.”

Anne Ford is a writer in Evanston, Ill.