SARS-CoV-2, the virus that causes COVID-19, can damage the heart in patients with ARDS (Acute Respiratory Distress Syndrome) without directly infecting heart tissue, a new study has found. These findings suggest it is systemic inflammation that causes this damage.
“The research also suggests that suppressing the inflammation through treatments might help minimize these complications,” said Michelle Olive, PhD, associate director of the Basic and Early Translational Research Program at the National Heart, Lung, and Blood Institute (NHLBI).
The study was published in the journal Circulation today. The senior author is Matthias Nahrendorf, MD, PhD, Center for Systems Biology, Massachusetts General Hospital.
It’s already known that COVID-19 increases the risk of heart attack, stroke, and Long COVID. Also, prior imaging research has shown that over 50% of people who get COVID-19 experience some inflammation or damage to the heart. What scientists did not know is whether the damage occurs because the virus infects the heart tissue, or because of systemic inflammation triggered by the body’s immune response to the virus.
“This was a critical question and finding the answer opens up a whole new understanding of the link between this serious lung injury [ARDS] and the kind of inflammation that can lead to cardiovascular complications,” said Olive.
The researchers focused on cardiac macrophages, which normally perform a critical role in keeping the tissue healthy but can turn inflammatory in response to injury such as heart attack or heart failure. The team analyzed heart tissue specimens from 21 patients who died from SARS-CoV-2-associated ARDS and compared them with specimens from 33 patients who died from non-COVID-19 causes. They also infected mice with SARS-CoV-2 to follow what happened to the macrophages after infection.
In both humans and mice, the team found that SARS-CoV-2 infection increased the total number of cardiac macrophages and also caused them to shift their activity, and become inflammatory.
The researchers then designed a mouse study to test whether the response they observed happened because SARS-CoV-2 was infecting the heart directly, or because the SARS-CoV-2 infection in the lungs was severe enough to render the heart macrophages more inflammatory. They saw the same heart macrophage shift both in the samples from patients who died of COVID-19 and the mice infected with SARS-CoV-2 infection.
“What this study shows is that after a COVID infection, the immune system can inflict remote damage on other organs by triggering serious inflammation throughout the body— and this is in addition to damage the virus itself has directly inflicted on the lung tissue,” said Nahrendorf. “These findings can also be applied more generally, as our results suggest that any severe infection can send shockwaves through the whole body.”
The research team also found that blocking the immune response with a neutralizing antibody in the mice stopped the flow of inflammatory cardiac macrophages and preserved cardiac function. While they have yet to test this in humans, Nahrendorf said a treatment like this could be used as a preventive measure to help COVID-19 patients with pre-existing conditions, or people who are likely to have more severe outcomes from SARS-CoV-2 associated ARDS.
