Virus that causes COVID-19 can damage heart even if heart tissue not directly affected

March 20, 2024

2 min read

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Key takeaways:

• The SARS-CoV-2 virus, which causes COVID-19, can cause damage to the heart via inflammation triggered by the immune system.
• This can happen even if there is no direct damage to heart tissues from the virus.

Among patients who died of acute respiratory distress syndrome associated with SARS-CoV-2, the virus that causes COVID-19, heart tissues were damaged even when they were not directly affected by the virus, researchers reported.

For the NHLBI-funded study, the researchers investigated whether COVID-19-related heart damage was caused by direct action on the heart from SARS-CoV-2 or resulted from systemic inflammation caused by the immune system’s response to SARS-CoV-2 infection among patients who died of acute respiratory distress syndrome (ARDS) as a result of COVID-19.

The SARS-CoV-2 virus, which causes COVID-19, can cause damage to the heart via inflammation triggered by the immune system. Image: Adobe Stock

“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,” Matthias Nahrendorf, MD, PhD, professor of radiology at Harvard Medical School, said in a press release. “These findings can also be applied more generally, as our results suggest that any severe infection can send shockwaves through the whole body.”

Nahrendorf and colleagues compared autopsy results, focusing on cardiac macrophages, of 21 people who died of ARDS as a result of COVID-19 and 33 people who died of other causes. They also conducted a study in mice determine what happens to cardiac macrophages after SARS-CoV-2 infection or lung injury not related to SARS-CoV-2.

Compared with people who died of other causes, in people who died of ARDS as a result of COVID-19, there were higher counts of total cardiac macrophages and a greater proportion of CCR2+ macrophages, which promote inflammation, Nahrendorf and colleagues found.

In mice, both infection with SARS-CoV-2 and lung injury not related to SARS-CoV-2 were associated with remodeling of cardiac resident macrophages and expansion of CCR2+ macrophages. In mice with lung injury not related to SARS-CoV-2, treatment with a tumor necrosis factor-alpha-inhibiting antibody reduced cardiac monocytes and CCR2+ macrophages and preserved cardiac function, and among those mice, those with preexisting HF were more likely to die, according to the researchers.

“Our data suggest that viral ARDS promotes cardiac inflammation by expanding the CCR2+ macrophage subset and that the associated cardiac phenotypes … can be elicited by activating the host immune system even without viral presence in the heart,” the researchers wrote.

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Sources/Disclosures

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Disclosures:
Nahendorf reports receiving funds or material research support from Alnylam, Biotronik, CSL Behring, GlycoMimetics, GlaxoSmithKline, Medtronic, Novartis and Pfizer and consultant fees from Biogen, Eli Lilly, Gimv, IFM Therapeutics, Molecular Imaging, Sigilon and Verseau Therapeutics. The other authors report no relevant financial disclosures.

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