University of Nebraska Medical Center

How lung distress from SARS-CoV-2 can cause heart damage


SARS-CoV-2, the virus that causes COVID-19, can trigger a life-threatening condition called acute respiratory distress syndrome (ARDS), in which fluid leaks into the lungs and prevents oxygen from passing into the body. Other complications of COVID-19 include systemic inflammation and cardiovascular complications.

Previous studies have found changes in the makeup of lung immune cells in patients with COVID-19. But it isn’t clear if COVID-19 causes similar changes to immune cells in heart tissue. Nor is it clear if such changes help contribute to cardiovascular complications.

An NIH-funded research team, led by Dr. Matthias Nahrendorf at Massachusetts General Hospital and Dr. Jana Grune at the German Heart Center at Charité in Berlin, investigated how ARDS-associated immune signals affect heart tissue and cardiovascular health. The study appeared in the journal Circulation on March 20, 2024.

The team examined heart tissue specimens from 21 people who died with SARS-CoV-2-associated ARDS. They compared these to specimens from 33 people who died from non-COVID-19 causes from before the COVID-19 pandemic. They focused on a type of immune cells called macrophages, which greatly multiply during ARDS. Macrophages engulf and digest pathogens. One type of macrophage normally lives in heart tissue, where they clear out pathogens and support metabolism in the heart muscle. Another type can accumulate in response to tissue damage and promote inflammation.

Heart tissue from people with COVID-19 had more macrophages than tissue from controls. More of the macrophages were of the inflammatory type, too. The researchers observed similar results in mice infected with SARS-CoV-2.

The team wanted to find out how SARS-CoV-2 infection led to the observed changes in heart macrophages. To do so, they developed a way to induce ARDS in mice without any virus infection. This “virus-like” ARDS (VLARDS) led to the same changes in heart macrophages as those seen in SARS-CoV-2 infection. Blocking part of the inflammatory response prevented these changes and preserved heart function. Mice with VLARDS were also more likely to die if they had pre-existing heart failure.

The results suggest that SARS-CoV-2 increases the inflammatory share of macrophages in the heart, leading to heart damage. This change appears to result from the immune response to lung injury rather than from viral infection of the heart itself. Targeting pro-inflammatory heart macrophages might thus relieve the cardiovascular complications of SARS-CoV-2. Dialing back the body’s immune response might also be an effective treatment.

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