How lung problems from SARS-CoV-2 can harm the heart. Transmission


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 oxygen is lost to the body. Prevents from. Other complications of COVID-19 include systemic inflammation and cardiovascular complications.

Previous studies have found changes in the composition of immune cells in the lungs in patients with COVID-19. But it is unclear whether COVID-19 causes similar changes in immune cells in heart tissue. Nor is it clear whether such changes contribute to cardiovascular complications.

An NIH-funded research team led by Dr. Matthias Nahrendorf at Massachusetts General Hospital and Dr. Jana Grüne at the German Heart Center at Charite in Berlin investigated how immune signals associated with ARDS affect heart tissue and cardiovascular health. Are. This study appeared in the journal Spreading On 20 March 2024.

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

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

The team wanted to find out how SARS-CoV-2 infection caused changes in cardiac macrophages. To do this, they developed a way to induce ARDS in mice without any virus infection. This “virus-like” ARDS (VLARDS) caused the same changes in cardiac macrophages that were seen in SARS-CoV-2 infection. Blocking part of the inflammatory response prevented these changes and preserved heart function. with rats VLIf people with ARDS already had heart failure, they were also more likely to die.

The results show that SARS-CoV-2 increases macrophage inflammation in the heart, leading to heart damage. This change appears to be a result of the immune response to lung injury rather than to viral infection of the heart. Targeting pro-inflammatory cardiac macrophages may relieve cardiovascular complications of SARS-CoV-2. Dialing back the body's immune response may also be an effective treatment.

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