NIH (National Institutes of Health)
SARS-CoV-2, the virus that causes COVID-19, can cause a life-threatening condition called acute respiratory distress syndrome (ARDS), when fluid leaks into the lungs and prevents oxygen from entering the body. This can lead to threatening conditions. Other complications of COVID-19 include systemic inflammation and cardiovascular complications.
Previous research has shown changes in the composition of lung immune cells in patients infected with the new coronavirus. However, it is not clear whether COVID-19 induces similar changes in immune cells in heart tissue. It is also unclear whether such changes contribute to cardiovascular complications.
An NIH-funded research team led by Dr. Matthias Nahlendorf of Massachusetts General Hospital and Dr. Jana Groen of the German Heart Center at the Charité in Berlin is investigating how ARDS-related immune signals influence heart tissue and cardiovascular health. We investigated whether it would have such an impact.The study was published in the journal Circulation March 20, 2024.
The research team examined heart tissue specimens from 21 people who died from SARS-CoV-2-related ARDS. They compared these with samples from 33 people who died from causes other than COVID-19 before the COVID-19 pandemic. They focused on a type of immune cell called macrophages that proliferate significantly during ARDS. Macrophages engulf and digest pathogens. One type of macrophage normally resides in heart tissue, where it eliminates pathogens and supports myocardial metabolism. Another type can accumulate in response to tissue damage and promote inflammation.
Heart tissue from patients with COVID-19 contained more macrophages than tissue from controls. Many of the macrophages were also of the inflammatory type. Researchers observed similar results in mice infected with SARS-CoV-2.
The research team wanted to investigate how SARS-CoV-2 infection caused the observed changes in cardiac macrophages. To do so, they developed a method to induce ARDS in mice without infecting them with the virus. This “virus-like” ARDS (VLARDS) caused changes in cardiac macrophages similar to those seen with SARS-CoV-2 infection. Blocking part of the inflammatory response prevented these changes and preserved heart function.mouse and VLAdditionally, people with ARDS are more likely to die if they have a history of heart failure.
This result suggests that SARS-CoV-2 increases the inflammatory proportion of macrophages within the heart, causing cardiac damage. This change appears to be due to an immune response to lung injury rather than a viral infection of the heart itself. Therefore, targeting pro-inflammatory cardiac macrophages may reduce cardiovascular complications caused by SARS-CoV-2. Suppressing the body’s immune response may also be an effective treatment.
