The research specifically examines damage to the hearts of patients with SARS-CoV2-associated acute respiratory distress syndrome (ARDS), a serious and fatal lung complication. However, its results could be relevant for organs other than the heart as well as for viruses other than SARS-CoV-2: previous research has thus suggested that the cerebral and neurological complications of COVID are rather correlated with inflammation than ‘to brain infection.
Scientists have long known that COVID-19 increases the risk of heart attacks, strokes and long COVID.
More than 50% of patients who develop COVID-19 have inflammation or damage to the heart.
However the question still arises whether the damage occurs because the virus infects heart tissue or because of systemic inflammation triggered by the immune response to the virus.
A whole new understanding of the link between lung injury and inflammation
One of the lead authors, Dr. Michelle Olive, director of basic and early translational research at NHLBI adds: “Research also suggests that suppressing inflammation could help minimize these complications.”
The study focused on cardiac macrophage immune cells, which normally play a critical role in maintaining the health of heart tissue but can become inflammatory in response to injuries such as heart attack or heart failure. The researchers thus analyzed heart tissue samples from 21 patients who died from ARDS associated with SARS-CoV-2 and compared them to samples from 33 patients who died from causes unrelated to COVID-19. Monitoring of macrophages after infection was also carried out in mouse models of SARS-CoV-2 infection. These studies carried out in humans and mice reveal that:
- SARS-CoV-2 infection increases the total number of cardiac macrophages and makes them more inflammatory;
- when macrophages no longer perform their normal function, which includes maintaining the heart’s metabolism and eliminating harmful bacteria or other foreign agents, they inflame and weaken the heart and the rest of the body;
- even in the absence of viruses, COVID mouse models mount immune responses strong enough to produce the same change in their cardiac macrophages as already observed in patients who died from COVID-19.
Taken together these observations confirm that after COVID infection, the immune system can inflict damage from a distance to other organs by triggering serious inflammation throughout the body. This systemic inflammation is in addition to the damage the virus inflicts directly on lung tissue.
Blocking the immune response with a neutralizing antibody makes it possible – again in mice – to stop the flow of inflammatory cardiac macrophages and preserve cardiac function.
In other words, this research supports the responsibility of inflammation, rather than infection, in the incidence of COVID-associated cardiac damage.
