"COVID-19 Lung Infection Linked to Heart Damage"

In a groundbreaking study supported by the National Institutes of Health (NIH), researchers have unveiled a pivotal discovery that unveils a new link between severe lung infection during COVID-19 and potential damage to the heart, even in cases where the virus does not directly infect heart tissue. Published in the esteemed journal Circulation, the study sheds light on the intricate interplay between SARS-CoV-2, the virus responsible for COVID-19, and the heart, particularly in individuals with SARS-CoV-2-associated acute respiratory distress syndrome (ARDS).

Traditionally, the medical community has noted an increased risk of heart complications such as heart attacks, strokes, and inflammation in individuals with COVID-19. However, what remained unclear was whether this damage stemmed from direct viral infiltration of heart tissue or from the body's exuberant immune response to the virus, leading to systemic inflammation.

Dr. Michelle Olive, associate director of the Basic and Early Translational Research Program at the National Heart, Lung, and Blood Institute, emphasized the critical nature of this research, stating that understanding this connection provides insights into the intricate relationship between severe lung injury and the inflammation that can trigger cardiovascular complications. The study suggests that targeting inflammatory responses could potentially mitigate these complications.

By focusing on cardiac macrophages, immune cells pivotal for heart health, the researchers examined heart tissue samples from deceased individuals with SARS-CoV-2-associated ARDS and compared them with samples from non-COVID-19 cases. Strikingly, both human samples and mouse models infected with SARS-CoV-2 exhibited an increase in inflammatory cardiac macrophages, indicating a significant shift from their normal functions towards a pro-inflammatory state.

Moreover, through a mouse study mimicking lung inflammation without the presence of the virus, researchers demonstrated that severe lung infection alone could induce the same inflammatory response in cardiac macrophages, suggesting a systemic mechanism at play. This finding implies that the immune system post-COVID-19 infection can induce damage in distant organs, exacerbating the impact of the virus on the body.

Dr. Matthias Nahrendorf, senior author on the study and a professor at Harvard Medical School, highlighted the broader implications of the research, indicating that severe infections, beyond COVID-19, could trigger profound systemic inflammation that adversely affects multiple organs throughout the body.

Excitingly, the research team discovered that blocking the immune response in mice halted the influx of inflammatory cardiac macrophages, preserving heart function. While this approach awaits human trials, it holds promise as a potential preventive strategy for COVID-19 patients with underlying conditions or those at risk of severe outcomes from SARS-CoV-2-associated ARDS.

This groundbreaking study not only deepens our understanding of the complex interplay between COVID-19 and cardiovascular health but also opens avenues for novel therapeutic interventions that could mitigate post-infection complications. As we unravel the intricate mechanisms underlying COVID-19 pathophysiology, this research underscores the critical importance of exploring the far-reaching impacts of viral infections on the human body.

Source: https://www.eurekalert.org/news-releases/1038032