Heart at risk from ARDS: Inflammatory responses fuel cardiovascular complications

By Hugo Francisco de SouzaMar 24 2024Reviewed by Benedette Cuffari, M.Sc. In a recent study published in the journal Circulation, researchers investigate the inflammatory response to acute respiratory distress syndrome within the heart.

Circulating immune cells may respond to COVID-19 by upregulating cytokine release, which can lead to myocardial injury. Cardiac macrophages, immune cells responsible for the myocardial inflammatory response, are increasingly being investigated for their role in ARDS. Recent evidence indicates that macrophage expansion, which can be accompanied by changes in the population size and relative abundances of various cardiac macrophages, is a characteristic feature of ARDS.

About the study In the present study, researchers investigate the role of viral- and non-viral-induced ARDS-associated immune signals in altering cardiac macrophage populations, thereby impacting CVD parameters, including systemic inflammation. Patient data included results obtained from electrocardiogram , echocardiography, lung computed tomography scan, blood gas analyses, body temperature evaluation, bronchoalveolar lavage fluid characterization, blood pressure measurements, and flow cytometry. Both human and murine autopsy samples were processed using ribonucleic acid isolation, real-time polymerase chain reaction assay, and enzyme-linked immunosorbent assays for protein and gene expression determinations.

In both non-infected ARDS and SARS-CoV-2-infected mice, an increased infiltration of interstitial macrophages and reduced levels of alveolar macrophages were observed. Although both mouse models exhibited increased levels of cardiac macrophages, this immune response was more pronounced in infected mice. Nevertheless, both models' subsets of cardiac macrophages were altered to similar levels.

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