Virus-Induced Acute Respiratory Distress Syndrome Causes Cardiomyopathy Through Eliciting Inflammatory Responses in the Heart
Authors' conclusion
Our data suggest that viral ARDS promotes cardiac inflammation by expanding the CCR2+ macrophage subset, and the associated cardiac phenotypes in mice can be elicited by activating the host immune system even without viral presence in the heart.
Study context
- Population
- Autopsy specimens of patients with COVID-19 acute respiratory distress syndrome (ARDS) and controls; mice with SARS-CoV-2 infection or virus-like ARDS (intratracheal TLR ligands and ACE2 inhibitor)
- Participants
- 21 vs 33
- Comparison
- SARS-CoV-2-associated ARDS vs other causes of death (humans); SARS-CoV-2 infection vs virus-free ARDS (mice)
- COVID-19n = 21
- Other causesn = 33reference
- Outcome
- Cardiac macrophage subsets
Methodological detailshuman autopsy specimens, mouse models
- Human autopsy specimens
- Mouse models
Main finding
As reported in the abstract
- In humans, SARS-CoV-2 increased total cardiac macrophage counts and the proportion of CCR2+ macrophages
- In mice, SARS-CoV-2 and virus-free lung injury triggered profound remodelling of cardiac resident macrophages, recapitulating expansion of CCR2+ macrophages
- TNFα-neutralizing antibody in virus-like ARDS reduced cardiac monocytes and inflammatory MHCIIlo CCR2+ macrophages and preserved cardiac function (mice)
- Virus-like ARDS elevated mortality in mice with pre-existing HF
Original publication
Virus-Induced Acute Respiratory Distress Syndrome Causes Cardiomyopathy Through Eliciting Inflammatory Responses in the Heart. Circulation. Published 20 March 2024. doi:10.
Summarised from the published abstract; every number is checked against it