Heart health in long Covid
Summary:
This study explores how virus-induced acute respiratory distress syndrome (ARDS) affects heart health, particularly focusing on the role of cardiac macrophages. The researchers examined autopsy specimens from COVID-19 patients with SARS-CoV-2-associated ARDS and compared them with those who died from other causes. They found that SARS-CoV-2 infection increased the number of cardiac macrophages, especially CCR2+ macrophages, which are associated with inflammation.
Note: Macrophages: Macrophages are a type of white blood cell that play a crucial role in the immune system. They are responsible for engulfing and digesting cellular debris, pathogens, and other harmful substances, as well as for regulating immune responses and inflammation.
In mouse models, both SARS-CoV-2 infection and virus-free lung injury led to significant changes in cardiac macrophages, similar to the human findings. These changes included an increase in CCR2+ macrophages, which were linked to cardiac inflammation and compromised heart function. Treatment with a tumor necrosis factor α–neutralizing antibody reduced the number of inflammatory macrophages and improved cardiac function.
The study concludes that viral ARDS triggers cardiac inflammation by expanding the CCR2+ macrophage subset, and this effect can be replicated by activating the immune system without direct viral infection of the heart. This highlights the importance of managing systemic inflammation to protect heart health during viral infections that cause ARDS.
Main Points:
- Background:
- Viral infections like SARS-CoV-2 can cause acute respiratory distress syndrome (ARDS), leading to systemic inflammation and cardiovascular complications.
- The role of heart macrophages in cardiac injury during viral ARDS was previously unknown.
- Methods:
- Analysis of cardiac macrophage subsets using immunofluorescence histology on autopsy specimens from 21 COVID-19 patients with SARS-CoV-2-associated ARDS and 33 non-ARDS patients.
- Comparison of cardiac immune cell dynamics in mice after SARS-CoV-2 infection and virus-free lung injury induced by intratracheal instillation of Toll-like receptor ligands and an ACE2 inhibitor.
- Results:
- Human Findings:
- SARS-CoV-2 infection increased total cardiac macrophage counts.
- Higher proportion of CCR2+ (C-C chemokine receptor type 2 positive) macrophages in the hearts of COVID-19 patients.
- Mouse Model Findings:
- Both SARS-CoV-2 infection and virus-free lung injury caused significant remodeling of cardiac resident macrophages, similar to human findings.
- Virus-like ARDS led to an increase in CCR2+ macrophages in the heart.
- Treatment with a tumor necrosis factor α–neutralizing antibody reduced cardiac monocytes and inflammatory MHCIIlo CCR2+ macrophages, preserving cardiac function.
- Elevated mortality observed in mice with pre-existing heart failure exposed to virus-like ARDS.
- Conclusions:
- Viral ARDS promotes cardiac inflammation by expanding the CCR2+ macrophage subset.
- The cardiac inflammation and related phenotypes can be induced by systemic immune activation without the presence of the virus in the heart.
- Managing systemic inflammation is crucial for protecting heart health during viral infections causing ARDS.
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
Long Covid The Answers
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Originally published 20 Mar 2024 https://doi.org/10.1161/CIRCULATIONAHA.123.066433Circulation. 2024;0
