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Immune Profile and MRI-Detected Cardiac Fibrosis and Edema in Hypertensive and Non-Hypertensive Patients with
Renata Moll-Bernardes1, Gabriel C Camargo1, Andréa Silvestre-Sousa1,2
1D'Or Institute for Research and Education, Rio de Janeiro 22281-100, Brazil.
Insights
COVID-19 survivors show immune dysregulation, with CD8+ T-cell activation linked to cardiac fibrosis and edema. This immune response may explain late heart damage in patients with and without hypertension.
Area of Science:
- Immunology
- Cardiology
- Infectious Diseases
Background:
- Cardiac sequelae are frequent in COVID-19 survivors, potentially driven by an overactive immune response.
- Hypertension may influence the immune profile and cardiac outcomes post-COVID-19.
Purpose of the Study:
- To investigate immune profiles in hypertensive and non-hypertensive COVID-19 survivors with late cardiac fibrosis or edema.
- To correlate cytokine and immune cell subset levels with cardiac magnetic resonance imaging (MRI) findings.
Main Methods:
- Cardiac MRI (measuring extracellular volume for fibrosis and T2 for edema) was performed post-discharge.
- Cytokine and immune cell subset levels during hospitalization were analyzed.
- Associations were examined in hypertensive and non-hypertensive patient groups.
Main Results:
- Hypertensive patients exhibited altered B-cell and natural killer cell percentages and elevated Interleukin (IL)-4, IL-5, IL-13, IL-17A, and tumor necrosis factor-β.
- CD8+ T-cell activation markers correlated with increased fibrosis and edema in hypertensive patients.
- Human Leukocyte Antigen DR (HLA-DR) intensity correlated with fibrosis in non-hypertensive patients.
Conclusions:
- COVID-19 survivors, with or without hypertension, display immune and cytokine dysregulation.
- CD8+ T-cell activation is moderately associated with myocardial fibrosis and edema markers.
- Findings enhance understanding of immune dysfunction in COVID-19-related cardiac remodeling.
Abstract:
Cardiac involvement in 2019 coronavirus disease (COVID-19) survivors has been reported frequently. An exacerbated immune response may be the main mechanism of myocardial injury and late cardiac sequelae in this population. Background/Objectives: We investigated the immune profile in hypertensive and non-hypertensive patients with COVID-19 who developed late cardiac fibrosis and edema, as detected by magnetic resonance imaging (MRI). Methods: We evaluated associations of cytokine and immune-cell subset levels during hospitalization for COVID-19 with the presence of myocardial interstitial fibrosis [represented by the extracellular volume (ECV)] or edema (represented by the T2), detected by cardiac MRI examination after discharge, in hypertensive and non-hypertensive patients. Results: Patients with hypertension had reduced B-cell percentages, increased natural killer cell percentages, and higher interleukin (IL)-4, IL-5, IL-13, IL-17A, and tumor necrosis factor-β levels compared to patients without hypertension. Larger percentages of human leukocyte antigen DR isotope+ blood cells, reflecting CD8+ T-cell activation, correlated with increased T2 and ECV in hypertensive patients. The HLA-DR mean fluorescence intensity was associated with ECV in non-hypertensive patients. Conclusions: Our findings reveal cytokine and immune-cell dysregulation in both hypertensive and non-hypertensive patients with COVID-19, along with moderate correlations between CD8+ T-cell activation and increased cardiac MRI markers of myocardial interstitial fibrosis and edema. These results contribute to a deeper understanding of immune dysfunction mechanisms involved in myocardial remodeling.
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