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IMMUNEPROFILE AND MRI-DETECTED CARDIAC FIBROSIS AND EDEMA IN HYPERTENSIVE AND NON-HYPERTENSIVE PATIENTS WITH COVID-19
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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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