Immune Profile and MRI-Detected Cardiac Fibrosis and Edema in Hypertensive and Non-Hypertensive Patients with COVID-19.

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. 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). 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. 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. 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.