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. 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.
Citação
@online{renata2024,
author = {Renata , Moll-Bernardes and Gabriel C. , Camargo and Andréa
, Silvestre-Sousa and Julia Machado , Barroso and Juliana R. ,
Ferreira and Mariana B. , Tortelly and Adriana L. , Pimentel and Ana
Cristina B. S. , Figueiredo and Eduardo B. , Schaustz and José
Carlos P. , Secco and Sergio C. , Fortier and Narendra , Vera and
Luciana , Conde and Mauro Jorge , Cabral-Castro and Denilson C. ,
Albuquerque and Paulo H. , Rosado-de-Castro and Martha V. T. ,
Pinheiro and Olga F. , Souza and Ronir R. , Luiz and Emiliano ,
Medei},
title = {Immune Profile and MRI-Detected Cardiac Fibrosis and Edema in
Hypertensive and Non-Hypertensive Patients with COVID-19},
volume = {13},
number = {23},
date = {2024-12-02},
doi = {10.3390/jcm13237317},
langid = {pt-BR},
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.}
}