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New Insights on the Mechanisms of Myocardial Injury in Hypertensive Patients With COVID-19
Renata Moll-Bernardes1, Juliana R Ferreira1,2, Eduardo B Schaustz1
1D'Or Institute for Research and Education, Rua Diniz Cordeiro, 30, 22281100, Rio de Janeiro, Brazil.
Insights
Hypertension and COVID-19 can cause myocardial injury. Immune biomarkers like lymphopenia and specific CD8+ cell markers are associated with this cardiac damage in affected patients.
Area of Science:
- Immunology
- Cardiology
- Infectious Diseases
Background:
- Myocardial injury is a frequent complication in hypertensive patients with COVID-19.
- The precise mechanisms linking immune dysregulation to cardiac injury in this population remain unclear.
Purpose of the Study:
- To investigate immune system alterations associated with myocardial injury in hypertensive patients hospitalized with COVID-19.
- To identify potential immune biomarkers for cardiac damage in this patient group.
Main Methods:
- Prospective, multicenter study comparing hypertensive COVID-19 patients with (cases) and without (controls) myocardial injury.
- Quantification of biomarkers and immune cell subsets.
- Multivariate logistic regression analysis to identify associations with myocardial injury.
Main Results:
- Cases exhibited lower total lymphocyte counts and specific T cell subset percentages compared to controls.
- Elevated levels of natural killer lymphocytes and specific CD8+ cell activation markers (CD8+CD38+MFI, CD8+HLA-DR+MFI) were observed in cases.
- Multivariate analysis confirmed associations between CD8+HLA-DR+MFI, CD8+CD38+MFI, and total lymphocyte count with myocardial injury.
Conclusions:
- Lymphopenia, CD8+CD38+MFI, and CD8+HLA-DR+MFI serve as immune biomarkers for myocardial injury in hypertensive COVID-19 patients.
- These immune signatures may elucidate mechanisms of cardiac injury and inform treatment strategies.
- Further research could lead to improved management of cardiovascular complications in this vulnerable population.
Purpose:
Myocardial injury is common in hypertensive patients with 2019 coronavirus disease (COVID-19). Immune dysregulation could be associated to cardiac injury in these patients, but the underlying mechanism has not been fully elucidated.
Methods:
All patients were selected prospectively from a multicenter registry of adults hospitalized with confirmed COVID-19. Cases had hypertension and myocardial injury, defined by troponin levels above the 99th percentile upper reference limit, and controls were hypertensive patients with no myocardial injury. Biomarkers and immune cell subsets were quantified and compared between the two groups. A multiple logistic regression model was used to analyze the associations of clinical and immune variables with myocardial injury.
Results:
The sample comprised 193 patients divided into two groups: 47 cases and 146 controls. Relative to controls, cases had lower total lymphocyte count, percentage of T lymphocytes, CD8+CD38+ mean fluorescence intensity (MFI), and percentage of CD8+ human leukocyte antigen DR isotope (HLA-DR)+ CD38-cells and higher percentage of natural killer lymphocytes, natural killer group 2A (NKG2A)+ MFI, percentage of CD8+CD38+cells, CD8+HLA-DR+MFI, CD8+NKG2A+MFI, and percentage of CD8+HLA-DR-CD38+cells. On multivariate regression, the CD8+HLA-DR+MFI, CD8+CD38+MFI, and total lymphocyte count were associated significantly with myocardial injury.
Conclusion:
Our findings suggest that lymphopenia, CD8+CD38+MFI, and CD8+HLA-DR+MFI are immune biomarkers of myocardial injury in hypertensive patients with COVID-19. The immune signature described here may aid in understanding the mechanisms underlying myocardial injury in these patients. The study data might open a new window for improvement in the treatment of hypertensive patients with COVID-19 and myocardial injury.
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