New Insights on the Mechanisms of Myocardial Injury in Hypertensive Patients With COVID-19

Abstract

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. Supplementary Information The online version contains supplementary material available at 10.1007/s10875-023-01523-6.