Phenotypic composition of peripheral blood monocytes in young patients with COVID-19 and its association with the risk of acute myocardial infarction

Background. COVID-19 is associated with systemic inflammation, endothelial dysfunction, and coagulopathy, significantly increasing the risk of thrombotic complications–including acute myocardial infarction (AMI) – including in young patients. The role of the monocyte–macrophage system in the pathogenesis of these complications remains insufficiently studied.

Aim. To investigate the phenotypic composition of peripheral blood monocytes in young patients with COVID-19 alone and in those with concomitant COVID-19 and AMI.

Methods. A comparative cross-sectional study included 223 male patients aged 36.4 (31.2; 41.6) years: 15 with moderate COVID-19 and AMI (main group), 179 with moderate COVID-19 without AMI (comparison group), and 29 healthy individuals (control group). Expression levels of CD14, HLA-DR, CD11b, CD206, CD32, TNFR1, TNFR2, CD68, TRAIL, and TGFβ1 on monocytes were assessed by flow cytometry.

Results. In patients with COVID-19, monocyte expression of CD14 and HLA-DR was significantly reduced compared to controls, while expression of TNFR2, TRAIL, TGFβ1, CD206, CD68, CD32, and CD11b was elevated. These alterations were more pronounced in patients with both COVID-19 and AMI, including increased TNFR1 expression relative to controls. Comparative analysis revealed significantly higher expression levels of TNFR1, TNFR2, TGFβ1, CD206, and TRAIL in the main group versus the comparison group. Significant correlations were found between monocyte marker expression (CD14, HLA-DR, CD206, TNFR1, TNFR2, TRAIL, TGFβ1) and the development of AMI in patients with COVID-19. ROC analysis confirmed the prognostic value of HLA-DR, CD206, TRAIL, and TGFβ1 as markers of high AMI risk in this population.

Conclusion. COVID-19 induces a phenotypic shift in monocytes toward an immunosuppressive, pro-inflammatory, and pro-fibrotic profile, thereby increasing the risk of AMI.

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