Key result
COVID-19 with STEMI is linked to increased senescent cells and worse long-term glycemic control.
Why the study?
STEMI induces long-term immune remodeling, and double-positive CD3+CD4+CD8+ T-lymphocytes are involved in chronic inflammation and immune adaptation. However, their long-term dynamics following STEMI, particularly in patients with concomitant COVID-19, remained unclear.
Does concomitant COVID-19 at the time of STEMI alter long-term double-positive CD4+CD8+ T-cell profiles and senescence-associated markers compared to pre-pandemic STEMI without COVID-19 in post-STEMI survivors?
Observational (n=60)
Does concomitant COVID-19 at the time of STEMI alter long-term double-positive CD4+CD8+ T-cell profiles and senescence-associated markers compared to pre-pandemic STEMI without COVID-19 in post-STEMI survivors?
Concomitant COVID-19 at the time of STEMI is associated with persistent immunosenescence, long-term metabolic dysregulation, and a cytotoxic shift in double-positive CD4+CD8+ T-cells 3-4 years post-infarction compared to STEMI without COVID-19.
Answers are grounded in this paper and cite their sources.
Concomitant COVID-19 may drive persistent immunosenescence and metabolic dysregulation post-STEMI; leaves open causal mechanisms and outcome impact in survivors.
Background ST-elevation myocardial infarction (STEMI) induces long-term immune remodeling. Double-positive (DP) CD3+CD4+CD8+ T-lymphocytes represent a minor but functionally plastic subset involved in chronic inflammation and immune adaptation. However, their long-term dynamics following STEMI, particularly in patients with concomitant COVID-19, remains unclear. Purpose To compare immune profiles 3-4 years after STEMI in patients (pts) treated before the COVID-19 pandemic and in pts with STEMI and concomitant COVID-19, focusing on DP T-cells and their associations with metabolic, inflammatory, endothelial, and senescence-associated markers. Methods Sixty post-STEMI pts were examined: 30 pts experienced STEMI in pre-pandemic period (group 1, G1), and 30 – during pandemic with concomitant COVID-19 (group 2, G2). Peripheral blood immunophenotyping was performed by flow cytometry. Senescent-associated heterochromatin foci (SAHF) were assessed by fluorescent microscopy. In addition, glucose metabolism markers, neutrophil-to-lymphocyte ratio (NLR), and brachial artery flow-mediated dilation (FMD) were analyzed. Correlations between DP T-cells (%) and clinical or immunological variables were evaluated. Results In group 1, DP T-cells were integrated into a classical acute-phase inflammatory profile characterized by higher NLR, relative lymphopenia and monocytosis (Table 1). Their positive association with FMD suggests that this inflammatory pattern was not accompanied by endothelial dysfunction. Group 2 demonstrated higher proportions of CD31−CD38+ and SAHF-positive cells, along with elevated glucose and HbA1c levels compared with group 1 indicating persistent immune activation and features of senescence. In this group, DP T-cells were increased and showed a strong positive correlation with SAHF-positive cells, as well as an inverse correlation with CD31−CD38+ activated lymphocytes accompanied by a loss of associations with NLR and FMD. An inverse relationship between CD4+CD8+ and CD4+CD8− cells, together with a direct correlation with CD4−CD8+ cells was observed. This pattern may reflect functional plasticity of DP T cells with a relative CD8-dominant phenotype, consistent with cytotoxic skewing in the context of chronic immune activation. Conclusion Years after STEMI, CD4+CD8+ DP T-cells in non-COVID survivors remain associated with acute-phase inflammatory markers and preserved endothelial and metabolic function, suggesting coordinated immune adaptation. In contrast, concomitant STEMI and COVID-19 are associated with persistent immunosenescence and long-term metabolic dysregulation, along with a cytotoxic shift in the DP subset, potentially reflecting a compensatory response to the accumulation of senescence-prone T-cells following combined ischemic and viral injury.
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Parkhomenko et al. (2026) conducted an observational in ST-elevation myocardial infarction (STEMI) with or without concomitant COVID-19 (n=60). Concomitant COVID-19 infection during STEMI vs. Pre-pandemic STEMI without COVID-19 was evaluated on Double-positive (CD3+CD4+CD8+) T-cell profiles and associations with metabolic, inflammatory, endothelial, and senescence-associated markers. Concomitant COVID-19 in STEMI patients (n=30 vs 30 pre-pandemic) was associated with increased CD4+CD8+ T-cells, elevated SAHF+ senescent cells, and higher glucose/HbA1c at 3-4 years.
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