Peripheral blood memory T cells and follicular helper T cells as potential biomarkers for assessing disease severity and in-hospital outcomes in acute myocardial infarction patients

外周血记忆性T细胞和滤泡辅助性T细胞作为评估急性心肌梗死患者疾病严重程度和住院预后的潜在生物标志物

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Abstract

BACKGROUND: Acute myocardial infarction (AMI) is a leading cause of morbidity and mortality worldwide. Understanding its pathogenesis is essential for improving treatment and outcomes. Memory T cells and follicular helper T cells (Tfh) may play a role in the immune response to AMI. This study aimed to investigate the association of these cells with AMI severity and hospital outcomes, exploring their potential as biomarkers. METHODS: We studied 403 AMI patients admitted to Shidao People's Hospital, Rongcheng City, between January 2019 and July 2023. Based on Gensini scores assessing coronary artery damage, patients were split into low-risk (LR) and high-risk (HR) groups. Additionally, we categorized patients by hospital outcomes: adverse outcomes (AO, including death or complications) or non-adverse outcomes (NAO). Memory T cell subsets and Tfh cells were quantified using flow cytometry. Heart function and inflammation markers were also measured. Statistical analyses were performed to correlate immune cell levels with AMI severity and outcomes. RESULTS: Patients in the HR group exhibited higher percentage and absolute numbers of CD3+ CD8+ effector memory (Tem) cells and Tfh cells. Elevated levels of these cells were associated with more severe AMI and poorer hospital outcomes. Higher levels of inflammation markers (ischemia-modified albumin [IMA], hypersensitive C-reactive protein [hs-CRP], pentraxin 3 [PTX3]) correlated with worse disease severity. Conversely, lower levels of CD4+ resting memory T cells were linked to worse outcomes, suggesting a potential protective role. Increases in central memory and effector memory T cells were also associated with poor outcomes. CONCLUSION: Our findings show clear links between specific types of T cell subsets and AMI severity and outcomes, highlighting the immune system's critical role in AMI pathogenesis.

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