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. 2022 Jun;36(6):e24469.
doi: 10.1002/jcla.24469. Epub 2022 May 6.

Th1, Th2, and Th17 cells are dysregulated, but only Th17 cells relate to C-reactive protein, D-dimer, and mortality risk in Stanford type A aortic dissection patients

Mowei Song  1 , Li Deng  2 , Hongtao Shen  3 , Guofu Zhang  4 , Hang Shi  4 , Erjun Zhu  4 , Qingping Xia  5 , Hongguang Han  6
Affiliations

Th1, Th2, and Th17 cells are dysregulated, but only Th17 cells relate to C-reactive protein, D-dimer, and mortality risk in Stanford type A aortic dissection patients

Mowei Song et al. J Clin Lab Anal. 2022 Jun.

Abstract

Background: T helper (Th) cells are closely involved in vascular inflammation, endothelial dysfunction, and atherogenesis, which are the hallmarks of aortic dissection (AD). This study aimed to evaluate the clinical value of Th1, Th2, and Th17 cell measurements in Stanford type A AD patients.

Methods: Stanford type A AD patients (N=80) and non-AD patients with chest pain (N = 40) were recruited. Then, Th1, Th2, and Th17 cells in peripheral blood CD4+ T cells from all participants were detected by flow cytometry. The 30-day mortality of Stanford type A AD patients was recorded.

Results: Th1 and Th17 cells were higher, while Th2 cells were lower in Stanford type A AD patients compared with non-AD patients (all p < 0.001). Meanwhile, Th1 cells (area under curve (AUC): 0.734, 95% confidence interval (CI): 0.640-0.828), Th2 cells (AUC: 0.841, 95% CI: 0.756-0.925), and Th17 cells (AUC: 0.898, 95% CI: 0.839-0.957) could distinguish Stanford type A patients from non-AD patients. Moreover, Th1 cells (p = 0.037) and Th17 cells (p = 0.001) were positively related to CRP, and Th17 cells (p = 0.039) were also positively associated with D-dimer in Stanford type A AD patients. Furthermore, Th17 cells were elevated in deaths compared with survivors (p = 0.001), also, it could estimate 30-day mortality risk in Stanford type A AD patients with an AUC of 0.741 (95% CI: 0.614-0.867), which was similar to the value of CRP (AUC: 0.771, 95% CI: 0.660-0.882), but lower than the value of D-dimer (AUC: 0.818, 95% CI: 0.722-0.913).

Conclusion: Th1, Th2, and Th17 cells are dysregulated, but only the Th17 cells relate to CRP, D-dimer, and 30-day mortality risk in Stanford type A AD patients.

Keywords: C-reactive protein; D-dimer; 30-day mortality risk; T helper cells; stanford type A aortic dissection.

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Conflict of interest statement

The authors declare that they have no conflicts of interest.

Figures

FIGURE 1
FIGURE 1
Th1, Th2, and Th17 cells were dysregulated in Stanford type A AD patients. Comparison of Th1 (A), Th2 (B), and Th17 cells (C) between Stanford type A AD patients and non‐AD patients. ROC curves of Th1, Th2, and Th17 cells in distinguishing Stanford type A AD patients from non‐AD patients (D). The comparison was made by the Wilcoxon rank sum test
FIGURE 2
FIGURE 2
Th17 cells were positively related to CRP and D‐dimer in Stanford type A AD patients. Correlation of Th1 (A), Th2 (B), and Th17 cells (C) with CRP. Association of Th1 (D), Th2 (E), and Th17 cells (F) with D‐dimer
FIGURE 3
FIGURE 3
Th17 cells, CRP, and D‐dimer predicted 30‐day mortality risk in Stanford type A AD patients. Comparison of Th1 (A), Th2 (B), and Th17 cells (C) between deaths and survivors. ROC curves of Th1, Th2, and Th17 cells in predicting 30‐day mortality risk (D). ROC curves of CRP and D‐dimer in estimating 30‐day mortality risk (E). The comparison was made by the Wilcoxon rank sum test
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References

    1. Sayed A, Munir M, Bahbah EI. Aortic dissection: a review of the pathophysiology, management and prospective advances. Curr Cardiol Rev. 2021;17(4):e230421186875. - PMC - PubMed
    1. Juraszek A, Czerny M, Rylski B. Update in aortic dissection. Trends Cardiovasc Med. 2021;15:200‐213. - PubMed
    1. Sherk WM, Khaja MS, Williams DM. Anatomy, pathology, and classification of aortic dissection. Tech Vasc Interv Radiol. 2021;24(2):100746. - PubMed
    1. Smedberg C, Steuer J, Leander K, Hultgren R. Sex differences and temporal trends in aortic dissection: a population‐based study of incidence, treatment strategies, and outcome in Swedish patients during 15 years. Eur Heart J. 2020;41(26):2430‐2438. - PMC - PubMed
    1. Jassar AS, Sundt TM 3rd. How should we manage type A aortic dissection? Gen Thorac Cardiovasc Surg. 2019;67(1):137‐145. - PubMed