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.

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.