Figure legends.
Figure 1. Cumulative MACE survival probability at the long-term follow-up, according to the quintiles of maximum levels hs-cTnT during the in-hospital stay. HR: 2.16; 95% CI: 1.82-2.58; p value <0.001 for each increasing quintile (multivariable COX regression analysis).
Figure 2. Troponin levels during hospitalization according to corticosteroid treatment in patients with hs-cTnT>0.014 µg/L. Data are expressed as adjusted marginal means (±SE) of log-transformed hs-cTnT levels (MANOVA analysis).
Figure 3. Kaplan–Meier estimates of time to MACE according to in-hospital corticosteroid treatment among patients with hs-cTnT > 0.014 µg/L during the in-hospital stay (log-rank test).
Figure 4. Serum sNox2-dp levels during hospitalization according to corticosteroid treatment in the whole cohort (panel A), in patients with hs-cTnT>0.014 µg/L (panel B) and in patients with hs-cTnT ≤ 0.014 0.014 µg/L (panel C). Data are expressed as adjusted marginal means (±SE) of log-transformed sNox2-dp levels (MANOVA analyses).
Figure 5. Glucocorticoids and oxidative stress. Nox2 activation (A) and H2O2 production (B) were evaluated in human peripheral blood mononuclear cells (PBMCs) incubated with scalar concentrations (150–600 ng/ml) of betamethasone or methylprednisolone and stimulated with LPS (40pg/ml) (n = 5 experiments) (*p value < 0.05; **p value <0.001;***p value <0.0001; Kruskal–Wallis test).
Figure 6. Glucocorticoids and pathway of oxidative stress. AKT (A) and p47phox (C) phosphorylation were analyzed in in human peripheral blood mononuclear cells (PBMCs) incubated with scalar concentrations (150–600 ng/ml) of betamethasone or methylprednisolone and stimulated with LPS (40pg/ml) (n = 3 experiments) (*p value < 0.05; **p value <0.001;***p value <0.0001; Kruskal–Wallis test). A representative western blot of AKT (B) and p47phox (D) phosphorylation in the presence or not of betamethasone or methylprednisolone (150–600 ng/ml).