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).