Elevated CRP levels were independently associated with increased 10-year risk of CHD in intermediate-Framingham-risk men and high-Framingham-risk women.
GDF-15 remained an independent predictor of CHD mortality in SA patients (P < 0.001). Addition of GDF-15 improved the prognostic accuracy of a clinical risk prediction model concerning CHD mortality.
No significant difference between the control (24.2 ± 5.7 g/L) and SA groups (26.3 ± 4.8 g/L). MPO levels in patients with ACS (93.6 ± 20.3 µg/L) were significantly higher than in patients with SA and the healthy control subjects (P < 0.05).
No correlation of SDF-1 with any biochemical parameter (except an inverse correlation with cholesterol levels, P = 0.035), either in the whole study population or in the SA group. No statistical difference in SDF-1 levels between NSTEMI and SA groups.
Increased PCT levels in ACS group than in SA group (P for trend was P < 0.0001). Increased PCT levels at baseline were related to higher cardiovascular mortality (P = 0.00018) and higher cardiovascular event rate (P = 0.026). Also, independently related to future cardiovascular death (HR: 1.34; 95% CI: 1.08–1.65; P = 0.0070) when adjusted for clinical variables.
Decreased fetuin-A levels in SA group than in controls. Higher fetuin-A levels in SA patients, compared to AMI patients (1.67 ± 0.20 ng/mL versus 1.56 ± 0.21 ng/mL, P = 0.020).
Both MMP-8 and MMP-9 levels did not correlate with clinical characteristics. No difference in serum or plasma levels of MMP-8/MMP-9 between SA patients and controls.
TIMP-1, TIMP-2
Brunner et al., 2010 [91], Fiotti et al., 2008 [94], Jönsson et al., 2011 [89]
No significant difference in TIMP-1/TIMP-2 levels between SA groups and controls.
Higher baseline copeptin levels in patients with family CAD history. Patients with serum level ≥20.4 pmol/L suffered more events of the combined primary endpoint and of all-cause death in 90 days.
