Identification of biomarker panels as predictors of severity in coronary artery disease

FIGURE 1. A, MMPs levels variation between CAD patient subgroups and controls. C: Controls, 0: Stable angina, 1: NSTEMI (CAD ST‐), 2: STEMI (CAD ST+), n.s: non‐significant, *P < .01, **P < .001, ***P < .0001. B, TIMPs levels variation between CAD patient subgroups and controls. C: Controls, 0: stable angina, 1: NSTEMI (CAD ST−), 2: STEMI (CAD ST+), n. s: non‐significant, *P < .01, **P < .001, ***P < .0001. C, Apolipoproteins levels variation between CAD patient subgroups and controls. C: Controls, 0: stable angina, 1: NSTEMI (CAD ST‐), 2: STEMI (CAD ST+), n. s: non‐significant, *P < .01, **P < .001, ***P < .0001. CAD, coronary artery diseases

FIGURE 2. A, MMPs levels variation between different number of stenosed vessels in patient subgroups and controls. Number of stenosed Vessels, C: Controls, 0: one stenosed vessel, 1: two stenosed vessels, 2: Three stenosed vessels, n.s: non‐significant, *P < .01, **P < .001, ***P < .0001. B, TIMPs levels variation between different number of stenosed vessels in patient subgroups and controls. Number of stenosed Vessels, C: Controls, 0: one stenosed vessel, 1: two stenosed vessels, 2: three stenosed vessels, n.s: non‐significant, *P < .01, **P < .001, ***P < .0001. C, Apolipoproteins levels variation between different number of stenosed vessels in patient subgroups and controls. Number of stenosed Vessels, C: Controls, 0: one stenosed vessel, 1: two stenosed vessels, 2:Three stenosed vessels, n.s: non‐significant, *P < .01, **P < .001, ***P < .0001

FIGURE 3. A, MMPs levels variation between different stent treatments in patient subgroups and controls. Stent treatment, C: Controls, 0: No stent treatment, 1: Bare‐metal stent, 2: Drug elution stent n.s: non‐significant, *P < .01, **P < .001, ***P < .0001. B, TIMPs levels variation between different stent treatment in patient subgroups and controls. Stent treatment, C: Controls, 0: No stent treatment, 1: Bare‐metal stent, 2: Drug elution stent n.s: non‐significant, *P < .01, **P < .001, ***P < .0001. C, Apolipoproteins levels variation between different stent treatments in patient subgroups and controls. Stent treatment, C: Controls, 0: No stent treatment, 1: Bare‐metal stent, 2: Drug elution stent, n.s: non‐significant, *P < .01, **P < .001, ***P < .0001

FIGURE 4. Heatmap showing study biomarkers and the associated discrimination between patient and control groups

FIGURE 5. A, Apo‐CIII, MMP‐9 and TIMP‐2 in patients vs controls, AUC = 0.991. B, Apo‐CII, MMP‐9 and TIMP‐2 in CAD patients subgroups vs controls, AUC = 0.997. C, Apo‐CII, MMP‐9 and TIMP‐2 in‐stent treatment patients subgroups vs controls, AUC = 0.9915. D, Apo‐CIII, MMP‐9 and TIMP‐2 in‐stent treatment patients subgroups Vs controls, AUC = 0.9914. E, Apo‐CIII, MMP‐9 and TIMP‐2 in number of stenosed vessel vs controls, AUC = 0.995. Diagnostic performance of a multiplex protein biomarker assay (Apo‐CII or Apo‐CIII, MMP‐9 and TIMP‐2). ROC was plotted to describe performance characteristics in the 757‐subject cohort (controls and different patient's subgroups) (Figure 3A–E). AUC, area under the curve; C, control; CAD, coronary artery diseases; P, patients, CAD subgroups (0: stable angina, 1: NSTEMI, 2: STEMI), stent treatment (0: no stent treatment, 1: BMS (Bare‐metal stent), 2: DES (Drug elution stent)), number of stenosed vessels (0: one stenosed vessel, 1: two stenosed vessels, 2: three stenosed vessels)