Table 1.
Patient characteristics.
Figure 1.
Systemic and local levels of proinflammatory and anti- inflammatory markers.
Serum levels of inflammatory markers in systemic, pre-, and post-procedural local samples were measured by ELISA. Results are expressed as mean ± IQRs. Differences between the samples are not significant, except for those indicated by *P<0.05.
Figure 2.
Comparison of proinflammatory and anti- inflammatory markers for plaque vulnerability.
Serum levels of proinflammatory and anti-inflammatory markers from vulnerable and stable plaques in systemic, pre-, and post-procedural local samples were measured by ELISA. Results are expressed as mean ± IQRs. Differences between the samples are not significant, except for those indicated by *P<0.05.
Figure 3.
Comparison of systemic and control samples.
Serum levels of proinflammatory and anti-inflammatory markers in systemic samples of patients with vulnerable and stable plaques, and controls were measured by ELISA. Results are expressed as mean ± IQRs. Differences between the samples are not significant, except for those indicated by *P<0.05.
Figure 4.
Immunochemical staining of atherosclerotic carotid endarterectomy specimens and emboli captured by distal protection devices.
Serial sections were stained with hematoxylin and eosin (HE) (A, B, C, Q, R), anti-IL-6 (D, E, F), anti-PTX3 (G, H, I), and anti-E-selectin (J, K, L) antibodies. Sections from CEA (A to L), quantification of immunohistochemistry analysis of IL-6, PTX3, and E-selectin staining of sections from CEA (M, N, O), and embolic debris from CAS captured by the distal filter device (P, Q, R) are shown. HE staining showed inflammatory cell infiltrations in the vulnerable plaques (A, B, Q) and cholesterin crystals in the stable plaques (C, R). IL-6 staining is observed in the vulnerable plaques with inflammatory cell infiltration (D, E) but not in the stable plaques (F). PTX3 expression is observed in endothelial and perivascular cells and in the basement membrane in the vulnerable plaques (G, H) but not in the stable plaques (I). Immunohistochemistry revealed E-selectin expression in endothelial cells in the vulnerable plaques (J, K) but not in the stable plaques (L). The second line on the left of the vulnerable plaques (B, E, H, K) shows enlargement of the cropped areas. Scale bar, 100 µm.
Figure 5.
Receiver-operating curve of PTX3 levels for predicting vulnerable plaque.
The area under the curve of PTX3 levels were obtained from all patients.
Figure 6.
Proinflammatory and anti-inflammatory biomarkers in vulnerable plaques.
Decreased adiponectin levels induce endothelial cell dysfunction with E-selectin release, with subsequent low IL-10 levels and high TNFα levels. Impaired endothelial cells release E-selectin, PTX3, and TNFα. Macrophages produce PTX3, TNFα, and IL-6.