Galectin-3, Carotid Plaque Vulnerability, and Potential Effects of Statin Therapy

• Published in: European journal of vascular and endovascular surgery Vol. 49; no. 1; pp. 4 - 9
• Main Authors: Kadoglou, N.P.E, Sfyroeras, G.S, Spathis, A, Gkekas, C, Gastounioti, A, Mantas, G, Nikita, K.S, Karakitsos, P, Liapis, C.D
• Format: Journal Article
• Language: English
• Published: England Elsevier Ltd 01.01.2015
• Subjects: Aged; Antigens, CD - analysis; Antigens, Differentiation, Myelomonocytic - analysis; C-Reactive Protein - analysis; Carotid Artery Diseases - complications; Carotid Artery Diseases - diagnostic imaging; Carotid Artery Diseases - pathology; Carotid Artery Diseases - therapy; Carotid atherosclerosis; Carotid Stenosis - etiology; Cross-Sectional Studies; Endarterectomy, Carotid; Female; Galectin 3 - analysis; Galectin 3 - blood; Galectin-3; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors - pharmacology; Immunohistochemistry; Laminin - analysis; Macrophages - immunology; Macrophages - pathology; Male; Plaque vulnerability; Plaque, Atherosclerotic - chemistry; Plaque, Atherosclerotic - diagnostic imaging; Regression Analysis; Statins; Stroke/transient ischemic attack; Surgery; Ultrasonography; Stroke/transient ischemic attack; Plaque vulnerability; Galectin-3; Carotid atherosclerosis; Statins
• DOI: 10.1016/j.ejvs.2014.10.009
• ISSN: 1078-5884

Objectives Galectin-3, a member of galectines, a family of β-galactoside-specific lectins, has been reported to propagate vascular inflammation. The role of galectin-3 in carotid atherosclerosis is controversial. The aim of this study was to investigate the relationship of galectin-3 with plaque vulnerability in patients with high grade carotid stenosis. Methods This was a cross sectional study of patients undergoing carotid endarterectomy (CEA). Carotid plaques obtained from 78 consecutive patients (40 symptomatic [SG], 38 asymptomatic [AG]) undergoing CEA were histologically analyzed for galectin-3, macrophages (CD68) and laminin. Pre-operatively the biochemical profile and plaque echogenicity (gray-scale median, GSM) score were determined. Results There were no significant differences in clinical and demographic parameters between SG and AG ( p  > .05). The SG had a lower GSM score (44.21 ± 18.24 vs. 68.79 ± 28.79, p  < .001) and a smaller positive stained area for galectin-3 (4.89 ± 1.60% vs. 12.01 ± 5.91%, p  < .001) and laminin (0.88 ± 0.71% vs. 3.46 ± 2.12%, p  < .001) than the AG. On the other hand, intra-plaque macrophage content was increased in SG ( p  < .001). For the whole cohort, symptomatic status was independently associated with intra-plaque contents of both galectin-3 (OR = 0.634, p  < .001), and GSM score (OR = 0.750, p  < .001). Notably, patients on long term statin treatment had elevated galectin-3 and lowered macrophage intra-plaque concentrations compared with those on short term treatment ( p  < .05). Conclusions A low galectin-3 intra-plaque concentration seems to correlate with clinically and ultrasonically defined unstable human carotid plaques. Long term statin treatment may induce increase of intra-plaque galectin-3 concentration mediating plaque stabilization.