Introduction: atherosclerosis is one of the leading causes of death and morbidity worldwide. It consists in the development of plaques in the intima media layers of arteries due to lipid accumulation and oxidation, causing massive inflammation. We aim to better understand the role of Galectin-3 (Gal-3) and Lipoprotein(a) [Lp(a)] as possible peripheral markers of plaque presence. Methods: Gal-3 and Lp(a) were measured in plasma samples from 99 patients undergoing carotid endarterectomy and 78 healthy controls, by immunometric assays. Plaques were classified histologically, according to the American Heart Association (AHA) guidelines as type Va (fibroatheroma), Vb (mainly calcific) and Vl (complicated lesion). Results: Gal-3 and Lp(a) plasma levels are higher in patients compared to controls [19.8 ng/mL (SD 5.8) vs 14.0 ng/mL (3.6)], p<0.0001 and 8.4 mg/dL (IQR 4.0-25.1) vs 4.7 mg/dL (2.4-12.7), p=0.0003, respectively). Analysis of ROC curves confirmed the discriminating power of these markers obtaining an area under the curve of 0.806 (p<0.0001) for Gal-3 and 0.657 (p=0.0001) for Lp(a). At multivariate logistic regression, Gal-3 and Lp(a) plasma levels were associated with plaque presence independently of each other as well as of age, sex, LDL-C levels and previous myocardial infarction with an odds ratio of 1.22 (95%CI 1.08-1.38, p=0.002) and 1.05 (1.00-1.09, p=0.048) respectively. No differences of Gal-3 and Lp(a) plasma levels were observed among the plaque types. Conclusion: our data showed that Gal-3 and Lp(a) are reliable markers of advanced atherosclerotic plaques. The absence of differences among the different lesion types suggests that the increase of Gal-3 and Lp(a) is independent of the specific plaque features.
|Number of pages||7|
|Publication status||Published - 2019|
- Clinical Biochemistry
- Medical Laboratory Technology
- Biochemistry, medical