Galectin-3 Plasma Levels and Coronary Artery Disease: A New Possible Biomarker of Acute Coronary Syndrome

Abstract

Inflammation plays a key role in atherosclerosis. Galectin-3 is a macrophage- and endothelium-derived mediator actively involved in the regulation of many aspects of inflammatory cell behaviour. The aim of this study is to quantify plasma Galectin-3 in patients with coronary artery disease (CAD) and different clinical manifestation at the moment of observation in order to verify whether Galectin-3 could be a useful biomarker of atherosclerotic state. We enrolled 125 patients affected by CAD, angiographically documented (70 stable, 55 unstable). They underwent accurate examinations and anamnestic data was collected. The most important traditional risk factors, such as age, hypertension, and body mass index, were reported. Plasma Galectin-3 was quantified using an ELISA kit. Unstable patients (n = 55) had a higher plasma Galectin-3 levels in respect to the stable subjects (27.75 ng/mL (19.27–39.09) vs 6.48 ng/ml (4.88–8.83), p<0.001. A trend in correlation between plasma Galectin-3 levels and number of vessels compromised seems to be present: CAD patients with three-vessel disease had higher levels of Galectin-3 than patients with one-or two-vessel disease (17.39 ng/ml (10.75–29.82) vs 9.18 ng/ml (5.56–23.22), p= 0.058. The significantly higher plasma Galectin-3 levels in patients with unstable angina in respect to the stable angina confirm the involvement of Galectin-3 in promoting macrophage activation and monocyte attraction. Despite the distribution of CAD in patients with acute and chronic coronary disease being similar, we may hypothesize that Galectin-3 could be a useful biomarker of atherosclerotic plaque and in particular of its destabilization.

The association between galectin-3 and clinical parameters in patients with fi rst acute myocardial infarction treated with primary percutaneous coronary angioplasty

“…Data from the Pravastatin or Atorvastatin Evaluation and Infection Therapy-Thrombolysis In Myocardial Infarction 22 trial (PROVEIT-TIMI 22) demonstrated that galectin-3 values above 16.7 µg/L (median), measured within 7 days after acute coronary syndrome, was significantly associated with higher risk of HF development during 2-year follow--up, but elevated levels of this biomarker were observed mostly in patients with hypertension, diabetes, prior HF and prior MI [16]. Falcone et al [17] analyzed a group of patients with angiographically documented coronary artery disease: unstable patients (n = 55) had higher galectin-3 levels in comparison to the stable subjects (27.75 ng/mL vs. 6.48 ng/mL, p < 0.001). Compared with these studies, we observed lower galectin-3 concentrations in our group of patients (median 13.0 ng/mL), which could be explained by our restrictive inclusion and exclusion criteria.…”

Galectin-3 in acute coronary syndrome

“…Firstly, the most common finding among such investigations is that circulating Gal-3 levels are elevated in ACS/AMI, being released during the acute phase of AMI [31,[33][34][35][36][37][38][39]. Indeed, Gal-3 could be part of a survival mechanism of the injured myocardium to cope with the ischemic insult [14].…”

Automatizáltan mérhető biomarkerek az akut myocardialis infarctus diagnosztikájában

“…Wilcoxon-próbát alkalmaztunk a felvételkori és a később (6 órán belül) elvégzett hsTn-mérés eredményeinek összehasonlítására. Beszédzavar (1) Apoplexia cerebri (1) Eszméletvesztés (35) AMI (3), delirium tremens (1), epilepszia (3), exsiccosis (1), hyperglikaemiás ketoacidosis (3), hypoglikaemia (2), ictus caloris (1), sokk (2), collapsus (2), pancreatitis acuta (2), fi brillatio auricularis (4), rhabdomyolysis (3), apoplexia cerebri (3), arrhythmia cardiaca (2), embolia pulmonum (2), infarctus cerebri (1) Fejfájás (2) Cephalalgia (1), hypertonia (1) Fulladás (30) Bronchitis acuta (5), COPD (1), hydrothorax (2), bronchitis chronica (1), decompensatio cardiaca (9), fi brillatio auricularis (3), pneumonia (4), neoplasma pulmonum malignum (2), oedema pulmonum (3) Gyengeség (20) Infarctus cerebri (1), cholecystitis (1), exsiccosis (2), anxietas (1), TIA (15) Hányás (3) Gastritis acuta (1), subileus (2) Hasfájás (5) Exsiccosis (1), hyperaciditas (1), pancreatitis acuta (1), szeptikus sokk (2) Lábduzzadás (5) MVT (2) [5]. Az AMI bekövetkezte utáni praenecrosis-és necrosis-biomarkerek koncentrációjának változását mutatja a 3. ábra.…”

“…A prognosztikai markerek (oldható OX40 ligand, MPO, rezisztin, oldható ST2 fehérje) egy esetleg későbbi időpontban bekövet-kező AMI valószínűségét jelzik [6,16,17,18]. A plakkmarkerek (visfatin, galectin-3, oldható lectinszerű oxidált LDL-receptor-1, lipoproteinasszociált foszfolipáz-A2, leukotrién-B4, extracelluláris mátrixmetalloproteináz, triptáz, oldható LR11 fehérje, oldható amyloid prekurzor fehérje 770, apelin, chitotriosidas, tenascin-C) az instabilitást, a sérülés bekövetkeztét, mértékét mutatják, így utalva az AMI lehetőségére [19,20,21,22,23,24,25,26,27,28,29,30]. Ígéretes korai markernek tűnik az ischaemiamodifi kált albumin, a hősokkfehérje-27, a katepszin-K, a C1q-kötő adiponectin, a sejtmentes keringő DNS, a májsejt-növekedési faktor, a glikogén foszforiláz BB izoenzim és a növekedést elkülönítő faktor 15 [31,32,33,34,35,36,37,38,39].…”