Short-term Changes in Gal 3 Circulating Levels After Acute Myocardial Infarction

Abstract

Background and aims: Galectin 3 (Gal 3) is a β-galactoside-binding lectin known to play a part in inflammation, adverse remodeling and fibrosis. Gal 3 seems to be linked to atherogenesis and Coronary Artery Disease (CAD), but less is known about the relationship between Gal 3 and acute myocardial infarction (AMI). The aim of the present study is to assess circulating levels of Gal 3 after AMI and to evaluate short-term changes of the biomarker within 5 days from the acute event.

Methods: Two hundred fifteen confirmed AMI patients (125 STEMI, M/F = 2.8; mean age: 65.4 ± 13.8 years) were enrolled in the present study; two blood samples were collected from each patient: first, within 1 h from admission to the Emergency Area (T1) and then upon discharge (T2).

Results: Kinetics of Gal 3 during AMI show that the marker boosts during the acute event (T1) and then decreases from baseline, being significantly lower at T2 (18 [14.2-25] vs. 16.8 [12.7-23.4]; p = 0.006). Gal 3 levels were correlated to hsTnI and eGFR on admission (r = 0.2; p <0.001 and r = -0.25; p <0.001, respectively). Linear regression analysis confirms an association between Gal 3 and ejection fraction (r² = 0.037; p = 0.005).

Conclusions: Gal 3 is reasonably supposed to be a part of those mechanisms leading to formation, destabilization and rupture of plaque; however, the usefulness of Gal 3 as a biomarker in CAD/AMI is far from being elucidated.

Keywords: AMI; CAD; Galectin 3; Inflammation; Plaque.