Galectin-3: Relation to infarct scar and left ventricular function after myocardial infarction

Abstract

Elevated serum levels of galectin-3, a member of the lectin family, have recently been reported in heart failure patients, aswell as in animal models of heart failure [1–3]. Apart from cardiac remodelling, upregulation of galectin-3 expression and release has also been associated with several other human fibrotic conditions including liver cirrhosis, idiopathic lung fibrosis, pancreatitis and renal failure. Therefore, this lectin is thought to play some regulatory role between inflammation and fibrosis [1]. Its direct mediation of profibrotic pathways such as cell adhesion and proliferation suggests that galectin-3 is involved in the development of heart failure [4,5]. After acute myocardial infarction (AMI), fibrosis and tissue remodelling are the leading causes for the development of heart failure. Cardiacmagnetic resonance (CMR) imagingwith its concept of late enhancement provides high-resolution delineation of myocardial infarction size with diagnostic accuracy and good reproducibility [6,7]. The aim of the present studywas to investigate the correlation of galectin-3 concentrations to CMR-determined myocardial infarction size as well as myocardial function measured four months after STelevation myocardial infarction (STEMI) treated with primary percutaneous coronary intervention (p-PCI). Blood samples of successfully reperfused STEMI patients (n=29, mean age: 58.1±10.1 yrs) were obtained four months after the acute event. Patients selected for this analysis had no history for any chronic disease. Galectin-3 was measured using an enzyme-linked immunoInternational Journal of Cardiology 163 (2013) 335–344