Galectin -3: an independent cardiac marker of left ventricular (LV) remodeling in chronic heart failure

Abstract

Introduction and Aim: Heart failure (HF) with increased morbidity and mortality is a critical condition where the cardiac pumping capacity fails to meet up with the body’s demand. Its development is silent due to slow, progressive remodeling presenting with symptoms later. Brain Natriuretic peptides (BNP) denotes ventricular loading status which do not reveal other mechanisms whereas a novel marker Galectin-3 (Gal-3) provides information about cardiac structural changes which includes inflammation, fibrosis, remodeling for guiding treatment. Research studies demonstrated that there is upregulation of Galectin- 3 in both acute and chronic heart failure (CHF) individuals. The objectives of our study were to compare Galectin- 3 levels in moderate and severe LVD CHF patients and determine whether serum Galectin -3 can be used as an independent cardiac marker of ventricular structural remodeling in such HF individuals. Materials and Methods: 80 patients between 20 - 80 years diagnosed with CHF using Framingham criteria with ejection fraction (EF) of 45% and classified into two groups:(i) moderate LVD and (ii) severe LVD. Those with abnormal kidney functions were excluded. Comparison was done between serum Galectin - 3 and BNP; Gal- 3 was determined to be an independent marker of structural remodeling of LV between the two categories. Results: Galectin-3 and BNP were significantly increased in HF with severe LVD than moderate LVD. Multivariate linear regression showed Galectin-3 as an independent predictor of LV remodeling with respect to changes in LV end- diastolic dimension with statistically significant p 0.001 whereas BNP did not show any such significance. Conclusion: Galectin -3 and BNP levels were elevated in severe LV dysfunction than moderate LVD and concluded that Gal-3 is an independent cardiac biomarker of LV remodeling in Chronic heart failure.