Abstract 12251: Galectin-3 as a Predictor of Myocardial Fibrosis in Kawasaki Disease
Background: Kawasaki disease (KD) is a self-limited, acute vasculitis of young children and the etiology remains unknown. Coronary artery aneurysms (CAA) are the most significant complication, but histologic examination of autopsies and biopsies of KD patients has revealed myocarditis and myocardial fibrosis (MF) in most cases.
Galectin-3 (Gal-3) is a matricellular protein that plays a multifunctional role in inflammation, fibrosis, and cell differentiation, and is expressed by fibroblasts and inflammatory cells including macrophages, activated T cells, and dendritic cells. Gal-3 is recognized as a cardiac fibrosis marker associated with heart failure and cardiovascular events. Gal-3 plays a role in adhesion and migration of inflammatory and fibroblastic cells. We postulated that Gal-3 may be involved in myocarditis and MF in KD.
Methods: Plasma Gal-3 levels were determined by ELISA in 63 pediatric (PKD) and 91 adult KD (AKD) subjects, 7 age-similar pediatric healthy controls (HC) and 69 age-similar adult HC. KD subjects were classified by coronary artery status (normal, aneurysm, giant aneurysm). Immunohistochemical analysis (IHCA) for Gal-3 was performed on 1 acute and 4 convalescent stage KD hearts.
Results: PKD subjects had significantly higher Gal-3 levels at all-time points compared to pediatric HC (p<0.05) and AKD subjects with normal CA or small aneurysms (p<0.001). AKD subjects with giant aneurysms had significantly higher Gal-3 levels compared to other AKD and adult HC (p<0.01)(Figure). For acute PKD, there was no correlation between Gal-3 levels [[Unable to Display Character: ​]][[Unable to Display Character: ​]]and inflammatory markers. IHCA showed Gal-3 expression in infiltrating inflammatory cells and in spindle-shaped cells in acute and convalescent myocardium, respectively.
Conclusion: Gal-3 levels are elevated in acute PKD and AKD with giant aneurysms, and may reflect on-going inflammation and subclinical MF. Elevated levels of Gal-3 at one year post-KD onset raise concern for future MF in PKD patients.
Author Disclosures: F. Numano: None. C. Shimizu: None. S.J. Fernandez: None. M. Vejar: None. A. Salgado: None. A.H. Tremoulet: None. J.B. Gordon: None. J.C. Burns: None. L.B. Daniels: None.
- © 2014 by American Heart Association, Inc.