Abstract 47: Expression of Galectin-3 in the Myocardium and Arterial Walls of Kawasaki Disease Patients

Abstract

Background: Although coronary artery aneurysms are the most significant complication of Kawasaki Disease (KD), histologic examination 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. It is a prognostic indicator of heart failure and cardiovascular events. Gal-3 plays a role in adhesion and migration of inflammatory and fibroblastic cells. We previously reported that plasma Gal-3 levels were elevated in acute pediatric KD and adult KD with giant aneurysms (GA). We postulated that Gal-3 may be involved in both acute inflammation and convalescent fibrosis in KD. Methods: Conventional H&E staining, Trichrome staining and immunohistochemical analysis for Gal-3 were performed on 1 acute stage KD subject and 10 convalescent stage KD hearts including 6 from subjects with GA and 4 from subjects without aneurysms who died of non-cardiovascular causes. Results: In the acute KD myocardium, round inflammatory cells were seen infiltrating the myocardium and positive staining for Gal-3 was noted. In the myocardium of convalescent KD with GA, widespread cardiomyocyte degeneration and necrosis with extensive bridging fibrosis were observed but inflammatory cells were not detected; spindle-shaped cells expressing Gal-3 in the cytoplasm were observed between cardiomyocytes. Myocardial fibrosis and Gal-3 expression were not observed in the myocardium of KD subjects without aneurysms. In the acute KD coronary arteries, Gal-3 positive inflammatory cells were observed in all layers, and the intima was already thickened by illness day 7. Destruction of the internal elastic lamina and intimal thickening with Gal-3-positive spindle-shaped cells were observed in coronary and systemic arteries of convalescent KD subjects. Conclusion: Gal-3 expression was related to inflammation in acute KD and tissue fibrosis in late convalescent KD with GA. Elevated levels of Gal-3 should raise concern for MF in KD patients with GA. However, in KD without aneurysms, myocardial fibrosis and Gal-3 expression were not observed; therefore myocarditis in KD patients with normal coronary arteries may improve without progression to MF.