Active Remodeling of the Coronary Arterial Lesions in the Late Phase of Kawasaki Disease

• DOI: 10.1161/01.cir.101.25.2935
• Publication Date: 2012-06-12T00:42:29Z
• Authors: Atsuko Suzuki; Sachiko Miyagawa-...; Keiko Komatsu; Toshio Nishikawa; Yasunari Sakomura; Toshinobu Horie; Makoto Nakazawa
• Keywords: Vascular Endothelial Growth Factor A; Lymphokines; Adolescent; Arteriosclerosis; Vascular Endothelial Growth Factors; Coronary Thrombosis; Coronary Disease; Arteries; Endothelial Growth Factors; Mucocutaneous Lymph Node Syndrome; Coronary Vessels; Immunohistochemistry; Muscle, Smooth, Vascular; 3. Good health; 03 medical and health sciences; 0302 clinical medicine; Reference Values; Child, Preschool; Humans; Receptors, Growth Factor; Child; Growth Substances

Background —Remodeling of the coronary artery lesions in Kawasaki disease has been observed in longitudinal angiographic studies. However, mechanisms of such remodeling have not yet been elucidated.

Methods and Results —We examined formalin-fixed specimens of the coronary arteries immunohistochemically by using antibodies against vascular growth factors (GFs) and their receptors in 7 children with Kawasaki disease, 9 children with no coronary disease, and 3 adults with atherosclerosis. In the thickened intima at stenotic sites and at recanalized vessels with Kawasaki disease, extensive expression of vascular GFs, such as transforming GF-β 1 , platelet-derived GF-A, and basic fibroblast GF, was observed both within and surrounding smooth muscle cells. Vascular endothelial GF was observed within smooth muscle cells. Furthermore, all of these GFs were strongly expressed in the newly formed microvessels within the intima. In the thinned media, these GFs were focally and weakly expressed. In contrast, these GFs were expressed only in the media in the control children. In cases of adult atherosclerosis, GFs were expressed diffusely in the media but focally and weakly if at all in the intima.

Conclusions —Active remodeling of the coronary artery lesions in Kawasaki disease continues in the form of luxuriant intimal proliferation and neoangiogenesis for several years after the onset of the disease. This process is distinct from adult-onset atherosclerosis.