Fig. 2

a Left, coronary artery tissue section from KD patient 6, demonstrating subacute chronic (SA/C) inflammation and luminal myofibroblastic proliferation (LMP) with resultant narrowing of the arterial lumen that is filled with blood. Right, coronary artery tissue section from control patient 4, demonstrating normal histology without inflammation. Hematoxylin and eosin stains, M = media, A = adventitia; b Heatmap demonstrating differential gene expression in KD and control coronary artery tissues, with low expression in blue and high expression in red; c KD coronary artery gene expression does not cluster by treatment, patient age, or time since onset of KD. The lack of clustering of gene expression by treatment is likely due to persistent arteritis in the treated patients despite therapy