Background: Kawasaki disease (KD) is a systemic vasculitis prevalent in infants and sometimes complicates coronary artery lesions (CALs). It has been well known that CALs gradually develop endothelial dysfunction, post-inflammatory arteriosclerotic changes, and finally coronary calcification. It has been also reported, recently, that vascular calcification is an active cell-driven process characterized by osteogenic differentiation of vascular smooth muscle cells, relating to the chronic inflammation and oxidative stress. In this study, in KD, we evaluated the possible implication of significant calcification prevalent in CALs to the long-term prognosis.
Methods: We included 42 patients with a history of KD (age:18.3±6.7 year-old). The breakdown was 17 patients without CALs and 25 with CALs; 12 without calcification and 13 with calcification on multi-detector computed tomography. We measured %FMD as an endothelial function marker and hs-CRPs as an inflammatory marker, serum hydroperoxide and urinary 8-OHdG as oxidative stress markers, and the bone mineral density (BMD). Patients in CALs(-) group took no medicine and those in CALs(+) group were under antiplatelet and/or anticoagulant therapy, particularly, those with calcification were additionally administrated statin or ARB.
Results: Values of %FMD in CALs(+) group were significantly lower compared with those in CALs(-) (p<0.05), and values in those with calcification were still lower than those without calcification (p<0.05). Values of hs-CRPs in CALs(+) group were significantly lower than those in CALs (p<0.05). 8-OHdG values as oxidative stress marker in CALs(+) group were significantly lower than those in CALs(-) (p<0.05). The BMD in CALs(+) group tended to be lower compared with the age-matched reference values (88.9±7.0% of normal).
Conclusions: In KD chronic stage, the decreased %FMD may be an essential condition to occur coronary calcification. Decreased BMD in patients with coronary calcification suggested the possible existence of the skeletal and the vascular system in KD, similar to the mechanism of common vascular calcification.