Objectives: To test the hypothesis that low grade inflammation persists after the acute phase and affects arterial stiffness in children with a history of Kawasaki disease.
Design and patients: A cohort of 106 children was studied, which comprised 43 patients with Kawasaki disease with coronary aneurysms (group I), 28 patients with Kawasaki disease with normal coronary arteries (group II), and 35 healthy age matched children (group III). Their systemic blood pressure, fasting cholesterol concentrations, serum high sensitivity C reactive protein (hs-CRP) concentrations, and carotid artery stiffness index were compared. Significant determinants of serum hs-CRP concentration and carotid artery stiffness were identified and the relation between hs-CRP concentration and arterial stiffness was investigated.
Setting: Tertiary paediatric cardiac centre.
Results: Serum hs-CRP concentration of group I patients (median 0.39 mg/l, interquartile range 0.28–0.65 mg/l) was significantly greater than that of group II (median 0.24 mg/l, interquartile range 0.17–0.29 mg/l, p < 0.001) and of group III patients (median 0.25 mg/l, interquartile range 0.18–0.40 mg/l, p < 0.01). Likewise, carotid artery stiffness index of group I patients (mean (SD) 5.07 (1.11)) was significantly greater than that of group II (4.27 (0.83), p = 0.002), and of group III patients (4.24 (0.86), p = 0.001). For the entire cohort, the carotid artery stiffness index correlated positively with log serum hs-CRP concentration (r = 0.24, p = 0.013). In multiple linear regression analysis, age (standardised β = 0.22, p = 0.02), systolic blood pressure (standardised β = 0.28, p = 0.01), log serum hs-CRP concentration (standardised β = 0.21, p = 0.017), and patient grouping (standardised β = −0.36, p < 0.001) were all independently associated with the carotid artery stiffness index.
Conclusions: These findings support the possibility of ongoing low grade inflammation late after the acute phase of Kawasaki disease in patients with coronary aneurysms. Furthermore, this low grade inflammation may have a role in increasing systemic arterial stiffness.