Cardiovascular status after Kawasaki disease in the UK
Heart, 2015•heart.bmj.com
Objective Kawasaki disease (KD) is an acute vasculitis that causes coronary artery
aneurysms (CAA) in young children. Previous studies have emphasised poor long-term
outcomes for those with severe CAA. Little is known about the fate of those without CAA or
patients with regressed CAA. We aimed to study long-term cardiovascular status after KD by
examining the relationship between coronary artery (CA) status, endothelial injury, systemic
inflammatory markers, cardiovascular risk factors (CRF), pulse-wave velocity (PWV) and …
aneurysms (CAA) in young children. Previous studies have emphasised poor long-term
outcomes for those with severe CAA. Little is known about the fate of those without CAA or
patients with regressed CAA. We aimed to study long-term cardiovascular status after KD by
examining the relationship between coronary artery (CA) status, endothelial injury, systemic
inflammatory markers, cardiovascular risk factors (CRF), pulse-wave velocity (PWV) and …
Objective
Kawasaki disease (KD) is an acute vasculitis that causes coronary artery aneurysms (CAA) in young children. Previous studies have emphasised poor long-term outcomes for those with severe CAA. Little is known about the fate of those without CAA or patients with regressed CAA. We aimed to study long-term cardiovascular status after KD by examining the relationship between coronary artery (CA) status, endothelial injury, systemic inflammatory markers, cardiovascular risk factors (CRF), pulse-wave velocity (PWV) and carotid intima media thickness (cIMT) after KD.
Methods
Circulating endothelial cells (CECs), endothelial microparticles (EMPs), soluble cell-adhesion molecules cytokines, CRF, PWV and cIMT were compared between patients with KD and healthy controls (HC). CA status of the patients with KD was classified as CAA present (CAA+) or absent (CAA−) according to their worst-ever CA status. Data are median (range).
Results
Ninety-two KD subjects were studied, aged 11.9 years (4.3–32.2), 8.3 years (1.0–30.7) from KD diagnosis. 54 (59%) were CAA−, and 38 (41%) were CAA+. There were 51 demographically similar HC. Patients with KD had higher CECs than HC (p=0.00003), most evident in the CAA+ group (p=0.00009), but also higher in the CAA− group than HC (p=0.0010). Patients with persistent CAA had the highest CECs, but even those with regressed CAA had higher CECs than HC (p=0.011). CD105 EMPs were also higher in the KD group versus HC (p=0.04), particularly in the CAA+ group (p=0.02), with similar findings for soluble vascular cell adhesion molecule 1 and soluble intercellular adhesion molecule 1. There was no difference in PWV, cIMT, CRF or in markers of systemic inflammation in the patients with KD (CAA+ or CAA−) compared with HC.
Conclusions
Markers of endothelial injury persist for years after KD, including in a subset of patients without CAA.
heart.bmj.com