Cardiovascular status after Kawasaki disease in the UK
V Shah1, G Christov2, T Mukasa2
1Infection, Inflammation and Rheumatology Section, UCL Institute of Child Health, London, UK.
Insights
Endothelial injury markers persist long after Kawasaki disease (KD), even in children without coronary artery aneurysms (CAA). This indicates a need for long-term cardiovascular monitoring in all KD survivors.
Area of Science:
- Cardiovascular Medicine
- Pediatric Rheumatology
- Vascular Biology
Background:
- Kawasaki disease (KD) is a leading cause of acquired heart disease in children, potentially leading to coronary artery aneurysms (CAA).
- Long-term cardiovascular outcomes for KD patients without CAA or with regressed CAA remain poorly understood.
- Assessing endothelial injury and cardiovascular risk factors is crucial for understanding long-term sequelae.
Purpose of the Study:
- To investigate long-term cardiovascular status in Kawasaki disease patients.
- To examine the relationship between coronary artery status, endothelial injury markers, and cardiovascular risk factors post-KD.
- To compare endothelial injury markers, pulse-wave velocity (PWV), and carotid intima-media thickness (cIMT) between KD patients and healthy controls.
Main Methods:
- Compared circulating endothelial cells (CECs), endothelial microparticles (EMPs), and soluble cell-adhesion molecules between 92 KD patients and 51 healthy controls (HC).
- Classified KD patients based on worst-ever coronary artery (CA) status: CAA present (CAA+) or absent (CAA-).
- Assessed cardiovascular risk factors (CRF), PWV, and cIMT in both groups.
Main Results:
- KD patients exhibited significantly higher CECs than HC, with the highest levels in the CAA+ group and elevated levels also observed in the CAA- group.
- Endothelial microparticles (CD105 EMPs) and specific soluble adhesion molecules were elevated in KD patients, particularly in the CAA+ group.
- No significant differences were found in PWV, cIMT, CRF, or systemic inflammation markers between KD patients and HC.
Conclusions:
- Endothelial injury markers, such as CECs, persist for years following Kawasaki disease.
- These markers of endothelial dysfunction are present even in KD patients who did not develop coronary artery aneurysms.
- Long-term monitoring for endothelial injury is warranted in all Kawasaki disease survivors, irrespective of initial coronary artery status.
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.
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