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Coronary artery disease
Original article
Cardiovascular status after Kawasaki disease in the UK
  1. V Shah1,
  2. G Christov2,
  3. T Mukasa2,
  4. K S Brogan1,
  5. A Wade3,
  6. D Eleftheriou1,
  7. M Levin4,
  8. RM Tulloh5,
  9. B Almeida1,
  10. MJ Dillon1,
  11. J Marek2,
  12. N Klein1,
  13. PA Brogan1
  1. 1Infection, Inflammation and Rheumatology Section, UCL Institute of Child Health, London, UK
  2. 2Department of Paediatric Cardiology, Great Ormond Street Hospital NHS Foundation Trust, London, UK
  3. 3Department of Clinical Epidemiology, Nutrition and Biostatistics Section, UCL Institute of Child Health, London, UK
  4. 4Paediatric Infectious diseases group, Division of Medicine, Imperial College London, London, UK
  5. 5Department of Paediatric Cardiology, Bristol Royal Hospital for Children, Bristol, UK
  1. Correspondence to Dr PA Brogan, Infection, Inflammation and Rheumatology Section, UCL Institute of Child Health, 30 Guilford Street, London WC1N 1 EH, UK; p.brogan{at}ucl.ac.uk

Abstract

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.

This is an Open Access article distributed in accordance with the terms of the Creative Commons Attribution (CC BY 4.0) license, which permits others to distribute, remix, adapt and build upon this work, for commercial use, provided the original work is properly cited. See: http://creativecommons.org/licenses/by/4.0/

https://doi.org/10.1136/heartjnl-2015-307734

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