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Importance of anatomical dominance in the evaluation of coronary dilatation in Kawasaki disease

Published online by Cambridge University Press:  19 September 2016

Audrey Dionne
Affiliation:
Division of Pediatric Cardiology, CHU Sainte-Justine, Montreal, Quebec, Canada
Baher Hanna
Affiliation:
Division of Pediatric Cardiology, CHU Sainte-Justine, Montreal, Quebec, Canada
Frédérick Trinh Tan
Affiliation:
Division of Pediatric Cardiology, CHU Sainte-Justine, Montreal, Quebec, Canada
Laurent Desjardins
Affiliation:
Division of Pediatric Cardiology, CHU Sainte-Justine, Montreal, Quebec, Canada Division of Pediatrics, Centre Hospitalier Universitaire de Quebec, Quebec, Canada
Chantale Lapierre
Affiliation:
Division of Radiology, CHU Sainte-Justine, Montreal, Quebec, Canada
Julie Déry
Affiliation:
Division of Radiology, CHU Sainte-Justine, Montreal, Quebec, Canada
Anne Fournier
Affiliation:
Division of Pediatric Cardiology, CHU Sainte-Justine, Montreal, Quebec, Canada
Nagib Dahdah*
Affiliation:
Division of Pediatric Cardiology, CHU Sainte-Justine, Montreal, Quebec, Canada
*
Correspondence to: N. Dahdah, MD, Division of Pediatric Cardiology (6 – Bloc 9), CHU Sainte-Justine, 3175, Cote Sainte-Catherine, Montreal, Quebec, Canada, H3T 1C5. Tel: 514 345 4931 (5403); Fax: 514 345 4896; E-mail: [email protected]

Abstract

Introduction

In Kawasaki disease, although coronary dilatation is attributed to vasculitis, the effect of myocardial inflammation is underestimated. Coronary dilatations are determined by Z-scores, which do not take into account dominance. The aim of the present study was to describe the impact of coronary dominance on dilatation in Kawasaki disease.

Methods

We performed a retrospective analysis of coronary dilatations according to angiography categorisation of dominance.

Results

Of 28 patients (2.6 [0.2–10.1] years), right dominance was present in 15 patients and left in 13. Early dilatation was present in all patients, of whom 11 were ipsilateral to the dominant segment and 17 contralateral. Ipsilateral dilatations were present at diagnosis (9/11 versus 6/17, p=0.02) compared with contralateral dilatations, which developed 2 weeks after diagnosis (9/11 versus 16/17, p=0.29). Coronary artery Z-scores of patients with contralateral dilatation increased at 2 weeks, before returning to baseline values (2.0±2.2 at diagnosis, 4.1±1.8 at 2 weeks, 1.8±1.2 at 3–6 months, p=0.001), compared with patients with ipsilateral dilatation in whom Z-scores were maximal at diagnosis and remained stable (3.0±0.9, 2.7±1.1 and 2.6±1.5, respectively, p=0.13). Dominant coronary artery Z-scores were higher compared with non-dominant segments at diagnosis (3.0±0.9 versus 1.0±0.8, p<0.001) and at late follow-up (2.6±1.5 versus 0.4±1.4, p=0.002) in patients with ipsilateral dilatation.

Conclusion

Progression of coronary dilatation after diagnosis may be a sign of dilatation secondary to vasculitis, as opposed to regression of Z-scores in ipsilateral dilatations, probably related to physiological vasodilatation in response to carditis. This needs to be validated in larger studies against vasculitic and myocardial inflammatory markers.

Type
Original Articles
Copyright
© Cambridge University Press 2016 

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