Abstract 165: Coronary Artery Dilatation in Kawasaki Disease is Associated with Anatomical Coronary Dominance

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Abstract

Introduction: Coronary artery (CA) dilatation in Kawasaki disease (KD) is best determined by elevated Z-scores. Z-score equations, do not take into account anatomical CA dominance. We hypothesize that, except for CA aneurysms, CA dominance influences dilatation status in KD (Z-score > 2.5).

Material and Methods: We retrospectively analyzed CA status in KD patients followed at our institution for persistent CA dilatation. All patients who had a diagnostic catheterization between 2002 and 2012 were considered. Serial echocardiographic dimensions of LCA, RCA, and LAD upon diagnosis, 1 week, 2 weeks, 4 weeks, 2 months, 3-6 months, and 9-12 months later were normalized to BSA using published CA Z-score equations. Data were contrasted with CA angiography description of CA dominance: right or left dominance was adopted when the respective CA supplies both diaphragmatic LV free wall and posterior inter ventricular septum (IVS); Co-dominance was when posterior IVS was supplied by RCA and diaphragmatic LV free wall by LCA.

Results: Of 69 potential patients, 16 were excluded (9 never presented a CA dilatation and 7 had CA aneurysms). The interval between acute onset and selective CA angiography of the remaining 53 patients was 69.5±52.8months at 9.2±5.2years old. Of the latter, 20(37.7%) had LCA-dominance, 31(58.5%) RCA-dominance, and 2(3.8%) Co-dominance. Upon KD onset, the LCA-dominant subset had 14/20(70%) ipsilateral dilatation vs. 6/20(30%) contralateral dilatation. Similarly, RCA-dominant dilatation was ipsilateral in 21/31(68%) vs. 10/31(32%) contralateral dilatation (p=0.89). On late follow-up, persistent CA dilatation was similar between LCA-dominance 6/14(43%) and RCA-dominance 10/21(47%) (p=0.94). The interval between onset and normalizing CA Z-score was 1.16±1.65 vs. 2.45±3.6years in ispilateral vs. contralateral subsets (p=0.19). From the inflammatory perspective, serum albumin was significantly lower in patients with contralateral CA dilatation (p=0.02). Nevertheless, other inflammatory markers did not show a significant difference.

Conclusion: Transitory CA dilatation following KD is closely related to anatomical dominance. This may be a reflection of vasodilation during immune carditis rather than coronary vasculitis.

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