These results indicate that in patients with Kawasaki disease the coronary disease accompanying impaired reactivity to nitroglycerin is present at the sites of regressed aneurysms as well as in angiographically normal coronary segments. We suggest that these sites with morphologic and functional abnormalities are related to the development of significant stenosis.

This study determined the long-term outcome for patients after myocardial infarction (MI) due to Kawasaki disease (KD). Retrospective analysis was performed for 60 patients who had experienced MI between 1976 and 2007. Their ages at the initial MI ranged from 3 months to 33 years (median, 2 years). The maximum follow-up period after the initial MI was 33 years (median, 16 years). Coronary angiography, left ventriculography, and radioisotope myocardial perfusion imaging (MPI) had been performed for 56 patients more than 2 months after MI when all were in stable condition. The survival rate and ventricular tachycardia (VT)-free survival rate were calculated after the initial MI by the Kaplan-Meier method. Both sustained and nonsustained VT were included. Furthermore, the Cox proportional hazards model was used to analyze which factors influenced the post-MI outcome and which influenced the appearance of VT. The 30-year survival rate was 62.7% (95% confidence interval [CI], 44.6-77.9%), and the 25-year VT-free survival rate after MI was 28.5% (95% CI 15.4-46.5%). The postinfarction left ventricular ejection fraction (LVEF) was related to the outcome in this population (hazard ratio 0.86; 95% CI 0.75-0.95; P = 0.002), whereas the development of VT was related to the post-LVEF and to perfusion abnormalities in MPI (P = 0.0002). The 30-year survival rate after MI was poor for the patients with a low LVEF. With aging, the existence of nonviable myocardium in the infarct area can induce fatal ventricular arrhythmia more than 10 years after the original MI.

Objectives: To evaluate the effectiveness and long term outcomes of catheter intervention for obstructive conduits between the right ventricle and pulmonary arteries. Design: Retrospective chart review. Setting: Tertiary care paediatric cardiology unit. Patients and interventions: 70 procedures in 68 children (median age at intervention 6 years, median interval after conduit insertion 3.4 years) were analysed. All children had haemodynamic indications for conduit replacement. Twenty four children underwent a second intervention (stent dilatation in 17, second stent implantation in seven). Results: Mean (SD) conduit pressure gradient decreased from 44 (18) mm Hg to 18 (12) mm Hg at the initial intervention (n = 62, p , 0.001) and from 39 (15) mm Hg to 23 (10) mm Hg at the second intervention (n = 16, p , 0.001). The percentage of the predicted right ventricular outflow area increased from 17 (9)% to 44 (22)% at the initial intervention (n = 62, p , 0.001) and from 24 (8)% to 29 (11)% at the second intervention (n = 21, p , 0.001). The conduit was subsequently replaced in 33 children. Freedom from conduit replacement from the time of stent implantation was 83%, 75%, and 47% at one, two, and five years, respectively, and from the time of the initial conduit surgery it was 87%, 64%, and 42% at five, eight, and 10 years, respectively. Body growth was maintained, no deaths were reported during follow up, and pulmonary insufficiency was well tolerated. Conclusion: A catheter treatment strategy for obstructive conduits is safe and effective in prolonging conduit function.