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Background Accurate prediction of coronary artery aneurysms ( CAAs ) in patients with Kawasaki disease remains challenging in North American cohorts. We sought to develop and validate a risk model for CAA prediction. Methods and Results A binary outcome of CAA was defined as left anterior descending or right coronary artery Z score ≥2.5 at 2 to 8 weeks after fever onset in a development cohort (n=903) and a validation cohort (n=185) of patients with Kawasaki disease. Associations of baseline clinical, laboratory, and echocardiographic variables with later CAA were assessed in the development cohort using logistic regression. Discrimination (c statistic) and calibration (Hosmer-Lemeshow) of the final model were evaluated. A practical risk score assigning points to each variable in the final model was created based on model coefficients from the development cohort. Predictors of CAAs at 2 to 8 weeks were baseline Z score of left anterior descending or right coronary artery ≥2.0, age 40-fold greater in the validation cohort (odds ratio, 44.0; 95% CI, 10.8-180 [ P

OBJECTIVES: We sought to analyze trends in admissions and to describe therapies used for acute Kawasaki disease over a 6-year period. METHODS: The Pediatric Health Information System provides patient data including demographic variables, International Classification of Diseases, Ninth Revision codes, and services billed to patients. Patient identifiers enable tracking of medication use in and across multiple admissions within a center. We analyzed data for patients with (1) a diagnosis code for Kawasaki disease, (2) intravenously administered immunoglobulin treatment during hospitalization, and (3) discharge between January 1, 2001, and December 30, 2006, from 27 hospitals contributing complete data over the study period. RESULTS: During the study period, 5197 Kawasaki disease admissions were identified for 4811 patients; numbers increased 32.6% from 2001 (n = 678) to 2006 (n = 899). Retreatment with intravenous immunoglobulin was administered to 712 patients (14.8%) over the study period. Other antiinflammatory therapies included intravenously administered methylprednisolone (5.8%), orally administered prednisone (2.8%), and infliximab (1%). Use of infliximab steadily increased from 0.0% (0 of 678 patients) in 2001 to 2.3% (21 of 899 patients) in 2006. Coronary artery aneurysms were coded for 3.3% of patients. Male patients, patients <1 year of age, and Hispanic patients were significantly more likely to have coding for coronary artery aneurysms. CONCLUSIONS: Our report provides the first large multicenter description of agents used in the treatment of intravenously administered immunoglobulin-resistant Kawasaki disease in the United States. Trends include increased numbers of admissions attributable to Kawasaki disease and increased usage of infliximab. [ABSTRACT FROM AUTHOR]

Introduction: Accurate prediction of coronary artery aneurysms (CAA) in patients (pts) with Kawasaki Disease (KD) is challenging in North American (NA) cohorts. We sought to develop and validate a risk model for CAA prediction in KD pts that included baseline demographic, clinical and echo data. Methods: The development cohort consisted of KD pts at 2 centers (n=726); pts enrolled in the Pediatric Heart Network's KD trial constituted the validation cohort (n=185). Pts were treated with IVIG within 10 days of fever onset; other therapies were permitted. A binary outcome of CAA was defined as LAD or RCA z score (zMax) ≥2.5 at 2-8 weeks after fever onset. Associations of baseline clinical, laboratory and echo variables with later CAA were assessed in the development cohort using logistic regression; discrimination (c statistic) and calibration (Hosmer Lemeshow) were evaluated in both cohorts. A simple risk score assigning points to each variable in the final model was created based on model coefficients in the development cohort. Results: Independent predictors of CAA at 2-8 wks were baseline zMax ≥2.0, age <6 months, Asian race and hemoglobin <10.2 mg/dL (c = 0.83 development, c = 0.89 validation, Table 1). The risk score assigned 2 points for baseline zMax ≥2.0 and 1 point for each of the other variables with creation of low (0-1), moderate (2) and high risk (3-5) groups. The odds of CAA was 20 fold greater in the high vs low risk groups (OR= 20.1, [10.8, 37.6], p <0.001, Table 2). Conclusion: We developed a risk model for CAA in KD pts consisting of baseline demographic, laboratory and echo variables. Our model had excellent predictive value, and should undergo future testing in larger NA populations. [ABSTRACT FROM AUTHOR]