Background-To prospectively apply an automated, quantitative 3-D approach to imaging and airway analysis to assess airway remodeling in asthma.

Background The development of asthma after respiratory syncytial virus (RSV) bronchiolitis has been demonstrated in case-control studies, although the determinants of post-RSV asthma remain undefined. Objectives We sought to evaluate the potential determinants of physician-diagnosed asthma after severe RSV bronchiolitis during infancy. Methods We enrolled 206 children during an initial episode of severe RSV bronchiolitis at 12 months of age or less in a prospective cohort study and followed these children for up to 6 years. In a subset of 81 children, we analyzed CCL5 (RANTES) mRNA expression in upper airway epithelial cells. Results Forty-eight percent of children had physician-diagnosed asthma before the seventh birthday. Independent determinants significantly associated with increased risk for physician-diagnosed asthma by the seventh birthday included maternal asthma (odds ratio [OR], 5.2; 95% CI, 1.7-15.9; P = .004), exposure to high levels of dog allergen (OR, 3.2; 95% CI, 1.3-7.7; P = .012), aeroallergen sensitivity at age 3 years (OR, 10.7; 95% CI, 2.1-55.0; P = .005), recurrent wheezing during the first 3 years of life (OR, 7.3; 95% CI, 1.2-43.3; P = .028), and CCL5 expression in nasal epithelia during acute RSV infection (OR, 3.8; 95% CI, 1.2-2.4; P < .001). White children (OR, 0.19; 95% CI, 0.04-0.93; P = .041) and children attending day care (OR, 0.18; 95% CI, 0.04-0.84; P = .029) had a decreased risk of physician-diagnosed asthma. Conclusions Approximately 50% of children who experience severe RSV bronchiolitis have a subsequent asthma diagnosis. The presence of increased CCL5 levels in nasal epithelia at the time of bronchiolitis or the development of allergic sensitization by age 3 years are associated with increased likelihood of subsequent asthma.

Background Respiratory syncytial virus (RSV) bronchiolitis in infancy is a major risk factor for recurrent wheezing and asthma. As azithromycin attenuated neutrophilic airway inflammation in a murine viral bronchiolitis model, demonstration of similar effects in humans may provide a strategy for the prevention of post-bronchiolitis recurrent wheezing. Objectives To investigate whether azithromycin treatment during RSV bronchiolitis reduces serum and nasal lavage IL-8 levels and the occurrence of post-bronchiolitis recurrent wheezing. Method A randomized, double-masked, placebo-controlled, proof-of-concept trial in 40 otherwise healthy infants hospitalized with RSV bronchiolitis who were treated with azithromycin or placebo for 14 days. IL-8 levels were measured in nasal lavage and serum on randomization, day 8, and day 15 (nasal lavage only). The occurrence of wheezing episodes was assessed monthly over the ensuing 50 weeks. Results Compared to placebo, azithromycin treatment did not reduce serum IL-8 levels at day 8 (p=0.6), but resulted in a greater decline in nasal lavage IL-8 by day 15 (p=0.03). 22% of azithromycin-treated participants experienced at least 3 wheezing episodes compared to 50% of participants in the placebo group (p=0.07). Azithromycin treatment resulted in prolonged time to the third wheezing episode (p=0.048), and in fewer days with respiratory symptoms over the subsequent year in comparison to placebo (36.7 vs. 70.1 days; p=0.01). Conclusion In this proof-of-concept study, azithromycin treatment during RSV bronchiolitis reduced upper airway IL-8 levels, prolonged the time to a third wheezing episode, and reduced overall respiratory morbidity over the subsequent year.

Purpose:To evaluate the relationships of right ventricular (RV) and left ventricular (LV) myocardial perfusion reserves with ventricular function and pulmonary hemodynamics in patients with pulmonary arterial hypertension (PAH) by using adenosine stress perfusion cardiac magnetic resonance (MR) imaging. Materials and Methods:This HIPAA-compliant study was institutional review board approved. Twenty-fi ve patients known or suspected to have PAH underwent right heart catheterization and adenosine stress MR imaging on the same day. Sixteen matched healthy control subjects underwent cardiac MR imaging only. RV and LV perfusion values at rest and at adenosine-induced stress were calculated by using the Fermi function model. The MR imaging-derived RV and LV functional data were calculated by using dedicated software. Statistical testing included KruskalWallis tests for continuous data, Spearman rank correlation tests, and multiple linear regression analyses. Results:Seventeen of the 25 patients had PAH: 11 with sclerodermaassociated PAH, and six with idiopathic PAH. The remaining eight patients had scleroderma without PAH. groups. There were signifi cant correlations between biventricular MPRI and both mean pulmonary arterial pressure (mPAP) (RV MPRI: r = 2 0.59, Bonferroni P = .036; LV MPRI: r = 2 0.79, Bonferroni P , .002) and RV stroke work index (RV MPRI: r = 2 0.63, Bonferroni P = .01; LV MPRI: r = 2 0.75, Bonferroni P , .002). In linear regression analysis, mPAP and RV ejection fraction were independent predictors of RV MPRI. mPAP was an independent predictor of LV MPRI. Conclusion:Biventricular vasoreactivity is signifi cantly reduced with PAH and inversely correlated with RV workload and ejection fraction, suggesting that reduced myocardial perfusion reserve may contribute to RV dysfunction in patients with PAH.q RSNA, 2010

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