Asian Science Citation Index is committed to provide an authoritative, trusted and significant information by the coverage of the most important and influential journals to meet the needs of the global scientific community.  
ASCI Database
308-Lasani Town,
Sargodha Road,
Faisalabad, Pakistan
Fax: +92-41-8815544
Contact Via Web
Suggest a Journal
Articles by E. J Orav
Total Records ( 3 ) for E. J Orav
  L. M Chen , A. K Jha , S Guterman , A. B Ridgway , E. J Orav and A. M. Epstein

Background  Hospitals face increasing pressure to lower cost of care while improving quality of care. It is unclear if efforts to reduce hospital cost of care will adversely affect quality of care or increase downstream inpatient cost of care.

Methods  We conducted an observational cross-sectional study of US hospitals discharging Medicare patients for congestive heart failure (CHF) or pneumonia in 2006. For each condition, we examined the association between hospital cost of care and the following variables: process quality of care, 30-day mortality rates, readmission rates, and 6-month inpatient cost of care.

Results  Compared with hospitals in the lowest-cost quartile for CHF care, hospitals in the highest-cost quartile had higher quality-of-care scores (89.9% vs 85.5%) and lower mortality for CHF (9.8% vs 10.8%) (P < .001 for both). For pneumonia, the converse was true. Compared with low-cost hospitals, high-cost hospitals had lower quality-of-care scores (85.7% vs 86.6%, P = .002) and higher mortality for pneumonia (11.7% vs 10.9%, P < .001). Low-cost hospitals had similar or slightly higher 30-day readmission rates compared with high-cost hospitals (24.7% vs 22.0%, P < .001 for CHF and 17.9% vs 17.3%, P = .20 for pneumonia). Nevertheless, patients initially seen in low-cost hospitals incurred lower 6-month inpatient cost of care compared with patients initially seen in hospitals with the highest cost of care ($12 715 vs $18 411 for CHF and $10 143 vs $15 138 for pneumonia, P < .001 for both).

Conclusions  The associations are inconsistent between hospitals' cost of care and quality of care and between hospitals' cost of care and mortality rates. Most evidence did not support the "penny wise and pound foolish" hypothesis that low-cost hospitals discharge patients earlier but have higher readmission rates and greater downstream inpatient cost of care.

  H. A Bischoff Ferrari , B Dawson Hughes , A Platz , E. J Orav , H. B Stahelin , W. C Willett , U Can , A Egli , N. J Mueller , S Looser , B Bretscher , E Minder , A Vergopoulos and R. Theiler

Background  Care of elderly patients after hip fracture is not well established.

Methods  We enrolled 173 patients with acute hip fracture who were 65 years or older (79.2% women; mean age, 84 years; 77.4% living at home). Using a factorial design, we randomly allocated patients to extended physiotherapy (PT) (supervised 60 min/d during acute care plus an unsupervised home program) vs standard PT (supervised 30 min/d during acute care plus no home program; single-blinded), and to cholecalciferol therapy, 2000 vs 800 IU/d (double-blinded). Primary outcome was rate of falls; secondary outcome was rate of hospital readmissions during the 12-month follow-up. All analyses included 173 individuals and used multivariate Poisson regression analyses.

Results  At baseline, 50.9% of participants had 25-hydroxyvitamin D levels of less than 12 ng/mL and 97.7% of less than 30 ng/mL. We documented 212 falls and 74 hospital readmissions. Because this was a factorial design trial, all analyses tested the main effect of each treatment while controlling for the other in 173 participants. Extended vs standard PT reduced the rate of falls by 25% (95% confidence interval [CI], –44% to –1%). Cholecalciferol treatment, 2000 vs 800 IU/d, did not reduce falls (28%; 95% CI, –4% to 68%), but reduced the rate of hospital readmissions by 39% (95% CI, –62% to –1%).

Conclusions  Extended PT was successful in reducing falls but not hospital readmissions, whereas cholecalciferol treatment, 2000 IU/d, was successful in reducing hospital readmission but not falls. Thus, the 2 strategies may be useful together because they address 2 different and important complications after hip fracture.

Trial Registration identifier: NCT00133640

  C. Y Ho , C Carlsen , J. J Thune , O Havndrup , H Bundgaard , F Farrohi , J Rivero , A. L Cirino , P. S Andersen , M Christiansen , B. J Maron , E. J Orav and L. Kober

Background— Genetic testing identifies sarcomere mutation carriers (G+) before clinical diagnosis of hypertrophic cardiomyopathy (HCM), allowing characterization of initial disease manifestations. Previous studies demonstrated that impaired relaxation develops before left ventricular hypertrophy (LVH). The precise impact of sarcomere mutations on systolic function in early and late disease is unclear.

Methods and Results— Comprehensive echocardiography with strain imaging was performed on 146 genotyped individuals with mutations in 5 sarcomere genes. Contractile parameters were compared in 68 preclinical (G+/LVH–), 40 overt (G+/LVH+) subjects with HCM, and 38 mutation (–) normal control relatives. All subjects had normal left ventricular ejection fraction. In preclinical HCM, global and regional peak systolic strain (sys) and longitudinal systolic strain rate were not significantly different from controls, but early diastolic mitral annular velocity (Ea) was reduced by 13%. In overt HCM, there was a significant 27% and 14% decrease in global longitudinal sys and systolic strain rate, respectively, compared with both preclinical HCM and controls (P<0.013 for all comparisons), and a 33% reduction in Ea.

Conclusions— Sarcomere mutations have disparate initial effects on diastolic and systolic functions. Preclinical HCM is characterized by impaired relaxation but preserved systolic strain. In contrast, both diastolic and longitudinal systolic abnormalities are present in overt disease despite normal ejection fraction. We propose that diastolic dysfunction is an early consequence of sarcomere mutations, whereas systolic dysfunction results from mutations combined with subsequent pathological remodeling. Identifying mechanistic pathways triggered by these mutations may begin to reshape the clinical paradigm for treatment, based on early diagnosis and disease prevention.

Copyright   |   Desclaimer   |    Privacy Policy   |   Browsers   |   Accessibility