Background: Indicators of hospital quality, such as hospital standardized mortality ratios (HSMR), have been used increasingly to assess and improve hospital quality. Our aim has been to describe and explain variation in new HSMRs for the Netherlands.
Methods: HSMRs were estimated using data from the complete population of discharged patients during 2003 to 2005. We used binary logistic regression to indirectly standardize for differences in case-mix. Out of a total of 101 hospitals 89 hospitals remained in our explanatory analysis. In this analysis we explored the association between HSMRs and determinants that can and cannot be influenced by hospitals. For this analysis we used a two-level hierarchical linear regression model to explain variation in yearly HSMRs.
Results: The average HSMR decreased yearly with more than eight percent. The highest HSMR was about twice as high as the lowest HSMR in all years. More than 2/3 of the variation stemmed from between-hospital variation. Year (-), local number of general practitioners (-) and hospital type were significantly associated with the HSMR in all tested models.
Conclusion: HSMR scores vary substantially between hospitals, while rankings appear stable over time. We find no evidence that the HSMR cannot be used as an indicator to monitor and compare hospital quality. Because the standardization method is indirect, the comparisons are most relevant from a societal perspective but less so from an individual perspective. We find evidence of comparatively higher HSMRs in academic hospitals. This may result from (good quality) high-risk procedures, low quality of care or inadequate case-mix correction.
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http://dx.doi.org/10.1186/1472-6963-8-73 | DOI Listing |
Alzheimers Dement
December 2024
Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Background: Clinical trials should strive to yield results that are clinically meaningful rather than solely relying on statistical significance. However, the determination of clinical meaningfulness of dementia clinical trials lacks standardization and varies based on the trial's nature. To tackle this issue, a proposed approach involves assessing the time saved before reaching a specific threshold in cognitive status.
View Article and Find Full Text PDFBackground: Human pluripotent stem cell (hPSC)-derived brain organoids patterned towards the cerebral cortex are valuable models of interactions occurring in vivo in cortical tissue. We and others have used these cortical organoids to model dominantly inherited FTD-tau. While these studies have provided essential insights, cortical organoid models have yet to reach their full potential.
View Article and Find Full Text PDFReal-world data on the uptake, effectiveness and safety of new diagnostics and disease-modifying (DMT) treatments for Alzheimer's Disease (AD) are imperative. This can be achieved through patient registries. A major challenge is how to embed registry data capture into routine clinical practice.
View Article and Find Full Text PDFLecanemab, a humanized IgG1 monoclonal antibody that binds with high affinity to amyloid-beta (Aβ) protofibrils, was formally evaluated as a treatment for early Alzheimer's disease in a phase 2 study (Study 201) and the phase 3 Clarity AD study. These trials both included an 18-month, randomized study (core) and an open-label extension (OLE) phase where eligible participants received open-label lecanemab for up to 30 months to date. Clinical (CDR-SB, ADAS-Cog14, and ADCS-MCI-ADL), biomarker (PET, Aβ42/40 ratio, and ptau181) and safety outcomes were evaluated.
View Article and Find Full Text PDFAlzheimer's disease pathophysiology is believed to involve various abnormalities, including those of amyloid beta (Ab) peptide and tau processing, inflammation, oxidative stress, and vascular risk factors. Aβ peptides exist in a dynamic continuum of conformational states from monomeric Aβ, to soluble progressively larger Aβ assemblies that include a range of low molecular weight oligomers to higher molecular weight protofibrils, and finally to insoluble fibrils (plaques). Various lines of evidence support the "amyloid hypothesis" that Aβ plays a central role in the pathogenesis of AD, and several immunotherapies have been developed to interact with this cascade in various different places which may reduce the number of soluble aggregates and insoluble Aβ fibrils deposited in the brain.
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