The Impact of the Medicare Access and CHIP Reauthorization Act on the Field of Ophthalmology.

PURPOSE: To analyze the impact of the Medicare Access and CHIP Reauthorization Act of 2015 (MACRA) on the field of ophthalmology. DESIGN: A perspective on the effects of MACRA's Quality Payment Program after analysis of the proposed rule, final rule, and commentary submitted by relevant stakeholders. RESULTS: Physicians will need to use 1 of 2 payment structures: Merit-Based Incentive Payment Systems (MIPS) or Alternative Payment Models (APMs). APMs and MIPS will focus on bundling payments and reimbursing based on "fee-for-service-plus" models, which take into account clinical outcomes, coordination of care, clinical improvement, and electronic information exchange and security. APMs have substantial advantages, with eligible participants receiving a bonus and a higher rate of annual adjustment over the program's life. For most ophthalmology practices, MIPS may be more appropriate owing to its broader applicability and the current paucity of APMs for ophthalmologists. CONCLUSION: The Quality Payment Program is a substantial improvement over the negative adjustments under the repealed Substantial Growth Rate model. Ophthalmologists will likely use the MIPS system; however, its comparatively lower reimbursements, as well as its cost, quality, and other reporting measures, may prove problematic.

Combined exposure to cigarette smoke and nontypeable Haemophilus influenzae drives development of a COPD phenotype in mice.

BACKGROUND: Cigarette smoke (CS) is the major etiologic factor of chronic obstructive pulmonary disease (COPD). CS-exposed mice develop emphysema and mild pulmonary inflammation but no airway obstruction, which is also a prominent feature of COPD. Therefore, CS may interact with other factors, particularly respiratory infections, in the pathogenesis of airway remodeling in COPD. METHODS: C57BL/6 mice were exposed to CS for 2 h a day, 5 days a week for 8 weeks. Mice were also exposed to heat-killed non-typeable H. influenzae (HK-NTHi) on days 7 and 21. One day after the last exposure to CS, mice were sacrificed and lung inflammation and mechanics, emphysematous changes, and goblet cell metaplasia were assessed. Mice exposed to CS or HK-NTHi alone or room air served as controls. To determine the susceptibility to viral infections, we also challenged these mice with rhinovirus (RV). RESULTS: Unlike mice exposed to CS or HK-NTHi alone, animals exposed to CS/HK-NTHi developed emphysema, lung inflammation and goblet cell metaplasia in both large and small airways. CS/HK-NTHi-exposed mice also expressed increased levels of mucin genes and cytokines compared to mice in other groups. CS/HK-NTHi-exposed mice infected with RV demonstrated increased viral persistence, sustained neutrophilia, and further increments in mucin gene and chemokine expression compared to other groups. CONCLUSIONS: These findings indicate that in addition to CS, bacteria may also contribute to development of COPD, particularly changes in airways. Mice exposed to CS/HK-NTHi are also more susceptible to subsequent viral infection than mice exposed to either CS or HK-NTHi alone.