Hospital Performance And Market Share: Implications For Patient Choice, Value-Based Care, And Health Equity

There is substantial hospital-level variation in the quality of healthcare delivered in the United States. Although patients now have greater access to public reporting of hospital quality than ever before, many individual, geographic, and structural factors limit patient choice. The degree to which hospital quality aligns with hospital market share is largely unknown. Using public performance measure score and volume data from CMS’s Hospital Care Compare, we assessed the association between publicly reported hospital performance scores and hospital market share for elective, semi-elective, and non-elective procedures. Using logistic regression, we found a significant association between hospitals’ risk-adjusted complication rate and their market share with a modest effect size for hip/knee replacement complication (-4.2; 95% CI: -6.56, -1.88; p\u3c.001) and acute myocardial infarction (AMI) readmission (-1.7; 95% CI: -3.10, -0.25; p=0.02). We did not find a significant association for AMI mortality or coronary artery bypass graft (CABG) readmission or mortality. These findings highlight a continued need to better align where patients receive care and the quality of care they receive for non-elective and semi-elective conditions/procedures. They support efforts to increase transparency and usability of hospital quality reporting, reduce constraints on patient choice, and increase the capacity and geographic distribution of high-quality hospitals. Value-based payment and healthcare delivery models are essential to efforts to advance the alignment of hospital quality and market share given their incentives around clinical outcomes. Expanding the implementation of these models could improve access to high-quality care. However, early evidence suggests that the structure of many of these programs may disincentivize providers from caring for more complex patients and worsen existing racial and socioeconomic health disparities, indicating an urgent need for refinement and optimization

The Effect of Moderation on Online Mental Health Conversations

Many people struggling with mental health issues are unable to access adequate care due to high costs and a shortage of mental health professionals, leading to a global mental health crisis. Online mental health communities can help mitigate this crisis by offering a scalable, easily accessible alternative to in-person sessions with therapists or support groups. However, people seeking emotional or psychological support online may be especially vulnerable to the kinds of antisocial behavior that sometimes occur in online discussions. Moderation can improve online discourse quality, but we lack an understanding of its effects on online mental health conversations. In this work, we leveraged a natural experiment, occurring across 200,000 messages from 7,000 conversations hosted on a mental health mobile application, to evaluate the effects of moderation on online mental health discussions. We found that participation in group mental health discussions led to improvements in psychological perspective, and that these improvements were larger in moderated conversations. The presence of a moderator increased user engagement, encouraged users to discuss negative emotions more candidly, and dramatically reduced bad behavior among chat participants. Moderation also encouraged stronger linguistic coordination, which is indicative of trust building. In addition, moderators who remained active in conversations were especially successful in keeping conversations on topic. Our findings suggest that moderation can serve as a valuable tool to improve the efficacy and safety of online mental health conversations. Based on these findings, we discuss implications and trade-offs involved in designing effective online spaces for mental health support.Comment: Accepted as a full paper at ICWSM 2021. 13 pages, 12 figures, 3 table

An Analysis of the Role of Tobacco-Specific Nitrosamines in the Carcinogenicity of Tobacco Smoke

Cigarette smoke is a complex mixture consisting of more than 4500 chemicals, including several tobacco-specific nitrosamines (TSNA). TSNA typically form in tobacco during the post-harvest period, with some fraction being transferred into mainstream smoke when a cigarette is burned during use. The most studied of the TSNA is 4-(methylnitrosamino)-l-(3-pyridyl)-l-butanone (NNK). NNK has been shown to be carcinogenic in laboratory animals. Studies examining the carcinogenicity of NNK frequently are conducted by injecting rodents with a single dose of 2.5 to 10 µmol of pure NNK; the amount of NNK contained in all of the mainstream smoke from about 3700 to 14,800 typical U.S. cigarettes. Extrapolated to a 70-kg smoker, the carcinogenic dose of pure NNK administered to rodents would be equivalent to the amount of NNK in all of the mainstream smoke of 22 to 87 million typical U.S. cigarettes. Furthermore, extrapolating results from rodent studies based on a single injection of pure NNK to establish a causative role for NNK in the carcinogenicity of chronic tobacco smoke exposure in humans is not consistent with basic pharmacological and toxicological principles. For example, such an approach fails to consider the effect of other smoke constituents upon the toxicity of NNK. In vitro studies demonstrate that nicotine, cotinine, and aqueous cigarette “tar” extract (ACTE) all inhibit the mutagenic activity of NNK. In vivo studies reveal that the formation of pulmonary DNA adducts in mice injected with NNK is inhibited by the administration of cotinine and mainstream cigarette smoke. Cigarette smoke has been shown to modulate the metabolism of NNK, providing a mechanism for the inhibitory effects of cigarette smoke and cigarette smoke constituents on NNK-induced tumorigenesis. NNK-related pulmoNary DNA adducts have not been detected in rodents exposed to cigarette smoke, nor has the toxicity of tobacco smoke or tobacco smoke condensate containing marked reductions in TSNA concentrations been shown to be reduced in any biological assay. In summary, there is no experimental evidence to suggest that reduction of TSNA will reduce the mutagenic, cytotoxic, or carcinogenic potential of tobacco smoke