Increases in smoking cessation interventions after a feedback and improvement initiative using electronic health records -- 19 community health centers, New York City, October 2010-March 2012.

Quitting smoking substantially reduces smokers' risk for smoking-related morbidity and mortality and can increase life expectancy by up to a decade. Most smokers want to quit and make at least one medical provider visit annually. Health care providers can play an important role in helping smokers quit by documenting patients' tobacco use, advising smokers to quit, and providing evidence-based cessation treatments or referrals for treatment, but many providers and practices do not regularly take these actions. Systems to increase provider screening and delivery of cessation interventions are available; in particular, electronic health records (EHRs) can be powerful tools to facilitate increased cessation interventions. This analysis reports on an EHR-based pay-for-improvement initiative in 19 community health centers (CHCs) in New York City (NYC) that sought to increase smoking status documentation and cessation interventions. At the end of the initiative, the mean proportion of patients who were documented as smokers in CHCs had increased from 24% to 27%, whereas the mean proportion of documented smokers who received a cessation intervention had increased from 23% to 54%. Public health programs and health systems should consider implementing strategies to equip and train clinical providers to use information technology to increase delivery of cessation interventions.

Hypotension, lipodystrophy, and insulin resistance in generalized PPARgamma-deficient mice rescued from embryonic lethality.

We rescued the embryonic lethality of global PPARgamma knockout by breeding Mox2-Cre (MORE) mice with floxed PPARgamma mice to inactivate PPARgamma in the embryo but not in trophoblasts and created a generalized PPARgamma knockout mouse model, MORE-PPARgamma knockout (MORE-PGKO) mice. PPARgamma inactivation caused severe lipodystrophy and insulin resistance; surprisingly, it also caused hypotension. Paradoxically, PPARgamma agonists had the same effect. We showed that another mouse model of lipodystrophy was hypertensive, ruling out the lipodystrophy as a cause. Further, high salt loading did not correct the hypotension in MORE-PGKO mice. In vitro studies showed that the vasculature from MORE-PGKO mice was more sensitive to endothelial-dependent relaxation caused by muscarinic stimulation, but was not associated with changes in eNOS expression or phosphorylation. In addition, vascular smooth muscle had impaired contraction in response to alpha-adrenergic agents. The renin-angiotensin-aldosterone system was mildly activated, consistent with increased vascular capacitance or decreased volume. These effects are likely mechanisms contributing to the hypotension. Our results demonstrated that PPARgamma is required to maintain normal adiposity and insulin sensitivity in adult mice. Surprisingly, genetic loss of PPARgamma function, like activation by agonists, lowered blood pressure, likely through a mechanism involving increased vascular relaxation.