Building a viable weight management program in a patient-centered medical home

.001), an average decrease in HbA1c of 0.2 points (P=.004), and an average blood pressure reduction of 2.8 mmHg systolic (P=.002) and 1.9 mmHg diastolic (P=.03). One-third of participants (n=60) achieved clinically significant weight loss (&gt5%) at 18 months. The program has become financially sustainable through billing for preventive counseling services and a $125 out-of-pocket enrollment fee. CONCLUSIONS: WMP provides one model for primary care practices to de-velop a financially sustainable and evidence-based behavioral therapy weight management program for their patients with obesity. Future work will include assessment of longer-term program benefits, quality metrics, and health care costs.BACKGROUND AND OBJECTIVES: The growing prevalence of obesity in the United States and globally highlights the need for innovative strategies to provide obesity treatment in primary care settings. This report describes and evaluates the Weight Management Program (WMP), an interprofessional program in an academic family medicine clinic delivering intensive behavioral therapy (IBT) following evidenced-based guidelines. METHODS: We extracted WMP participant health data from the electronic health record and evaluated retrospectively. Eligible participants completed at least four WMP visits and had a baseline weight, blood pressure, and he-moglobin A1c (HbA1c) recorded within 1 year prior to their first visit. Paired t tests were used to assess changes in, weight, HbA1c and systolic and diastolic blood pressures from baseline. RESULTS: WMP counseled 673 patients over 3,895 visits from September 2015 to June 2019. Of these, 186 met eligibility criteria (at least four vis-its), with a median of eight visits (mean=11.3, SD=8.1). Participants saw an average weight decrease during program participation of 9.7 lbs (P&l

Vorapaxar in the secondary prevention of atherothrombotic events

Item does not contain fulltextBACKGROUND: Thrombin potently activates platelets through the protease-activated receptor PAR-1. Vorapaxar is a novel antiplatelet agent that selectively inhibits the cellular actions of thrombin through antagonism of PAR-1. METHODS: We randomly assigned 26,449 patients who had a history of myocardial infarction, ischemic stroke, or peripheral arterial disease to receive vorapaxar (2.5 mg daily) or matching placebo and followed them for a median of 30 months. The primary efficacy end point was the composite of death from cardiovascular causes, myocardial infarction, or stroke. After 2 years, the data and safety monitoring board recommended discontinuation of the study treatment in patients with a history of stroke owing to the risk of intracranial hemorrhage. RESULTS: At 3 years, the primary end point had occurred in 1028 patients (9.3%) in the vorapaxar group and in 1176 patients (10.5%) in the placebo group (hazard ratio for the vorapaxar group, 0.87; 95% confidence interval [CI], 0.80 to 0.94; P<0.001). Cardiovascular death, myocardial infarction, stroke, or recurrent ischemia leading to revascularization occurred in 1259 patients (11.2%) in the vorapaxar group and 1417 patients (12.4%) in the placebo group (hazard ratio, 0.88; 95% CI, 0.82 to 0.95; P=0.001). Moderate or severe bleeding occurred in 4.2% of patients who received vorapaxar and 2.5% of those who received placebo (hazard ratio, 1.66; 95% CI, 1.43 to 1.93; P<0.001). There was an increase in the rate of intracranial hemorrhage in the vorapaxar group (1.0%, vs. 0.5% in the placebo group; P<0.001). CONCLUSIONS: Inhibition of PAR-1 with vorapaxar reduced the risk of cardiovascular death or ischemic events in patients with stable atherosclerosis who were receiving standard therapy. However, it increased the risk of moderate or severe bleeding, including intracranial hemorrhage. (Funded by Merck; TRA 2P-TIMI 50 ClinicalTrials.gov number, NCT00526474.)