Publications

OBJECTIVES

In 2010, the Veterans Health Administration (VA) began national implementation of its patient-centered medical home (PCMH) model, called Patient Aligned Care Teams (PACTs), to improve access, coordination, and patient-centered care. We evaluated changes in reported implementation of PCMH components in all VA primary care clinics, and patients' utilization of acute and non-acute care and total costs after 2 years.

STUDY DESIGN

Longitudinal study of 2,607,902 patients from 796 VA primary care clinics.

METHODS

Clinics were surveyed for their implementation of PCMH components. Patient outcomes were measured by outpatient visits for primary care, specialty care, telephone care, and emergency department (ED) care; hospitalizations for an ambulatory care-sensitive condition (ACSC); and costs of VA care in fiscal years (FYs) 2009 and 2011. Multi-level, multivariable models predicted changes in utilization and costs, adjusting for patients' health status, clinic PCMH component scores, and a patient fixed effect.

RESULTS

Clinics reported large improvements in adoption of all PCMH components from FY 2009 to FY 2011. Higher organization of practice scores was associated with fewer primary care visits (P = .012). Greater care coordination/transitions was modestly associated with more specialty care visits (P = .010) and fewer ED visits (P = .018), but quality/performance improvement was associated with more ED visits (P = .032). None of the PCMH components were significantly related to telephone visits, ACSC hospitalizations, or total healthcare costs.

CONCLUSIONS

Improvements under organization of practice and care coordination/transitions appear to have impacted outpatient care, but reductions in acute care were largely absent.

Clearing cellular debris after brain injury represents an important mechanism in regaining tissue homeostasis and promoting functional recovery. Triggering receptor expressed on myeloid cells-2 (TREM2) is a newly identified receptor expressed on microglia and is thought to phagocytose damaged brain cells. The precise role of TREM2 during ischemic stroke has not been fully understood. We explore TREM2 in both in vitro and in vivo stroke models and identify a potential endogenous TREM2 ligand. TREM2 knockdown in microglia reduced microglial activation to an amoeboid phenotype and decreased the phagocytosis of injured neurons. Phagocytosis and infarcted brain tissue resorption was reduced in TREM2 knock-out (KO) mice compared with wild-type (WT) mice. TREM2 KO mice also had worsened neurological recovery and decreased viable brain tissue in the ipsilateral hemisphere. The numbers of activated microglia and phagocytes in TREM2 KO mice were decreased compared with WT mice, and foamy macrophages were nearly absent in the TREM2 KO mice. Postischemia, TREM2 was highly expressed on microglia and TREM2-Fc fusion protein (used as a probe to identify potential TREM2 binding partners) bound to an unknown TREM2 ligand that colocalized to neurons. Oxygen glucose deprivation-exposed neuronal media, or cellular fractions containing nuclei or purified DNA, but not cytosolic fractions, stimulated signaling through TREM2. TREM2-Fc fusion protein pulled down nucleic acids from ischemic brain lysate. These findings establish the relevance of TREM2 in the phagocytosis of the infarcted brain and emphasize its role in influencing neurological outcomes following stroke. Further, nucleic acids may be one potential ligand of TREM2 in brain ischemia.