Unlocking Deprescribing Potential in Nursing Homes: Insights from a Focus Group Study with Healthcare Professionals.

BACKGROUND: The nursing home population is characterized by multimorbidity and disabilities, which often result in extensive prescription of medication and subsequent polypharmacy. Deprescribing, a planned and supervised process of dose reduction or total cessation of medication, is a solution to combat this. OBJECTIVE: This study aimed to identify barriers and enablers of deprescribing as experienced by nursing home physicians (NHPs) and collaborating pharmacists in the specific nursing home setting. METHODS: This qualitative study utilized a semi-structured interview format with two focus groups consisting of a mix of NHPs and pharmacists. Directed content analysis was performed based on the Theoretical Domains Framework, a validated framework for understanding determinants of behavior change among health care professionals. RESULTS: Sixteen health care professionals participated in two focus groups, including 13 NHPs and three pharmacists. The participating NHPs and pharmacists believed that deprescribing is a valuable process with enablers, such as multidisciplinary collaboration, good communication with patients and family, and involvement of the nursing staff. NHPs and pharmacists view deprescribing as a core task and feel assured in their ability to carry it out successfully. However, they also noted barriers: deprescribing is time-consuming; communication with residents, their relatives or medical specialists is difficult; and electronic patient systems often do not adequately support it. CONCLUSIONS: This study provides insight into the various barriers and enablers faced by NHPs and pharmacists when deprescribing in nursing homes. Specific for this population, deprescribing barriers focus on communication (with residents and their relatives, and also with medical specialists) and resources, while knowledge and expertise are mentioned as enablers.

Myeloid PHD2 Conditional Knockout Improves Intraplaque Angiogenesis and Vascular Remodeling in a Murine Model of Venous Bypass Grafting.

BACKGROUND: Intraplaque angiogenesis occurs in response to atherosclerotic plaque hypoxia, which is driven mainly by highly metabolically active macrophages. Improving plaque oxygenation by increasing macrophage hypoxic signaling, thus stimulating intraplaque angiogenesis, could restore cellular function and neovessel maturation, and decrease plaque formation. Prolyl hydroxylases (PHDs) regulate cellular responses to hypoxia. We therefore aimed to elucidate the role of myeloid PHD2, the dominant PHD isoform, on intraplaque angiogenesis in a murine model for venous bypass grafting. METHODS AND RESULTS: Myeloid PHD2 conditional knockout (PHD2cko) and PHD2 wild type mice on an Ldlr-/- background underwent vein graft surgery (n=11-15/group) by interpositioning donor caval veins into the carotid artery of genotype-matched mice. At postoperative day 28, vein grafts were harvested for morphometric and compositional analysis, and blood was collected for flow cytometry. Myeloid PHD2cko induced and improved intraplaque angiogenesis by improving neovessel maturation, which reduced intraplaque hemorrhage. Intima/media ratio was decreased in myeloid PHD2cko vein grafts. In addition, PHD2 deficiency prevented dissection of vein grafts and resulted in an increase in vessel wall collagen content. Moreover, the macrophage proinflammatory phenotype in the vein graft wall was attenuated in myeloid PHD2cko mice. In vitro cultured PHD2cko bone marrow-derived macrophages exhibited an increased proangiogenic phenotype compared with control. CONCLUSIONS: Myeloid PHD2cko reduces vein graft disease and ameliorates vein graft lesion stability by improving intraplaque angiogenesis.