Improving hypertension control through a collaboration between an academic medical center and a chain community pharmacy

IntroductionApproximately one-third of adults in the United States have hypertension (HTN), leading to increased morbidity and mortality.ObjectivesThis quality improvement intervention was designed to improve HTN control among community-dwelling adults through collaboration between patient-centered medical homes (PCMH) within an academic medical center and chain community pharmacies.MethodsFour PCMH sites in Ann Arbor, Michigan that were in close proximity to two Meijer pharmacies participated in this study between September 2016 and March 2017, which compared HTN outcomes for patients seen at two community pharmacies where the pharmacists received training on HTN management for patients who received usual care at their PCMH. The primary outcome was percent of patients who met their blood pressure (BP) goal of either <140/90-mmHg or-<-150/90-mmHg compared with matched controls who received usual care at the PCMH. Secondary outcomes included number of medication recommendations made, percent of recommendations accepted by the primary care provider (PCP), and patient satisfaction.ResultsPatients who received care at the community pharmacy (n = 155) had a higher rate of BP control at 3-months than matched controls (61.8% vs 47.7%, P = 0.013). A total of 29 medication recommendations were made by community pharmacists and 26 were accepted by the PCP. Nearly 95% of patients rated the care they received as excellent or very good and over 95% stated that they would recommend the pharmacist at the Meijer pharmacy to their family and friends.ConclusionPatients who received HTN management services as part of a collaboration between an academic medical center and chain community pharmacy were significantly more likely to have controlled BP at 3-months compared with matched controls who received standard care. This model shows promise as being a strategy to expand access to care for patients while being mutually beneficial for community pharmacies and health systems.Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/151336/1/jac51158_am.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/151336/2/jac51158.pd

Practical dyspnea assessment: relationship between the 0–10 numerical rating scale and the four-level categorical verbal descriptor scale of dyspnea intensity

Context—Measurement of dyspnea is important for clinical care and research. Objectives—To characterize the relationship between the 0–10 Numerical Rating Scale (NRS) and four-level categorical Verbal Descriptor Scale (VDS) for dyspnea assessment. Methods—This was a substudy of a double-blind randomized controlled trial comparing palliative oxygen to room air for relief of refractory breathlessness in patients with life-limiting illness. Dyspnea was assessed with both a 0–10 NRS and a four-level categorical VDS over the one-week trial. NRS and VDS responses were analyzed in cross section and longitudinally. Relationships between NRS and VDS responses were portrayed using descriptive statistics and visual representations. Results—Two hundred twenty-six participants contributed responses. At baseline, mild and moderate levels of breathlessness were reported by 41.9% and 44.6% of participants, respectively. NRS scores demonstrated increasing mean and median levels for increasing VDS intensity, from a mean (SD) of 0.6 (±1.04) for VDS none category to 8.2 (1.4) for VDS severe category. The Spearman correlation coefficient was strong at 0.78 (P < 0.0001). Based on the distribution of NRS scores within VDS categories, we calculated test characteristics of two different cutpoint models. Both models yielded 75% correct translations from NRS to VDS; however, Model A was more sensitive for moderate or greater dyspnea, with fewer misses downcoded. Conclusion—There is strong correlation between VDS and NRS measures for dyspnea. Proposed practical cutpoints for the relationship between the dyspnea VDS and NRS are 0 for none, 1–4 for mild, 5–8 for moderate, and 9–10 for severe

Stimulation of the Sphenopalatine Ganglion Induces Reperfusion and Blood-Brain Barrier Protection in the Photothrombotic Stroke Model

The treatment of stroke remains a challenge. Animal studies showing that electrical stimulation of the sphenopalatine ganglion (SPG) exerts beneficial effects in the treatment of stroke have led to the initiation of clinical studies. However, the detailed effects of SPG stimulation on the injured brain are not known.The effect of acute SPG stimulation was studied by direct vascular imaging, fluorescent angiography and laser Doppler flowmetry in the sensory motor cortex of the anaesthetized rat. Focal cerebral ischemia was induced by the rose bengal (RB) photothrombosis method. In chronic experiments, SPG stimulation, starting 15 min or 24 h after photothrombosis, was given for 3 h per day on four consecutive days. Structural damage was assessed using histological and immunohistochemical methods. Cortical functions were assessed by quantitative analysis of epidural electro-corticographic (ECoG) activity continuously recorded in behaving animals.Stimulation induced intensity- and duration-dependent vasodilation and increased cerebral blood flow in both healthy and photothrombotic brains. In SPG-stimulated rats both blood brain-barrier (BBB) opening, pathological brain activity and lesion volume were attenuated compared to untreated stroke animals, with no apparent difference in the glial response surrounding the necrotic lesion.SPG-stimulation in rats induces vasodilation of cortical arterioles, partial reperfusion of the ischemic lesion, and normalization of brain functions with reduced BBB dysfunction and stroke volume. These findings support the potential therapeutic effect of SPG stimulation in focal cerebral ischemia even when applied 24 h after stroke onset and thus may extend the therapeutic window of currently administered stroke medications

At the Crossroads of Sustainability: The Natural Recompositioning of Architecture

It is widely acknowledged that the mantra of sustainability has triggered a fundamental reversal in the core of design practice: If the original purpose of architecture was to protect humans from the destructive actions of nature,today it should protect nature from the damaging actions of humans. But sustainable design is far from being a coherent body of fully totalized ideas:it has a broad spectrum of disputing interpretations that oscillate between the deterministic models of energy control and technological efficiencies, and the moralistic and romantic approaches that attempt to see in nature and natural processes a fundamental way to de-escalate the global urban footprint and its associated patterns of consumption. However, mainstream green design has been evolving by progressively absorbing the narrative of deep ecology. Nature has been being integrated into architecture literally, by inserting vegetation onto buildings; digitally, by bringing environmental data into the design process (climate records, wind streams, sun rotation and air flows are computed, modelled and effectually shape architectures), and transcendentally, by claiming that sustainable architecture nurtures “the existing and evolving connections between spiritual and material consciousness.” The acknowledgement of the inexorable affiliation between architecture and the environment is, of course, not exactly new. What is distinctive today is the reification of the role of nature in architecture as an ideological stance, now totally intertwined with state-of-art data processing and the market-driven tools brought by Natural Capitalism. This paper will examine emblematic “green” buildings produced by leading architects such as Pelli Clarke Pelli, William McDonough, Stefano Boeri, Norman Foster and BIG in the light of Tim Morton’s, Slavoj Zizek and Bruno Latour’s critique of nature. It will illustrate how, despite being able to successfully forge new creative freedoms by exploring hybridizations between the domains of design and science, sustainability’s self-righteous “naturalistic” narrative is enabling a vision of the architect as an “expert manager” focused on producing projects of ecologic “beautification” while assumed to be “saving the world,” effectively depoliticizing the architectural practice. Nevertheless, these examples attest that there is a vast and fertile field of ideas to be explored and in this regard it is important to underline that we are still in the embryonic outset of the engagement of architecture with sustainability

Neurovascular unit dysfunction with blood-brain barrier hyperpermeability contributes to major depressive disorder: a review of clinical and experimental evidence

About one-third of people with major depressive disorder (MDD) fail at least two antidepressant drug trials at 1 year. Together with clinical and experimental evidence indicating that the pathophysiology of MDD is multifactorial, this observation underscores the importance of elucidating mechanisms beyond monoaminergic dysregulation that can contribute to the genesis and persistence of MDD. Oxidative stress and neuroinflammation are mechanistically linked to the presence of neurovascular dysfunction with blood-brain barrier (BBB) hyperpermeability in selected neurological disorders, such as stroke, epilepsy, multiple sclerosis, traumatic brain injury, and Alzheimer’s disease. In contrast to other major psychiatric disorders, MDD is frequently comorbid with such neurological disorders and constitutes an independent risk factor for morbidity and mortality in disorders characterized by vascular endothelial dysfunction (cardiovascular disease and diabetes mellitus). Oxidative stress and neuroinflammation are implicated in the neurobiology of MDD. More recent evidence links neurovascular dysfunction with BBB hyperpermeability to MDD without neurological comorbidity. We review this emerging literature and present a theoretical integration between these abnormalities to those involving oxidative stress and neuroinflammation in MDD. We discuss our hypothesis that alterations in endothelial nitric oxide levels and endothelial nitric oxide synthase uncoupling are central mechanistic links in this regard. Understanding the contribution of neurovascular dysfunction with BBB hyperpermeability to the pathophysiology of MDD may help to identify novel therapeutic and preventative approaches

Sarcoidosis in black women in the United States: Data from the Black Women\u27s Health Study

Background: Sarcoidosis is a systemic granulomatous disorder of unknown cause that occurs among men and women of all races. In the United States, black women are most frequently and most severely affected. There have been few epidemiologic studies of sarcoidosis focusing on black women. Methods: In this article, we present data on incidence, prevalence, and clinical characteristics of sarcoidosis among participants in the Black Women\u27s Health Study, a cohort study of 59,000 black women from across the United States. Data on incident disease and potential risk factors are obtained through biennial questionnaires. Follow-up has been \u3e80% through six completed cycles. Results: There were 685 prevalent cases of sarcoidosis at baseline in 1995 and 435 incident cases reported during 611,585 person-years of follow-up through 2007, for an average annual incidence rate of 71/100,000 and a current prevalence of 2.0%. The sarcoid diagnosis was confirmed in 96% of self-reported cases for whom medical records or physician checklists were obtained. The most frequently affected site was the lung. Most patients also had extrapulmonary involvement, with the most common sites being lymph nodes, skin, and eyes. Prednisone had the highest prevalence of use, followed by inhaled corticosteroids. Conclusions: This study confirms previous reports of high incidence and prevalence of sarcoidosis among black women, as well as the extent of extrapulmonary disease, frequent need for steroid therapy, and comorbid conditions in this population. The prospective identification of sarcoidosis cases from a defined population will enable a valid assessment of risk factors for incident disease as follow-up continues. © 2011 American College of Chest Physicians

Sarcoidosis-associated pulmonary hypertension: Outcome with long-term epoprostenol treatment

Rationale: Pulmonary hypertension is a known complication of sarcoidosis and is associated with increased mortality. Little is known about the outcome of sarcoidosis-associated pulmonary hypertension, including response to treatment. Objective: To determine the characteristics and outcome of patients with sarcoidosis-associated pulmonary hypertension treated with IV epoprostenol. Design: Retrospective chart review of all cases of pulmonary hypertension with a concomitant diagnosis of sarcoidosis evaluated in the Boston University Pulmonary Hypertension Center from 2000 to 2004. Measurements: Data collected included patient demographics, sarcoidosis stage, pulmonary function, echocardiography results, treatment, baseline and posttreatment hemodynamic measurements, and clinical outcome. Results: Eight patients were identified; four of the patients had stage IV pulmonary sarcoidosis. Pulmonary function test results were notable for severe diffusion impairment (mean diffusion capacity of the lung for carbon monoxide, 30% of predicted), with only mild-to-moderate restrictive physiology (mean FVC, 59% of predicted). Seventy-five percent of patients required supplemental oxygen at the time of presentation. All patients had moderate or severe pulmonary hypertension and were New York Heart Association (NYHA)/World Health Organization (WHO) class III or IV. A vasodilator trial with epoprostenol was performed in seven of the eight patients; six of the seven patients had a significant hemodynamic response (\u3e 25% reduction in pulmonary vascular resistance). All but one of the responders (five of six patients) continued on therapy. Average clinical improvement was one to two NYHA/WHO classes at a mean follow-up of 29 months (range, 15 to 49 months). Conclusions: In patients with sarcoidosis-associated pulmonary hypertension, the severity of pulmonary vascular disease occurs out of proportion to lung function abnormalities. The majority of our patients responded to epoprostenol; survival may be improved in this group