Heart Failure Management in Nursing Homes: A Scoping Literature Review

Heart failure (HF) affects 20% of nursing home (NH) residents, causing high morbidity and mortality. The optimal approach to HF management in NHs remains elusive. We conducted a scoping review of published guidelines and HF management interventions in NHs. A search for English publications since 1990 was conducted using PubMed, EMBASE, CINAHL, and Scopus, for scientific statements, guidelines, recommendations, or intervention studies that addressed at least 1 principle of HF management. Of 2545 records retrieved, 19 articles were retained after screening, and 2 additional articles identified through reference list manual searches. Six articles represented 5 guidelines and 15 described interventions. All guidelines endorsed the applicability of general HF guidelines to NH residents, tailored to comorbidities, frailty, and advance care preferences. Four addressed quality assurance but not feasibility and sustainability. Methodological quality of the interventions was poor, although results suggest that guideline-based HF management in NHs can improve nursing staff knowledge and job satisfaction, prescribing, and reduce acute care utilization. Clinically-based education for staff, and access to specialist mentorship are important. NH physician involvement was limited, and resident/family education potentially ineffective. Concerns about feasibility, sustainability, and quality assurance were identified in most interventions, and advance care planning was rarely addressed. HF guidelines for NH support the applicability of general HF guidelines to the care of NH residents, and published interventions suggest that guideline-based HF management in NHs is effective. Future work should support greater physician and resident engagement, advance care planning, and provide robust guidelines on developing feasible and sustainable interventions.     

Measurement of Novel Biomarkers to Predict Chronic Heart Failure Outcomes and Left Ventricular Remodeling

Myocardial remodeling is pivotal in the progression and complication of chronic heart failure (HF). We assessed serial measurement of five biomarkers with biologic links to remodeling (biglycan, secreted frizzled-related protein 3, endostatin, insulin-like growth factor binding protein 7 [IGFBP7], mimecan) in 142 patients with HF followed through 882 office visits. IGFBP7 and mimecan were most associated with events; in fully adjusted models, lower IGFBP7 concentrations across visits independently predicted fewer events (odds ratio [OR]?=?0.83; 95 % confidence interval [CI]?=?0.73–0.95, p?=?0.01). Subjects with rising mimecan had greater decrease in left ventricular end diastolic (p?=?0.07) and systolic (p?=?0.01) volumes, greater increase in ejection fraction (p?=?0.02), and had lowest event rates. Statistical models suggested several HF medications might lead to changes in both IGFBP7 and mimecan values. The results suggest serial measurement of IGFBP7 provides prognostic information, while changes in mimecan provide unique information regarding myocardial remodeling.     

Infective endocarditis in heroin addicts: epidemiological observations and some unusual cases

The total number of cases of heroin-induced endocarditis occurring over a four-year period were reviewed in order to explain an increase in the number of cases in the last year studied (1975). Brown heroin was noted to be used more frequently by addicts during the period of increased incidence. Cultures of "street samples" of brown and white heroin as well as cocaine were obtained in order to elucidate a possible relationship between the increased use of brown heroin and the increased number of endocarditis cases. Despite frequent contamination of both white and brown heroin, none of the common endocarditis-causing pathogens were isolated from the samples. Staphylococcus aureus, the most common etiological agent, frequently resulted in tricuspid endocarditis. That the accepted criteria for tricuspid endocarditis may be present without actual cardiac valve involvement is demonstrated by a most unusual case of hepatic vasculature infection.     

Predicted hexameric structure of the Agrobacterium VirB4 C terminus suggests VirB4 acts as a docking site during type IV secretion

The Agrobacterium T-DNA transporter belongs to a growing class of evolutionarily conserved transporters, called type IV secretion systems (T4SSs). VirB4, 789 aa, is the largest T4SS component, providing a rich source of possible structural domains. Here, we use a variety of bioinformatics methods to predict that the C-terminal domain of VirB4 (including the Walker A and B nucleotide-binding motifs) is related by divergent evolution to the cytoplasmic domain of TrwB, the coupling protein required for conjugative transfer of plasmid R388 from Escherichia coli. This prediction is supported by detailed sequence and structure analyses showing conservation of functionally and structurally important residues between VirB4 and TrwB. The availability of a solved crystal structure for TrwB enables the construction of a comparative model for VirB4 and the prediction that, like TrwB, VirB4 forms a hexamer. These results lead to a model in which VirB4 acts as a docking site at the entrance of the T4SS channel and acts in concert with VirD4 and VirB11 to transport substrates (T-strand linked to VirD2 or proteins such as VirE2, VirE3, or VirF) through the T4SS.     

Expression of a dominant-negative type II transforming growth factor β (TGF-β) receptor in the epidermis of transgenic mice blocks TGF-β-mediated growth inhibition

To determine whether a functional type II receptor of transforming growth factor β (TGF-β) is required to mediate the growth inhibitory effect of TGF-β on the skin in vivo, we have generated transgenic mice that overexpress a dominant negative-type II TGF-β receptor (ΔβRII) in the epidermis. The ΔβRII mice exhibited a thickened and wrinkled skin, and histologically the epidermis was markedly hyperplastic and hyperkeratotic. In vivo labeling with BrdUrd showed a 2.5-fold increase in the labeling index over controls, with labeled nuclei occurring in both basal and suprabasal cells of transgenic epidermis. In heterozygotes, this skin phenotype gradually diminished, and by 10–14 days after birth the transgenic mice were indistinguishable from their normal siblings. However, when F₁ mice were mated to homozygosity, perinatal lethality occurred due to the severe hyperkeratotic phenotype, which restricted movement. Cultured primary keratinocytes from ΔβRII mice also exhibited an increased rate of growth in comparison with nontransgenic controls, and were resistant to TGF-β-induced growth inhibition. These data document the role of the type II TGF-β receptor in mediating TGF-β-induced growth inhibition of the epidermis in vivo and in maintenance of epidermal homeostasis.     

Health Services Research in Rehabilitation and Disability—The Time is Now

Policy drives practice, and health services research (HSR) is at the intersection of policy, practice, and patient outcomes. HSR specific to rehabilitation and disability is particularly needed. As rehabilitation researchers and providers, we are uniquely positioned to provide the evidence that guides reforms targeting rehabilitative care. We have the expertise to define the value of rehabilitation in a policy-relevant context. HSR is a powerful tool for providing this evidence. We need to continue building capacity for conducting rigorous, timely rehabilitation-related HSR. Fostering stakeholder engagement in these research efforts will ensure we maintain a patient-centered focus as we address the “Triple Aim” of better care, better health, and better value. In this Special Communication we discuss the role of rehabilitation researchers in HSR. We also provide information on current resources available in our field for conducting HSR and identify gaps for capacity building and future research. Health care reforms are a reality, and through HSR we can give rehabilitation a strong voice during these transformative times.     

The Pattern of Fatty Acids Displaced by EPA and DHA Following 12 Months Supplementation Varies between Blood Cell and Plasma Fractions

Eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) are increased in plasma lipids and blood cell membranes in response to supplementation. Whilst arachidonic acid (AA) is correspondingly decreased, the effect on other fatty acids (FA) is less well described and there may be site-specific differences. In response to 12 months EPA + DHA supplementation in doses equivalent to 0–4 portions of oily fish/week (1 portion: 3.27 g EPA+DHA) multinomial regression analysis was used to identify important FA changes for plasma phosphatidylcholine (PC), cholesteryl ester (CE) and triglyceride (TAG) and for blood mononuclear cells (MNC), red blood cells (RBC) and platelets (PLAT). Dose-dependent increases in EPA + DHA were matched by decreases in several n-6 polyunsaturated fatty acids (PUFA) in PC, CE, RBC and PLAT, but were predominantly compensated for by oleic acid in TAG. Changes were observed for all FA classes in MNC. Consequently the n-6:n-3 PUFA ratio was reduced in a dose-dependent manner in all pools after 12 months (37%–64% of placebo in the four portions group). We conclude that the profile of the FA decreased in exchange for the increase in EPA + DHA following supplementation differs by FA pool with implications for understanding the impact of n-3 PUFA on blood lipid and blood cell biology.