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Background: Despite large reductions from 2005-2012, hospital-onset methicillin-resistant Staphylococcus aureus bloodstream infections (HO MRSA BSIs) continue be a major source of morbidity and mortality.Aim: To describe risk factors for and underlying sources of HO MRSA BSIs.Methods: We investigated HO MRSA BSIs at eight high-burden short-stay acute care hospitals. A case was defined as first isolation of MRSA from a blood specimen collected in 2016 on hospital day ≥4 from a patient without an MRSA-positive blood culture in the 14 days prior. We reviewed case-patient demographics and risk factors by medical record abstraction. The potential clinical source(s) of infection were determined by consensus by a clinician panel.Findings: Of the 195 eligible cases, 186 were investigated. Case-patients were predominantly male (63%); median age was 57 years (range 0-92). In the two weeks prior to the BSI, 88% of case-patients had indwelling devices, 31% underwent a surgical procedure, and 18% underwent dialysis. The most common locations of attribution were intensive care units (ICUs) (46%) and step-down units (19%). The most commonly identified non-mutually exclusive clinical sources were CVCs (46%), non-surgical wounds (17%), surgical site infections (16%), non-ventilator healthcare-associated pneumonia (13%), and ventilator-associated pneumonia (11%).Conclusions: Device-and procedure-related infections were common sources of HO MRSA BSIs. Prevention strategies focused on improving adherence to existing prevention bundles for device-and procedure-associated infections and on source control for ICU patients, patients with certain indwelling devices, and patients undergoing certain high-risk surgeries are being pursued to decrease HO MRSA BSI burden at these facilities. [ABSTRACT FROM AUTHOR]

Nursing homes (NHs) provide care in a congregate setting for residents at high risk of severe outcomes from SARS-CoV-2 infection. In spring 2020, NHs were implementing new guidance to minimize SARS-CoV-2 spread among residents and staff. To assess whether telephone and video-based infection control assessment and response (TeleICAR) strategies could efficiently assess NH preparedness and help resolve gaps. We incorporated Centers for Disease Control and Prevention COVID-19 guidance for NH into an assessment tool covering 6 domains: visitor restrictions; health care personnel COVID-19 training; resident education, monitoring, screening, and cohorting; personal protective equipment supply; core infection prevention and control (IPC); and communication to public health. We performed TeleICAR consultations on behalf of health departments. Adherence to each element was documented and recommendations provided to the facility. Health department–referred NHs that agreed to TeleICAR consultation. We assessed overall numbers and proportions of NH that had not implemented each infection control element (gap) and proportion of NH that reported making ≥1 change in practice following the assessment. During April 13 to June 12, 2020, we completed TeleICAR consultations in 629 NHs across 19 states. Overall, 524 (83%) had ≥1 implementation gap identified; the median number of gaps was 2 (interquartile range: 1-4). The domains with the greatest number of facilities with gaps were core IPC practices (428/625; 68%) and COVID-19 education, monitoring, screening, and cohorting of residents (291/620; 47%). TeleICAR was an alternative to onsite infection control assessments that enabled public health to efficiently reach NHs across the United States early in the COVID-19 pandemic. Assessments identified widespread gaps in core IPC practices that put residents and staff at risk of infection. TeleICAR is an important strategy that leverages infection control expertise and can be useful in future efforts to improve NH IPC. [ABSTRACT FROM AUTHOR]

Abstract: Background: Although oxidative stress is considered a key pathogenic step in mediating vascular dysfunction and atherosclerosis development, their association has not been evaluated in human coronary circulation in vivo. Accordingly, we hypothesized that higher oxidative stress would be associated with abnormal coronary epicardial structure and microvascular function. Methods: We measured coronary flow velocity reserve (CFVR) and hyperemic microvascular resistance (HMR) as indices of microvascular function, and epicardial plaque volume and necrotic core using intravascular ultrasound (IVUS) in 47 patients undergoing cardiac catheterization. Plasma glutathione, cystine and their ratio served as measures of oxidative stress while high-sensitivity C-reactive protein (hs-CRP) served as a measure of inflammation. Results: Lower glutathione, a measure of increased oxidative stress was associated with impaired microvascular function [CFVR (r =0.39, p =0.01) and HMR (r =−0.43, p =0.004)], greater plaque burden (r =−0.32, p =0.03) and necrotic core (r =−0.39, p =0.008). Similarly, higher cystine/glutathione ratio was associated with impaired microvascular function [CFVR (r =−0.29, p =0.04)] and greater necrotic core (r =0.37, p =0.01). In comparison, higher hs-CRP was associated only with greater necrotic core (r =0.45, p =0.003). After multivariate adjustment for age, gender, hypertension, diabetes, acute coronary syndrome presentation, body mass index, tobacco abuse, statin use and hs-CRP, glutathione remained an independent predictor of CFVR, HMR and necrotic core (p <0.05). Conclusions: Lower plasma glutathione level a measure of increased oxidative stress, was an independent predictor of impaired coronary microvascular function and plaque necrotic core. [Copyright &y& Elsevier]

Objectives: The primary objective of this study was to elucidate mechanisms underlying the link between vitamin D status and cardiovascular disease by exploring the relationship between 25-hydroxyvitamin D (25-OH D), an established marker of vitamin D status, and vascular function in healthy adults. Background: Mechanisms underlying vitamin D deficiency-mediated increased risk of cardiovascular disease remain unknown. Vitamin D influences endothelial and smooth muscle cell function, mediates inflammation, and modulates the renin-angiotensin-aldosterone axis. We investigated the relationship between vitamin D status and vascular function in humans, with the hypothesis that vitamin D insufficiency will be associated with increased arterial stiffness and abnormal vascular function. Methods: We measured serum 25-OH D in 554 subjects. Endothelial function was assessed as brachial artery flow-mediated dilation, and microvascular function was assessed as digital reactive hyperemia index. Carotid-femoral pulse wave velocity and radial tonometry-derived central augmentation index and subendocardial viability ratio were measured to assess arterial stiffness. Results: Mean 25-OH D was 31.8 ± 14 ng/ml. After adjustment for age, sex, race, body mass index, total cholesterol, low-density lipoprotein, triglycerides, C-reactive protein, and medication use, 25-OH D remained independently associated with flow-mediated vasodilation (β = 0.1, p = 0.03), reactive hyperemia index (β = 0.23, p < 0.001), pulse wave velocity (β = −0.09, p = 0.04), augmentation index (β = −0.11, p = 0.03), and subendocardial viability ratio (β = 0.18, p = 0.001). In 42 subjects with vitamin D insufficiency, normalization of 25-OH D at 6 months was associated with increases in reactive hyperemia index (0.38 ± 0.14, p = 0.009) and subendocardial viability ratio (7.7 ± 3.1, p = 0.04), and a decrease in mean arterial pressure (4.6 ± 2.3 mm Hg, p = 0.02). Conclusions: Vitamin D insufficiency is associated with increased arterial stiffness and endothelial dysfunction in the conductance and resistance blood vessels in humans, irrespective of traditional risk burden. Our findings provide impetus for larger trials to assess the effects of vitamin D therapy in cardiovascular disease. [Copyright &y& Elsevier]

A shared understanding of medical conditions between patients and their health care providers may improve self-care and outcomes. In this study, the concordance between responses to a medical history self-report (MHSR) form and the corresponding provider documentation in electronic health records (EHRs) of 19 select co-morbidities and habits in 230 patients with heart failure were evaluated. Overall concordance was assessed using the κ statistic, and crude, positive, and negative agreement were determined for each condition. Concordance between MHSR and EHR varied widely for cardiovascular conditions (κ = 0.37 to 0.96), noncardiovascular conditions (κ = 0.06 to 1.00), and habits (κ = 0.26 to 0.69). Less than 80% crude agreement was seen for history of arrhythmias (72%), dyslipidemia (74%), and hypertension (79%) among cardiovascular conditions and lung disease (70%) and peripheral arterial disease (78%) for noncardiovascular conditions. Perfect agreement was observed for only 1 of the 19 conditions (human immunodeficiency virus status). Negative agreement >80% was more frequent than >80% positive agreement for a condition (15 of 19 [79%] vs 8 of 19 [42%], respectively, p = 0.02). Only 20% of patients had concordant MSHRs and EHRs for all 7 cardiovascular conditions; in 40% of patients, concordance was observed for ≤5 conditions. For noncardiovascular conditions, only 28% of MSHR-EHR pairs agreed for all 9 conditions; 37% agreed for ≤7 conditions. Cumulatively, 39% of the pairs matched for ≤15 of 19 conditions. In conclusion, there is significant variation in the perceptions of patients with heart failure compared to providers'' records of co-morbidities and habits. The root causes of this variation and its impact on outcomes need further study. [Copyright &y& Elsevier]