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1.
Intern Med J ; 52(5): 755-762, 2022 05.
Artículo en Inglés | MEDLINE | ID: mdl-34580964

RESUMEN

BACKGROUND: Conversion from paper-based to electronic medical records (EMR) may affect the quality and timeliness of the completion of Goals-of-Care (GOC) documents during hospital admissions and this may have been further impacted by the COVID-19 pandemic. AIMS: To determine the impact of EMR and COVID-19 on the proper completion of GOC forms and the factors associated with inpatient changes in GOC. METHODS: We conducted a cross-sectional study of adult general medicine admissions (August 2018-September 2020) at Dandenong Hospital (Victoria, Australia). We used interrupted time series to model the changes in the rates of proper GOC completion (adequate documented discussion, completed ≤2 days) after the introduction of EMR and the arrival of COVID-19. RESULTS: We included a total of 5147 patients. The pre-EMR GOC proper completion rate was 27.7% (overall completion, 86.5%). There was a decrease in the proper completion rate by 2.21% per month (95% confidence interval (CI): -2.83 to -1.58) after EMR implementation despite an increase in overall completion rates (91.2%). The main reason for the negative trend was a decline in adequate documentation despite improvements in timeliness. COVID-19 arrival saw a reversal of this negative trend, with proper completion rates increasing by 2.25% per month (95% CI: 1.35 to 3.15) compared with the EMR period, but also resulted in a higher proportion of GOC changes within 2 days of admission. CONCLUSIONS: EMR improved the timeliness and overall completion rates of GOC at the cost of a lower quality of documented discussion. COVID-19 reversed the negative trend in proper GOC completion but increased the number of early revisions.


Asunto(s)
COVID-19 , Adulto , COVID-19/epidemiología , Estudios Transversales , Registros Electrónicos de Salud , Objetivos , Humanos , Pandemias , Victoria
2.
Clin Sci (Lond) ; 135(15): 1859-1871, 2021 08 13.
Artículo en Inglés | MEDLINE | ID: mdl-34296277

RESUMEN

BACKGROUND AND AIMS: Preterm birth is associated with increased risk of cardiovascular disease (CVD). This may reflect a legacy of inflammatory exposures such as chorioamnionitis which complicate pregnancies delivering preterm, or recurrent early-life infections, which are common in preterm infants. We previously reported that experimental chorioamnionitis followed by postnatal inflammation has additive and deleterious effects on atherosclerosis in ApoE-/- mice. Here, we aimed to investigate whether innate immune training is a contributory inflammatory mechanism in this murine model of atherosclerosis. METHODS: Bone marrow-derived macrophages and peritoneal macrophages were isolated from 13-week-old ApoE-/- mice, previously exposed to prenatal intra-amniotic (experimental choriomanionitis) and/or repeated postnatal (peritoneal) lipopolysaccharide (LPS). Innate immune responses were assessed by cytokine responses following ex vivo stimulation with toll-like receptor (TLR) agonists (LPS, Pam3Cys) and RPMI for 24-h. Bone marrow progenitor populations were studied using flow cytometric analysis. RESULTS: Following postnatal LPS exposure, bone marrow-derived macrophages and peritoneal macrophages produced more pro-inflammatory cytokines following TLR stimulation than those from saline-treated controls, characteristic of a trained phenotype. Cytokine production ex vivo correlated with atherosclerosis severity in vivo. Prenatal LPS did not affect cytokine production capacity. Combined prenatal and postnatal LPS exposure was associated with a reduction in populations of myeloid progenitor cells in the bone marrow. CONCLUSIONS: Postnatal inflammation results in a trained phenotype in atherosclerosis-prone mice that is not enhanced by prenatal inflammation. If analogous mechanisms occur in humans, then there may be novel early life opportunities to reduce CVD risk in infants with early life infections.


Asunto(s)
Aterosclerosis/inmunología , Corioamnionitis/inmunología , Inmunidad Innata , Macrófagos Peritoneales/inmunología , Células Progenitoras Mieloides/inmunología , Peritonitis/inmunología , Animales , Aterosclerosis/genética , Aterosclerosis/metabolismo , Células Cultivadas , Corioamnionitis/inducido químicamente , Corioamnionitis/metabolismo , Citocinas/metabolismo , Modelos Animales de Enfermedad , Femenino , Mediadores de Inflamación/metabolismo , Lipopolisacáridos , Macrófagos Peritoneales/metabolismo , Ratones Noqueados para ApoE , Células Progenitoras Mieloides/metabolismo , Peritonitis/inducido químicamente , Peritonitis/metabolismo , Fenotipo , Embarazo
3.
Clin Sci (Lond) ; 133(10): 1185-1196, 2019 05 31.
Artículo en Inglés | MEDLINE | ID: mdl-31088858

RESUMEN

Atherosclerosis is a chronic inflammatory disease that has its origins in early life. Postnatal inflammation exacerbates atherosclerosis, but the possible effect of intrauterine inflammation is largely unexplored. Exposure to inflammation in utero is common, especially in infants born preterm, who have increased cardiovascular risk in adulthood. We hypothesised that exposure to inflammation before birth would accelerate the development of atherosclerosis, with the most severe atherosclerosis following exposure to both pre- and postnatal inflammation. Here we studied the effect of prenatal and postnatal inflammation on the development of atherosclerosis by combining established techniques for modelling histological chorioamnionitis and atherosclerosis using apolipoprotein E (ApoE) knockout mice. A single intra-amniotic (IA) injection of lipopolysaccharide (LPS) caused intrauterine inflammation, and increased atherosclerosis at 13 weeks of postnatal age. In mice exposed to postnatal LPS, chorioamnionitis modulated subsequent responses; atherosclerotic lesion size, number and severity were greatest for mice exposed to both intrauterine and postnatal inflammation, with a concomitant decrease in collagen content and increased inflammation of the atherosclerotic plaque. In conclusion, pre- and postnatal inflammation have additive and deleterious effects on the development of atherosclerosis in ApoE knockout mice. The findings are particularly relevant to preterm human infants, whose gestations are frequently complicated by chorioamnionitis and who are particularly susceptible to repeated postnatal infections. Human and mechanistic studies are warranted to guide preventative strategies.


Asunto(s)
Aterosclerosis/etiología , Corioamnionitis , Inflamación/complicaciones , Efectos Tardíos de la Exposición Prenatal , Animales , Femenino , Masculino , Ratones Noqueados para ApoE , Embarazo
4.
Clin Sci (Lond) ; 129(8): 769-84, 2015 Oct 01.
Artículo en Inglés | MEDLINE | ID: mdl-26223841

RESUMEN

Cardiovascular disease continues to be the leading cause of global morbidity and mortality. Traditional risk factors account for only part of the attributable risk. The origins of atherosclerosis are in early life, a potential albeit largely unrecognized window of opportunity for early detection and treatment of subclinical cardiovascular disease. There are robust epidemiological data indicating that poor intrauterine growth and/or prematurity, and perinatal factors such as maternal hypercholesterolaemia, smoking, diabetes and obesity, are associated with adverse cardiovascular intermediate phenotypes in childhood and adulthood. Many of these early-life risk factors result in a heightened inflammatory state. Inflammation is a central mechanism in the development of atherosclerosis and cardiovascular disease, but few studies have investigated the role of overt perinatal infection and inflammation (chorioamnionitis) as a potential contributor to cardiovascular risk. Limited evidence from human and experimental models suggests an association between chorioamnionitis and cardiac and vascular dysfunction. Early life inflammatory events may be an important mechanism in the early development of cardiovascular risk and may provide insights into the associations between perinatal factors and adult cardiovascular disease. This review aims to summarise current data on the early life origins of atherosclerosis and cardiovascular disease, with particular focus on perinatal inflammation.


Asunto(s)
Aterosclerosis/etiología , Corioamnionitis , Enfermedades del Recién Nacido , Inflamación/complicaciones , Animales , Femenino , Humanos , Recién Nacido , Embarazo
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