Association of the clinical frailty scale with hospital outcomes.

BACKGROUND: The clinical frailty scale (CFS) was validated as a predictor of adverse outcomes in community-dwelling older people. In our hospital, the use of the CFS in emergency admissions of people aged ≥ 75 years was introduced under the Commissioning for Quality and Innovation payment framework. AIM: We retrospectively studied the association of the CFS with patient characteristics and outcomes. DESIGN: Retrospective observational study in a large tertiary university National Health Service hospital in UK. METHODS: The CFS was correlated with transfer to specialist Geriatric ward, length of stay (LOS), in-patient mortality and 30-day readmission rate. RESULTS: Between 1st August 2013 and 31st July 2014, there were 11 271 emergency admission episodes of people aged ≥ 75 years (all specialties), corresponding to 7532 unique patients (first admissions); of those, 5764 had the CFS measured by the admitting team (81% of them within 72 hr of admission). After adjustment for age, gender, Charlson comorbidity index and history of dementia and/or current cognitive concern, the CFS was an independent predictor of in-patient mortality [odds ratio (OR) = 1.60, 95% confidence interval (CI): 1.48 to 1.74, P < 0.001], transfer to Geriatric ward (OR = 1.33, 95% CI: 1.24 to 1.42, P < 0.001) and LOS ≥ 10 days (OR = 1.19, 95% CI: 1.14 to 1.23, P < 0.001). The CFS was not a multivariate predictor of 30-day readmission. CONCLUSIONS: The CFS may help predict in-patient mortality and target specialist geriatric resources within the hospital. Usual hospital metrics such as mortality and LOS should take into account measurable patient complexity.

Conditions permitting suppression of stretch-induced and vasoconstrictor tone by basal nitric oxide activity in porcine cerebral artery.

This study examined the ability of basal nitric oxide activity to suppress intrinsic and vasoconstrictor tone in isolated rings of porcine cerebral artery. Following stretch of approximately 1 g, N(G)-nitro-L-arginine methyl ester (L-NAME, 100 microM) produced a rise in tone in endothelium-containing but not endothelium-denuded rings. Thus, intrinsic tone was present and was powerfully suppressed by basal nitric oxide activity. Nevertheless, when concentration-response curves were constructed to U46619 and 5-hydroxytryptamine (5-HT), no endothelium-dependent depression of vasoconstriction was observed. It therefore appeared that basal nitric oxide activity was able to suppress intrinsic but not vasoconstrictor tone in these vessels. Stretch-tension curves generated following the application of stretch over the range 0 - 5. 5 g on endothelium-denuded rings showed that tension was stretch-induced. Experiments conducted in the presence of L-NAME (100 microM) revealed that the level of tone present in endothelium-containing rings was substantially higher than in endothelium-denuded rings across the entire range of stretch. When endothelium-containing and endothelium-denuded rings were set at similar levels of stretch-induced tone, rather than similar levels of stretch, the presence of the endothelium now depressed significantly vasoconstrictor responses to U46619 and 5-HT. Thus, when endothelium-containing and endothelium-denuded rings of porcine cerebral artery are set at similar points along their respective stretch-tension curves, rather than at similar levels of stretch, basal nitric oxide activity can be seen to inhibit both stretch-induced and vasoconstrictor tone.

Remodelling and enhanced myogenic tone in cerebral resistance arteries isolated from genetically hypertensive Brattleboro rats.

In this study, we examined the structural and functional properties of cerebral resistance arteries isolated from normotensive (Di/N), and hypertensive (Di/H), vasopressin-deficient rats. Di/H rats had a significantly higher mean arterial blood pressure (MAP, 159+/-3 mm Hg) than Di/N rats (125+/-2 mm Hg). Vessels were set up in a pressure myograph, and the internal diameter and wall thickness were determined at increasing intraluminal pressures under passive (calcium-free) conditions. Arteries were then pressurized to the MAP of the animal, from which they were isolated and fixed with glutaraldehyde, embedded in araldite, sectioned and examined histologically. Under passive conditions, the middle cerebral artery (MCA) from Di/H rats had a smaller internal diameter than the MCA isolated from Di/N rats at all distending pressures. This smaller internal diameter of vessels from hypertensive rats is characteristic of eutrophic inward remodelling, whereby a similar amount of wall material is organized around a smaller lumen, without vascular growth or an alteration in artery distensibility. We have previously shown that similar structural alterations occur in mesenteric resistance arteries isolated from Di/H rats. In the presence of extracellular calcium (1.6 mmol/l), the MCA isolated from Di/H rats had significantly more intrinsic tone than the MCA isolated from Di/N rats in the pressure range of 10-110 mm Hg, although arteries from both strains had a similar myogenic index. The increased intrinsic constriction was a specific enhancement of pressure-induced tone, since responses to the thromboxane mimetic, U46619, were decreased, rather than increased, in the MCA isolated from Di/H rats. Furthermore, it is unlikely that the increased intrinsic tone in arteries isolated from Di/H rats was due to an impaired endothelial function since responses to the endothelium-dependent vasodilator, bradykinin, were enhanced in these vessels compared to arteries isolated from Di/N rats.

Pressure-induced myogenic responses in human isolated cerebral resistance arteries.

BACKGROUND AND PURPOSE: Pressure-induced myogenic responses have been demonstrated in cerebral resistance arteries isolated from a number of species. In the present study, we determined the response of human isolated cerebral resistance arteries to a pressure stimulus. METHODS: Arteries were set up in a pressure myograph and exposed to alterations in intravascular pressure. RESULTS: Human isolated cerebral resistance arteries developed spontaneous intrinsic tone in response to a pressure stimulus over the pressure range of 20 to 90 mm Hg that was not apparent in the absence of extracellular calcium. This intrinsic tone may be an inherent property of the vascular smooth muscle, since it remained after functional removal of the endothelium. CONCLUSIONS: Human isolated cerebral resistance arteries spontaneously contract when exposed to raised intravascular pressure. This pressure-induced myogenic response may contribute to cerebral autoregulation of blood flow.