In comatose patients after out-of-hospital cardiac arrest, the incidence of death or severe disability was similar regardless of whether a restrictive or a liberal oxygenation strategy was used.
This trial showed no significant difference in the percentage of patients who died or had severe disability or coma when higher or lower blood-pressure targets were used after an out-of-hospital ...cardiac arrest.
Abstract
Funding Acknowledgements
Type of funding sources: None.
Background
Patients who are successfully resuscitated from out-of-hospital cardiac arrest (OHCA) and admitted to the hospital in a ...comatose stage are in high risk for anoxic brain injury. Multimodal approach for neuroprognostication include measurement of neuron-specific enolase (NSE) as a biomarker for neurological injury. NSE has been intensively studied over the past years and has shown a valid predictive value for neurological outcome. However, there has been no clinical studies comparing NSE analyzed on plasma and serum samples.
Purpose
To compare NSE at 48 hours obtained from both in serum and plasma samples, and to investigate the performance of both these measuring techniques in predicting all-cause mortality at 365-days among patients resuscitated from out-of-hospital cardiac arrest.
Methods
This is a post-hoc sub study of the BOX trial in which resuscitated OHCA patients admitted to the hospital in comatose stage were included. NSE was measured 48 hours after admission, both in serum samples used for clinical analysis with no freeze-thaw cycle (NSE-Serum), and plasma samples from biobank (NSE-Plasma). The comparison of NSE-Serum and NSE-Plasma was performed by Spearmans correlation. The area under the receiver operating characteristics curve (AUROC) for predicting all-cause mortality at 365-days for both NSE-Serum and NSE-Plasma were determined.
Results
369 patients had NSE values from both serum and plasma at 48 hours available for comparison. In these patients the NSE-Serum was median 21.2 µg/L (IQR 15.7 - 45.5), NSE-Plasma was median 19.3 µg (IQR 11.3 - 40.9), and mortality at 365-days was 32.5%. The correlation between NSE-Serum and NSE-Plasma was r=0.63 P<0.001. AUROC for NSE-Serum and NSE-Plasma were 0.94 and 0.83 respectively (FIGURE), and the differences in AUROC was -0.10 (95% confidence limits: -0.14 to -0.06), p<0.001.
Conclusion
In this sub study, we found moderate correlation between serum NSE values and plasma NSE values. Moreover, both measuring techniques had good predictive value against 1 year mortality, with clinically measured NSE from serum being slightly superior to NSE from plasma in predicting mortality.
Introduction
Hypophosphataemia is common in critically ill patients, but neither its prevalence nor its association with outcome have been investigated specifically in patients with aneurysmal ...subarachnoid haemorrhage (aSAH).
Methods
Patients with aSAH and at least one phosphate measurement were included from two independent cohorts; an American cohort extracted from two open‐access databases (Medical Information Mart for Intensive Care‐III and eICU Collaborative Research Database v. 2.0) and a Danish cohort consisting of patients with aSAH admitted to Rigshospitalet, Denmark over a 4‐year period. In each cohort, we calculated the prevalence of mild (0.32–0.80 mmol/L) and severe (<0.32 mmol/L) hypophosphataemia and their association with in‐hospital mortality before and after propensity‐score matching.
Results
Hypophosphataemia occurred in 72.4% (95% CI: 68.1–76.3) of patients in the American cohort (n = 471) and 54.9% (50.0–59.7) in the Danish cohort (n = 419). However, it was not associated with mortality in neither full (American: Mild, Odds ratio (OR) 0.99 (0.91–1.07), Severe OR 1.20 (0.95–1.51); Danish: Mild, OR 1.01 (0.95–1.08), Severe OR 1.20 (0.95–1.51)) nor propensity‐score matched cohorts (American (n = 168): Mild, OR 1.06 (0.88–1.28), Severe OR 1.46 (0.96–2.12); Danish (n = 44): Mild, OR 1.16 (0.82–1.65), Severe OR 0.45 (0.13–1.55)).
Conclusion
In this retrospective study of patients with aSAH, hypophosphataemia was common.
Introduction
Increased plasma levels of C‐reactive protein (CRP) in midlife are associated with increased risk of Alzheimer's disease (AD), whereas in older age the opposite association is observed. ...Whether genetically determined CRP is associated with AD remains unclear.
Methods
A total of 111,242 White individuals from the Copenhagen General Population Study and the Copenhagen City Heart Study were included. Plasma levels of CRP and four regulatory genetic variants in the CRP gene were determined.
Results
For CRP percentile group 1 to 5 (lowest plasma CRP) versus the 50 to 75 group (reference), the hazard ratio for AD was 1.69 (95% confidence interval 1.29–2.16). Genetically low CRP was associated with increased risk of AD in individuals with body mass index ≤25 kg/m2 (P = 4 × 10−6).
Discussion
Low plasma levels of CRP at baseline were associated with high risk of AD in individuals from the general population. These observational findings were supported by genetic studies.
Essentials
It is unknown how regular exercise affects platelet function after menopause.
We studied the effect of 3‐months of high‐intensity exercise in pre‐ and postmenopausal women.
Platelet ...sensitivity to the inhibitory effect of arterially infused prostacyclin was increased.
Reduced basal platelet reactivity was seen in the premenopausal women only.
Summary
Background
The risk of atherothrombotic events increases after the menopause. Regular physical activity has been shown to reduce platelet reactivity in younger women, but it is unknown how regular exercise affects platelet function after the menopause.
Objectives
To examine the effects of regular aerobic exercise in late premenopausal and recent postmenopausal women by testing basal platelet reactivity and platelet sensitivity to prostacyclin and nitric oxide.
Methods
Twenty‐five sedentary, but healthy, late premenopausal and 24 matched recently postmenopausal women, mean (95% confidence interval) 49.1 (48.2–49.9) and 53.7 (52.5–55.0) years old, participated in an intervention study: 3‐month high‐intensity supervised aerobic spinning‐cycle training (1 h, × 3/week). Basal platelet reactivity was analyzed in platelet‐rich plasma from venous blood as agonist‐induced % aggregation. In a subgroup of 13 premenopausal and 14 postmenopausal women, platelet reactivity was tested ex vivo after femoral arterial infusion of prostacyclin, acetylcholine, a cyclooxygenase inhibitor, and after acute one‐leg knee extensor exercise.
Results
Basal platelet reactivity (%aggregation) to TRAP‐6 (1 μm) was higher in the postmenopausal, 59% (50–68), than the premenopausal women, 45% (35–55). Exercise training reduced basal platelet reactivity to collagen (1 μg mL−1) in the premenopausal women only: from 63% (55–71%) to 51% (41–62%). After the training intervention, platelet aggregation was more inhibited by the arterial prostacyclin infusion and the acute exercise in both premenopausal and postmenopausal women.
Conclusions
These results highlight previously unknown cardioprotective aspects of regular aerobic exercise in premenopausal and postmenopausal women, improving their regulation of platelet reactivity through an increased platelet sensitivity to prostacyclin, which may counterbalance the increased atherothrombotic risk associated with the menopause.
To understand hindbrain pathways involved in the control of food intake, we examined roles for calcitonin receptor (CALCR)-containing neurons in the NTS. Ablation of NTS Calcr abrogated the long-term ...suppression of food intake, but not aversive responses, by CALCR agonists. Similarly, activating CalcrNTS neurons decreased food intake and body weight but (unlike neighboring CckNTS cells) failed to promote aversion, revealing that CalcrNTS neurons mediate a non-aversive suppression of food intake. While both CalcrNTS and CckNTS neurons decreased feeding via projections to the PBN, CckNTS cells activated aversive CGRPPBN cells while CalcrNTS cells activated distinct non-CGRP PBN cells. Hence, CalcrNTS cells suppress feeding via non-aversive, non-CGRP PBN targets. Additionally, silencing CalcrNTS cells blunted food intake suppression by gut peptides and nutrients, increasing food intake and promoting obesity. Hence, CalcrNTS neurons define a hindbrain system that participates in physiological energy balance and suppresses food intake without activating aversive systems.
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•NTS Calcr mediates food intake suppression but not aversive responses to sCT•Activating NTS Calcr neurons non-aversively suppresses feeding•These neurons act via non-CGRP PBN neurons•These neurons control long-term energy balance, not just short-term feeding
While the hindbrain is often postulated to control only short-term parameters of feeding via circuits that mediate aversive responses when activated strongly, Cheng et al. have identified a hindbrain system that participates in the physiological control of energy balance and suppresses food intake without activating aversive systems or symptoms.
Summary
Uncertainty exists regarding the relation of body size and weight change with dementia risk. As populations continue to age and the global obesity epidemic shows no sign of waning, reliable ...quantification of such associations is important. We examined the relationship of body mass index, waist circumference, and annual percent weight change with risk of dementia and its subtypes by pooling data from 19 prospective cohort studies and four clinical trials using meta‐analysis. Compared with body mass index–defined lower‐normal weight (18.5‐22.4 kg/m2), the risk of all‐cause dementia was higher among underweight individuals but lower among those with upper‐normal (22.5‐24.9 kg/m2) levels. Obesity was associated with higher risk in vascular dementia. Similarly, relative to the lowest fifth of waist circumference, those in the highest fifth had nonsignificant higher vascular dementia risk. Weight loss was associated with higher all‐cause dementia risk relative to weight maintenance. Weight gain was weakly associated with higher vascular dementia risk. The relationship between body size, weight change, and dementia is complex and exhibits non‐linear associations depending on dementia subtype under scrutiny. Weight loss was associated with an elevated risk most likely due to reverse causality and/or pathophysiological changes in the brain, although the latter remains speculative.
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