Are health assets associated with improved outcomes for hospitalised older adults? A systematic review

Objective Health assets are protective factors that support health and wellbeing, rather than risk factors that are associated with disease. This concept was developed in the community setting. In hospitalised older adults, the dominant approach has been to identify risk factors, with little examination of health assets. The purpose of this systematic review was to determine whether, in hospitalised older people, individual health assets decrease the risk of post hospital mortality, functional decline, new need for residential care, readmission or longer length of stay. Methods MEDLINE, EMBASE, CINAHL and PsycINFO were searched to identify studies examining outcomes for hospitalised older adults. Included studies examined at least one potential individual health asset, which was a psychosocial characteristic or health characteristic. Study quality was assessed, and findings are narratively described. Results Nine prospective cohort and two retrospective cohort studies were identified. subjective, functional and biological health assets were identified. Health assets were associated with decreased risk of post-hospital mortality, functional decline, new need for residential care and readmission. Conclusion The complex interplay between health status and psychological and social factors is incompletely understood. Health assets are associated with improved outcomes for hospitalised older adults. The small number of studies suitable for inclusion indicates the need for further research in this area

The clinical frailty scale predicts functional decline and mortality when used by junior medical staff: a prospective cohort study

Increasing frailty is associated with risk of mortality and functional decline in hospitalized older adults, but there is no consensus on the best screening method for use by non-geriatricians. The objective of this study is to determine whether the clinical frailty scale (CFS) can be used to identify patient baseline frailty status in the acute general medical setting when used by junior medical staff using information obtained on routine clinical assessment.This was a prospective cohort study in an acute general medical unit. All patients aged 65 and over admitted to a general medical unit during August and September 2013 were eligible for the study. CFS score at baseline was documented by a member of the treating medical team. Demographic information and outcomes were obtained from medical records. The primary outcomes were functional decline and death within three months.Frailty was assessed in 95\ua0% of 179 eligible patients. 45\ua0% of patients experienced functional decline and 11\ua0% died within three months. 40\ua0% of patients were classified as vulnerable/mildly frail, and 41\ua0% were moderately to severely frail. When patients in residential care were excluded, increasing frailty was associated with functional decline (p = 0.011). Increasing frailty was associated with increasing mortality within three months (p = 0.012).A high proportion of eligible patients had the frailty measure completed, demonstrating the acceptability of the CFS to clinicians. Despite lack of training for medical staff, increasing frailty was correlated with functional decline and mortality supporting the validity of the CFS as a frailty screening tool for clinicians

Frailty indexes in perioperative and critical care: a systematic review

Background/objectives: Frail patients are increasingly presenting for both perioperative and intensive care, highlighting the need for simple, valid and scaleable frailty measurement. Frailty indexes comprehensively assess a range of deficits in health, and can incorporate routinely collected data. The purpose of this systematic review was to evaluate the effect of frailty indexes on surgical and intensive care risk stratification and patient outcomes (mortality, complications, length of stay, and discharge location). Methods: A prospectively registered systematic review was performed. MEDLINE, EMBASE, and CINAHL were searched to identify studies enrolling adult surgical or intensive care patients which used a frailty index. Included studies were those published subsequent to 1990, of any study design, which utilised a frailty index consisting of ≥30 health deficits. Primary outcome was mortality; secondary outcomes were complications, length of stay (LOS) and discharge location. Study and frailty index quality were critically appraised by three independent reviewers, with findings narratively described. Results: 2026 articles were screened, from which nine prospective and four retrospective cohort studies (enrolling 2539 patients) were included. Frailty prevalence ranged between 19–62%; frailty indexes identified patients at risk of increased death [mortality rates ranging between 1.9–73.1%; reported odds ratios (ORs) for death ranging between 1.76–3.09 for frail vs. non-frail patients], surgical complications (ORs = 1.67–4.4), increased LOS, and discharge to residential care (ORs = 1.9–3.64). The term “frailty index” was found to be applied to a number of alternative measurement scales. Conclusion: Frail patients are at significantly increased risk in critical illness and the perioperative period. Better standardisation of frailty indexes is recommended

ACTN3 genotype infuences muscle performance through the regulation of calcineurin signaling

α-Actinin-3 deficiency occurs in approximately 16% of the global population due to homozygosity for a common nonsense polymorphism in the ACTN3 gene. Loss of α-actinin-3 is associated with reduced power and enhanced endurance capacity in elite athletes and nonathletes due to "slowing" of the metabolic and physiological properties of fast fibers. Here, we have shown that α-actinin-3 deficiency results in increased calcineurin activity in mouse and human skeletal muscle and enhanced adaptive response to endurance training. α-Actinin-2, which is differentially expressed in α-actinin-3-deficient muscle, has higher binding affinity for calsarcin-2, a key inhibitor of calcineurin activation. We have further demonstrated that α-actinin-2 competes with calcineurin for binding to calsarcin-2, resulting in enhanced calcineurin signaling and reprogramming of the metabolic phenotype of fast muscle fibers. Our data provide a mechanistic explanation for the effects of the ACTN3 genotype on skeletal muscle performance in elite athletes and on adaptation to changing physical demands in the general population. In addition, we have demonstrated that the sarcomeric α-actinins play a role in the regulation of calcineurin signaling