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      Implications of low muscle mass across the continuum of care: a narrative review

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          Abstract

          Abnormalities in body composition can occur at any body weight. Low muscle mass is a predictor of poor morbidity and mortality and occurs in several populations. This narrative review provides an overview of the importance of low muscle mass on health outcomes for patients in inpatient, outpatient and long-term care clinical settings. A one-year glimpse at publications that showcases the rapidly growing research of body composition in clinical settings is included. Low muscle mass is associated with outcomes such as higher surgical and post-operative complications, longer length of hospital stay, lower physical function, poorer quality of life and shorter survival. As such, the potential clinical benefits of preventing and reversing this condition are likely to impact patient outcomes and resource utilization/health care costs. Clinically viable tools to measure body composition are needed for routine screening and intervention. Future research studies should elucidate the effectiveness of multimodal interventions to counteract low muscle mass for optimal patient outcomes across the healthcare continuum. Key messages Low muscle mass is associated with several negative outcomes across the healthcare continuum. Techniques to identify and counteract low muscle mass in clinical settings are needed.

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          Most cited references146

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          Epidemiology and risk profile of heart failure.

          Heart failure (HF) is a major public health issue, with a prevalence of over 5.8 million in the USA, and over 23 million worldwide, and rising. The lifetime risk of developing HF is one in five. Although promising evidence shows that the age-adjusted incidence of HF may have plateaued, HF still carries substantial morbidity and mortality, with 5-year mortality that rival those of many cancers. HF represents a considerable burden to the health-care system, responsible for costs of more than $39 billion annually in the USA alone, and high rates of hospitalizations, readmissions, and outpatient visits. HF is not a single entity, but a clinical syndrome that may have different characteristics depending on age, sex, race or ethnicity, left ventricular ejection fraction (LVEF) status, and HF etiology. Furthermore, pathophysiological differences are observed among patients diagnosed with HF and reduced LVEF compared with HF and preserved LVEF, which are beginning to be better appreciated in epidemiological studies. A number of risk factors, such as ischemic heart disease, hypertension, smoking, obesity, and diabetes, among others, have been identified that both predict the incidence of HF as well as its severity. In this Review, we discuss key features of the epidemiology and risk profile of HF.
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            Alternative definitions of sarcopenia, lower extremity performance, and functional impairment with aging in older men and women.

            To compare two methods for classifying an individual as sarcopenic for predicting decline in physical function in the Health, Aging and Body Composition Study. Observational cohort study with 5 years of follow-up. Communities in Memphis, Tennessee, and Pittsburgh, Pennsylvania. Men and women aged 70 to 79 (N=2,976, 52% women, 41% black). Appendicular lean mass (aLM) was measured using dual energy x-ray absorptiometry, and participants were classified as sarcopenic first using aLM divided by height squared and then using aLM adjusted for height and body fat mass (residuals). Incidence of persistent lower extremity limitation (PLL) was measured according to self-report, and change in objective lower extremity performance (LEP) measures were observed using the Short Physical Performance Battery. There was a greater risk of incident PLL in women who were sarcopenic using the residuals sarcopenia method than in women who were not sarcopenic (hazard ratio (HR)=1.34, 95% confidence interval (CI)=1.11-1.61) but not in men. Those defined as sarcopenic using the aLM/ht(2) method had lower incident PLL than nonsarcopenic men (HR=0.76, 95% CI=0.60-0.96) and women (HR=0.75, 95% CI=0.60-0.93), but these were no longer significant with adjustment for body fat mass. Using the residuals method, there were significantly poorer LEP scores in sarcopenic men and women at baseline and Year 6 and greater 5-year decline, whereas sarcopenic men defined using the aLM/ht(2) method had lower 5-year decline. Additional adjustment for fat mass attenuated this protective effect. These findings suggest that sarcopenia defined using the residuals method, a method that considers height and fat mass together, is better for predicting disability in an individual than the aLM/ht(2) method, because it considers fat as part of the definition.
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              Sarcopenic obesity and myosteatosis are associated with higher mortality in patients with cirrhosis

              Abstract Background and aims Obesity is frequently associated with cirrhosis, and cirrhotic patients may develop simultaneous loss of skeletal muscle and gain of adipose tissue, culminating in the condition of sarcopenic obesity. Additionally, muscle depletion is characterized by both a reduction in muscle size and increased proportion of muscular fat, termed myosteatosis. In this study, we aimed to establish the frequency and clinical significance of sarcopenia, sarcopenic obesity and myosteatosis in cirrhotic patients. Methods We analysed 678 patients with cirrhosis. Sarcopenia, sarcopenic obesity and myosteatosis were analysed by CT scan using the third lumbar vertebrae skeletal muscle and attenuation indexes, using previously validated gender‐and body mass index‐specific cutoffs. Results Patients were predominately men (n = 457, 67%), and cirrhosis aetiology was hepatitis C virus in 269 patients (40%), alcohol in 153 (23%), non‐alcoholic steatohepatitis/cryptogenic in 96 (14%), autoimmune liver disease in 55 (8%), hepatitis B virus in 43 (6%), and others in 5 patients (1%). Sarcopenia was present in 292 (43%), 135 had sarcopenic obesity (20%) and 353 had myosteatosis (52%). Patients with sarcopenia (22 ± 3 vs. 95 ± 22 months, P < 0.001), sarcopenic obesity (22 ± 3 vs. 95 ± 22 months, P < 0.001), and myosteatosis (28 ± 5 vs. 95 ± 22 months, P < 0.001) had worse median survival than patients without muscular abnormalities. By multivariate Cox regression analysis, both sarcopenia [hazard ratio (HR) 2.00, 95% confidence interval (CI) 1.44–2.77, P < 0.001], and myosteatosis (HR 1.42, 95% CI 1.02–1.07, P = 0.04) were associated with mortality. Conclusions Sarcopenia, sarcopenic obesity and myosteatosis are often present in patients with cirrhosis, and sarcopenia and myosteatosis are independently associated with a higher long‐term mortality in cirrhosis.
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                Author and article information

                Journal
                Annals of Medicine
                Annals of Medicine
                Informa UK Limited
                0785-3890
                1365-2060
                September 12 2018
                September 12 2018
                : 1-19
                Affiliations
                [1 ] Department of Agricultural, Food and Nutritional Science, Division of Human Nutrition, University of Alberta, Edmonton, Alberta, Canada;
                [2 ] Abbott Nutrition, Abbott Laboratories, Columbus, OH, USA;
                [3 ] Center for Translational Research in Aging and Longevity, Department of Health and Kinesiology, Texas A and M University, TX, USA;
                [4 ] Kingston General Hospital, Clinical Evaluation Research Unit, Kingston, Ontario, Canada;
                [5 ] Florida Hospital, Sanford Burnham Prebys Medical Discovery Institute, Translational Research Institute for Metabolism and Diabetes, Orlando, FL, USA;
                [6 ] Department of Food Science and Human Nutrition, University of Illinois at Urbana-Champaign, Urbana, IL, USA;
                [7 ] Pennington Biomedical Research Center, Baton Rouge, LA, USA
                Article
                10.1080/07853890.2018.1511918
                6370503
                30169116
                33d26420-43e6-4b85-91b3-68cc2d9ea893
                © 2018
                History

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