Thus mortality among elderly subjects with or without CHF increases with frailty. Moreover, frailty is more predictive of long-term mortality in elderly subjects with than in those without CHF. Hence, frailty represents a new independent variable for predicting long-term mortality in elderly subjects with CHF.

No abstract

Modifications of lean mass are a frequent critical determinant in the pathophysiology and progression of heart failure (HF). Sarcopenia may be considered one of the most important causes of low physical performance and reduced cardiorespiratory fitness in older patients with HF. Sarcopenia is frequently misdiagnosed as cachexia. However, muscle wasting in HF has different pathogenetic features in sarcopenic and cachectic conditions. HF may induce sarcopenia through common pathogenetic pathways such as hormonal changes, malnutrition, and physical inactivity; mechanisms that influence each other. In the opposite way, sarcopenia may favor HF development by different mechanisms, including pathological ergoreflex. Paradoxically, sarcopenia is not associated with a sarcopenic cardiac muscle, but the cardiac muscle shows a hypertrophy which seems to be “not-functional.” First-line agents for the treatment of HF, physical activity and nutritional interventions, may offer a therapeutic advantage in sarcopenic patients irrespective of HF. Thus, sarcopenia is highly prevalent in patients with HF, contributing to its poor prognosis, and both conditions could benefit from common treatment strategies based on pharmacological, physical activity, and nutritional approaches.

No abstract

Long-term mortality was higher in elderly subjects with than in those without COPD. The clinical frailty score also significantly predicted mortality in subjects without and, even more, in those with COPD. Thus, clinical frailty may be considered a new prognostic factor to identify COPD subjects at high risk of mortality.

Elderly subjects are characterized by a high prevalence of diabetes and clinical frailty. This study aimed to examine the predictive role of clinical frailty on long-term mortality in elderly subjects with and without diabetes. The study evaluated mortality after 12-year follow-up in 188 subjects with diabetes and 1,100 subjects without diabetes selected in 1992. Clinical frailty was assessed according to the "Frailty Staging System" and stratified in tertiles. After 12-year follow-up, mortality was 50.5 % in subjects without and 66.5 % in subjects with diabetes (p < 0.001). With increasing frailty, mortality increases from 57.9 to 79.0 % (p for trend <0.01) in subjects without and from 75.9 to 87.0 % in subjects with diabetes (p for trend <0.001). Multivariate analysis shows that both diabetes (hazard ratio = 1.38; 95 % confidence interval = 1.12-1.95; p = 0.02) and frailty score (hazard ratio = 1.58 for each unit of increase; 95 % confidence interval = 1.41-2.35; p = 0.04) are predictive of long-term mortality. Moreover, when Cox regression analysis was performed by selecting sex, frailty increases the risk of long-term mortality for each unit of increase by 14 % (hazard ratio = 1.14; 95 % confidence interval = 1.10-1.18; p < 0.01) in women and by 60 % in men (hazard ratio = 1.60; 95 % confidence interval = 1.21-2.12; p < 0.001) in the absence and by 31 % (Hazard ratio = 1.31, 95 % confidence interval = 1.03-1.85, p = 0.03) in women and by 60 % in men (hazard ratio = 1.99, 95 % confidence interval = 1.75-3.05, p < 0.001) in the presence of diabetes, respectively. We concluded that diabetes predicts long-term mortality in elderly subjects. Moreover, clinical frailty significantly predicts mortality in subjects without and even more in those with diabetes. This phenomenon is particularly evident in men. Thus, clinical frailty may be considered a new prognostic factor to identify subjects with diabetes at high risk of mortality.

Treatment for chronic heart failure (CHF) is strongly focused on evidence-based medicine. However, large trials are often far away from the "real world" of geriatric patients and their messages are poorly transferable to the clinical management of CHF elderly patients. Precipitating factors and especially non-cardiac comorbidity may decompensate CHF in the elderly. More importantly, drugs of first choice, such as angiotensin-converting enzyme inhibitors and β-blockers, are still underused and effective drugs on diastolic dysfunction are not available. Poor adherence to therapy, especially for cognitive and depression disorders, worsens the management. Electrical therapy is indicated, but attention to the older age groups with reduced life expectancy has to be paid. Physical exercise, stem cells, gene delivery, and new devices are encouraging, but definitive results are still not available. Palliative care plays a key role to the end-stage of the disease. Follow-up of CHF elderly patient is very important but tele-medicine is the future. Finally, self-care management, caregiver training, and multidimensional team represent the critical point of the treatment for CHF elderly patients.

IFi is a valid measure of frailty after the comprehensive geriatric assessment in an Italian cohort of non-institutionalized patients.