Four different frailty models predict health outcomes in older patients with stable chronic obstructive pulmonary disease.

BACKGROUND: Frail patients with chronic obstructive pulmonary disease (COPD) face a higher risk of adverse outcomes, but there is no clear consensus on which frailty measures are most suitable for COPD patients. Herein we evaluated the ability of frailty measurements in predicting 1-year acute exacerbation, hospitalization, and mortality in older patients with COPD. METHODS: A total of 302 patients [median age: 86 years (IQR: 80-90), 22.2% female] were admitted to the Department of Geriatric Medicine were prospectively enrolled in this study. Frailty status was assessed using the Fried Frailty Phenotype (FFP), Clinical Frailty Scale (CFS), Frailty Index of Accumulative Deficits (FI-CD), and Short Physical Performance Battery (SPPB). Cox proportional hazard regression and Poisson regression were used to evaluating the association of the adverse outcomes with frailty as assessed using the four instruments. The discrimination accuracy of these tools in predicting the 1-year all-cause mortality was also compared. RESULTS: Prevalence of frailty ranged from 51% (using FFP) to 64.2% (using CFS). The four frail instruments were associated with 1-year mortality. After an average follow-up time of 2.18 years (IQR: 1.56-2.62 years), frailty as defined by four instruments (except for FI-CD), was associated with death [FFP: Hazard ratio (HR) = 3.11, 95% confidence interval (CI) 1.30-7.44; CFS: HR = 3.68, 95% CI 1.03-13.16; SPPB: HR = 3.74, 95% CI 1.39-10.06). Frailty was also associated with acute exacerbation (using FFP) and hospitalization (using FFP, CFS, and FI-CD). Frail showed a moderate predictive ability [area under the curve ranging (AUC) 0.70-0.80] and a high negative predictive value (0.98-0.99) for 1-year mortality. CONCLUSIONS: With the four different frailty assessment tools, frailty was associated with poor prognosis in older patients with stable COPD. The FFP, CFS, FI-CD, and SPPB instruments showed similar performance in predicting 1-year mortality.

Impact of Frailty on the Risk of Exacerbations and All-Cause Mortality in Elderly Patients with Stable Chronic Obstructive Pulmonary Disease.

RATIONALE: For the high prevalence of frail in patients with chronic obstructive pulmonary disease (COPD), further study should explore an in-depth understanding of the relationship between frailty and prognosis of COPD. OBJECTIVE: To determine the correlation between frailty and risk of acute exacerbation, hospitalizations, and mortality in older patients with stable COPD. PARTICIPANTS AND METHODS: Consecutive older adults (≥65) diagnosed with stable COPD from January 2018 to July 2019, with an average follow-up of 546 days (N = 309). Frailty was defined by the Fried frailty phenotype. Poisson regression was performed to assess the influence of frailty on the incidence of acute exacerbations of COPD (AECOPD) and all-cause hospitalizations in a year. Cox regression was performed to evaluate the effect of frailty on all-cause mortality in patients with stable COPD. RESULTS: The prevalence of frailty was 49.8%. The most common phenotypic characteristics were weakness (99.4%) followed by slowness (92.9%). After adjustment, frailty increased the incidence of AECOPD (IRR = 1.75, 95% CI: 1.09-2.82) and all-cause hospitalizations (IRR = 1.39, 95% CI 1.04-1.87) within a year. Slowness was associated with AECOPD (IRR = 1.77, 95% CI: 1.03-3.03), and weakness was associated with increased all-cause hospitalizations (IRR = 1.53, 95% CI: 1.04-2.25). The all-cause mortality risk was more than twofold higher in frail patients (HR = 2.54, 95% CI: 1.01-6.36) than non-frail patients. Low physical activity (HR = 2.66, 95% CI: 1.17-6.05) and weight loss (HR = 2.15, 95% CI: 1.02-4.51) were significantly associated with increased all-cause mortality in patients with COPD. CONCLUSION: Frailty increased the incidence of acute exacerbation and hospitalization, as well as increased mortality in older patients with stable COPD. This knowledge will help physicians identify high-risk groups with COPD and frailty who may benefit from targeted interventions to prevent disease progression.

The implication of cigarette smoking and cessation on macrophage cholesterol efflux in coronary artery disease patients.

We investigated ATP-binding cassette transporters A1/G1 expression and function in mediating cholesterol efflux by examining the macrophages of cigarette-smoking patients with coronary artery disease (CAD) before and after smoking abstinence. Peripheral blood monocyte cells were collected from nonsmokers (n = 17), non-CAD (NCAD) smokers (n = 35), and CAD smokers (n = 32) before and after 3 months of smoking cessation. We found that the ABCA1 expression level was lower in macrophages from NCAD and CAD smokers than from nonsmokers at baseline. The ABCA1 function of mediating cholesterol efflux was reduced in NCAD and CAD smokers as compared with nonsmokers. After 3 months of smoking cessation, ABCA1 expression and function were improved in CAD smokers. However, ABCG1 expression and function did not change after smoking cessation. Furthermore, ABCA1 expression was inhibited by tar in human acute monocytic leukemia cell line THP-1-derived macrophages through the inhibition of liver X receptors. Nicotine and carbon monoxide did not inhibit ABCA1 expression. Our results indicate that chronic cigarette smoking impaired ABCA1-mediated cholesterol efflux in macrophages and that tobacco abstinence reversed the function and expression of ABCA1, especially in CAD patients. It was tobacco tar, rather than nicotine or carbon monoxide, that played a major role in the tobacco-induced disturbance of cellular cholesterol homeostasis.