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Objectives To examine the association between midlife cardiovascular health and physical performance 25 years later. Design Cohort study (Atherosclerosis Risk in Communities Study); multinomial logistic and logistic regression adjusted for demographic characteristics and clinical measures. Setting Four U.S. communities: Forsyth County, North Carolina; Washington County, Maryland; Minneapolis, Minnesota; and Jackson, Mississippi. Participants: Individuals aged 54.2 ± 5.8 at baseline (N = 15,744; 55% female, 27% black). Measurements Cardiovascular health was measured at baseline using the American Heart Association's Life's Simple 7 ( LS7) score (0-14) and LS7 component categories (poor, intermediate, ideal) for each risk factor. The Short Physical Performance Battery ( SPPB) was used to quantify physical function as ordinal (0-12) and categorical (low (0-6), fair (7-9), good (10-12) outcomes. Results Mean baseline LS7 score was 7.9 ± 2.4; 6,144 (39%) individuals returned 25 years later for the fifth ARIC examination, at which point the SPPB was administered. Of 5,916 individuals who completed the SPPB, 3,288 (50%) had good physical performance. Each 1-unit increase in LS7 score was associated with a 17% higher SPPB score (rate ratio ( RR) = 1.17, 95% confidence interval ( CI) = 1.15-1.19) and a 29% greater chance of having a late-life SPPB score of 10 or greater compared to SPPB score of less than 10 ( RR = 1.29, 95% CI = 1.25-1.34). Ideal baseline glucose ( RR = 2.53, 95% CI = 2.24-2.87), smoking ( RR = 1.97, 95% CI = 1.81-2.15), blood pressure ( RR = 1.70, 95% CI = 1.54-1.88), body mass index ( RR = 1.51, 95% CI = 1.37-1.66), and physical activity ( RR = 1.31, 95% CI = 1.20-1.43) had the strongest associations with late-life SPPB score, adjusting for other LS7 components. Conclusion Better cardiovascular health during midlife may lead better physical functioning in older age. [ABSTRACT FROM AUTHOR]

Objectives To evaluate whether fibroblast growth factor 23 ( FGF-23) is related to frailty and to characterize the nature of their joint association with mortality. Design Cross-sectional analysis for frailty and longitudinal cohort analysis for mortality. Setting Cardiovascular Health Study. Participants Community-dwelling individuals (N = 2,977; mean age 77.9 ± 4.7, 40% male, 83% white). Measurements The predictor was serum FGF-23 concentration (C-terminal enzyme-linked immunosorbent assay), and the outcomes were frailty status (determined according to frailty phenotype criteria of weight loss, weakness, exhaustion, slowness, and low physical activity) and mortality. Multinomial logistic regression was used to assess the cross-sectional association between FGF-23 and frailty and prefrailty, adjusting for demographic characteristics, cardiovascular disease and risk factors, and kidney markers. Proportional hazards Cox proportional hazards regression was used to assess the association between FGF-23, frailty, and all-cause mortality. Results Mean estimated glomerular filtration rate ( eGFR) was 64 ± 17 mL/min per 1.73 m2. Median FGF-23 was 70.3 RU/mL (interquartile range 53.4-99.2); 52% were prefrail, and 13% were frail. After multivariate adjustment, each doubling in FGF-23 concentration was associated with 38% (95% confidence interval (CI) = 17-62%) higher odds of frailty than of nonfrailty and 16% (95% CI = 3-30%) higher odds of prefrailty. FGF-23 (hazard ratio ( HR) = 1.16, 95% CI = 1.10-1.23) and frailty (HR = 1.82, 95% CI = 1.57-2.12) were independently associated with mortality, but neither association was meaningfully attenuated when adjusted for the other. Conclusion In a large cohort of older adults, higher FGF-23 was independently associated with prevalent frailty and prefrailty. FGF-23 and frailty were independent and additive risk factors for mortality. FGF-23 may be a marker for functional outcomes. [ABSTRACT FROM AUTHOR]

The development of myocardial and large vessel stiffness with aging underlies the development of diastolic heart failure and isolated systolic hypertension. Nonenzymatic reaction between glucose and proteins (Maillard reaction) leading to collagen crosslinking in the myocardium and arterial wall has been implicated in age-related increase in cardiovascular stiffness. In the present issue, Chang et al. show that aminoguanidine, an inhibitor of protein crosslinking, retards age-related decline in the elastic properties of the left ventricle and arteries. The significance of these findings is discussed in this commentary. [ABSTRACT FROM AUTHOR]