Gait speed (GS) is emerging as a marker of frailty and predictor

Gait speed (GS) is emerging as a marker of frailty and predictor of outcomes in older adults undergoing cardiovascular intervention. The objective of this study was to delineate the prevalence of

slow GS, evaluate the association of GS with factors used in standard cardiovascular assessments, and evaluate the association of GS with dependence in activities of daily living (ADLs) in older adults with AS. Hypothesis We hypothesized that gait speed would not be associated with clinical factors, but would be associated with ADLs. Methods We evaluated GS, ADLs dependence, and Society of Thoracic Surgery score along with clinical and functional assessments in 102 older adults with AS being evaluated for transcatheter valve. Gait speed <0.5 m/s was considered slow, and GS =0.5 m/s was considered preserved. We assessed the association of covariates with GS as well as with ADLs dependence. Results Median GS was 0.37 m/s (interquartile GW786034 order Momelotinib mw range, 0.00.65 m/s). Sixty-four (63%)

subjects had slow GS. Of commonly employed clinical covariates, only prior coronary intervention and serum albumin were weakly associated with GS. However, GS was independently associated with ADLs dependence (Odds ratio: 1.52 [1.21-1.91] for every 0.1 m/s decrease in GS; P = 0.0003). Conclusions Although the prevalence of slow GS in a population of elderly patients with severe AS being screened for transcatheter valve was high, there were only weak associations between GS and other risk stratifying tools. The strong association between GS and dependent functional status suggests that assessment of gait speed is a useful, objectively measurable, risk stratification tool in this population. Dr. Maurer is supported by a grant from the NIH/NIA AG036778-02. The other authors have no funding, financial relationships, or conflicts of interest to disclose.”
“Atrophy of brain white matter (WM) often is considered a signature injury of alcohol use disorders (AUDs). However, investigations into AUD-related changes in WM volume have yielded complex findings that are difficult to synthesize in a narrative review. The objective of this study was to obtain an averaged effect

PFTα clinical trial size (ES) for WM volume reduction associated with AUD diagnosis and to test potential moderators of ES. Study inclusion criteria were: (1) English language; (2) peer reviewed; (3) published before December 2011; (4) use of magnetic resonance imaging (MRI); (5) human participants; (6) inclusion of AUD group; (7) inclusion of non-AUD comparison group; and (8) reporting or testing of total or cerebral WM volume. Moderators included study design, MRI methodology and AUD characteristics. Nineteen studies with a total of 1302 participants (70% male) were included, and calculated ESs were confirmed by the corresponding author for 12 studies. The magnitude of the averaged ES adjusted for small sample bias (Hedges’ g) for WM reduction in AUDs was 0.304 (standard error=0.134, range=0.571.21).

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