Cross-Sectional Study of the Relation of Health Literacy to Primary Language and Emergency Department Length of Stay.

OBJECTIVES: The primary aim of this study was to determine whether emergency department (ED) length of stay (LOS) or primary language was related to the degree of health literacy of patients. METHODS: Adult English-speaking and Spanish-speaking patients were recruited for the study. Participants completed the Newest Vital Sign (NVS) tool (English and Spanish versions), a 6-question validated scale. Patients with NVS scores of 0 to 3 were considered to be at risk for limited health literacy, whereas those with adequate health literacy were defined as scoring a 4 to 6. After completion of their ED visit, a retrospective chart review was performed to identify the patient's ED LOS (time from registration to time of disposition) and ED disposition. In addition, 2 single-item questions were compared with the NVS for validity. RESULTS: Participants included 250 English-speaking and 257 Spanish-speaking subjects. Per the NVS, 71% (359 of 507) of all patients had limited health literacy. By language group, significantly more Spanish-speaking than English-speaking patients had limited health literacy (93% vs 48%, diff 45%, 95% confidence interval 37-51). There was no significant difference in LOS between the limited health literacy group and adequate health literacy group (medians 440 vs 461 min). The 2 single-item questions had fair validity in comparison to the NVS scale (κ 0.2-0.3). CONCLUSIONS: There was a significant difference in health literacy based on language, with 93% of all Spanish-speaking patients in our sample having limited health literacy. We found no significant difference in ED LOS between patients with limited health and adequate health literacy in an academic urban ED setting.

Maintaining PGC-1α expression following pressure overload-induced cardiac hypertrophy preserves angiogenesis but not contractile or mitochondrial function.

During pathological hypertrophy, peroxisome proliferator-activated receptor coactivator 1α (PGC-1α) is repressed in concert with reduced mitochondrial oxidative capacity and fatty acid oxidation (FAO). We therefore sought to determine if maintaining or increasing PGC-1α levels in the context of pressure overload hypertrophy (POH) would preserve mitochondrial function and prevent contractile dysfunction. Pathological cardiac hypertrophy was induced using 4 wk of transverse aortic constriction (TAC) in mice overexpressing the human PGC-1α genomic locus via a bacterial artificial chromosome (TG) and nontransgenic controls (Cont). PGC-1α levels were increased by 40% in TG mice and were sustained following TAC. Although TAC-induced repression of FAO genes and oxidative phosphorylation (oxphos) genes was prevented in TG mice, mitochondrial function and ATP synthesis were equivalently impaired in Cont and TG mice after TAC. Contractile function was also equally impaired in Cont and TG mice following TAC, as demonstrated by decreased +dP/dt and ejection fraction and increased left ventricular developed pressure and end diastolic pressure. Conversely, capillary density was preserved, in concert with increased VEGF expression, while apoptosis and fibrosis were reduced in TG relative to Cont mice after TAC. Hence, sustaining physiological levels of PGC-1α expression following POH, while preserving myocardial vascularity, does not prevent mitochondrial and contractile dysfunction.