Background The relationship between hemoglobin concentration and all-cause mortality in acute ischemic stroke (AIS) patients remains unclear due to conflicting findings. This study aims to evaluate the impact of hemoglobin concentration on the risk of both short-term and long-term all-cause mortality in AIS patients from a nationwide stroke registry. Method We utilized data from the Singapore Stroke Registry (SSR), including patients >18years old at first AIS onset, and received treatment at a local hospital between 2005 and 2020. Patients were stratified according to sex-specific hemoglobin concentration cut-offs on anemia severity and polycythemia from the World Health Organization. Multivariate logistic regression and Cox proportional hazards modeling were performed, adjusting for demographics and cardiovascular risk factors. Results A total of 56,884 ischemic stroke patients were included, of which 66.8% had no anemia, 15.7% had mild anemia, 12.2% had severe anemia, and 5.3% had polycythemia. The cohort was predominantly male (57%), with a median age of 68 years. The median follow-up duration was 10-years (IQR 7–13). Compared to patients with normal-range hemoglobin, both mild and severe anemia was associated with elevated short-term and long-term risks of all-cause mortality. Severe anemia was associated with the highest risk of all-cause mortality, with hazard ratios of 1.99 (95%CI:1.92–2.06) at 30-days, 1.73 (95%CI:1.66–1.81) at 1-year, and 1.52 (95%CI:1.41–1.64) at 5-years. However, the excess risk associated with severe anemia appeared to attenuate at 10-years, whilst the elevated risk persisted among patients with mild anemia. Conclusion In this nationwide stroke registry, anemia is prevalent among AIS patients and is significantly associated with both short-term and long-term mortality.
C. E. Low, H. Wong, C. Yau et al.· Frontiers in stroke· 0 citations
Epigenetic clocks have emerged as markers of biological aging. Understanding their association with age-related functional decline may provide insights into DNA-mediated mechanisms underlying frailty-related functional decline and reveal which clocks best associate with accelerated functional decline. We therefore examined associations between established epigenetic clock measures and longitudinal trajectories of cognitive function, grip strength, and walking speed. We analyzed data from 4,018 participants in the Health and Retirement Study with available DNA methylation data and up to 12 years of follow-up data. Using linear mixed-effects models, we examined retrospective associations between twelve epigenetic clocks and longitudinal trajectories of frailty-related functional decline, modeling interactions between each epigenetic clock and time, adjusting for chronological age and sociodemographic covariates. In longitudinal analyses controlling for chronological age, older epigenetic age was associated with faster cognitive decline for Hannum (β = -0.0054, 95% CI: -0.0095, -0.0014, p = 0.009) and DNAmGrimAge (β = -0.0141, 95% CI: -0.0174, -0.0107, p < 0.001). Higher DNAmGrimAge was associated with accelerated decline in grip strength (β = -0.024, 95% CI: -0.033, -0.015, p < 0.001) and decline in walking speed (β = -0.0008, 95% CI: -0.0013, -0.0004, p < 0.001). Higher epigenetic clock biological age estimates, particularly DNAmGrimAge, are retrospectively associated with accelerated frailty-related functional decline across multiple functional domains. Systematic comparison of clock derivations may reveal specific epigenetic patterns underlying age-related functional deterioration.
Savvina Prapiadou, Tamara N. Kimball, B. Tan et al.· The journals of gerontology....· 0 citations
We use cookies to run the site and, with your consent, for analytics and to show ads.
See our Cookie Policy.
