Search

Background: Sodium intake reduction is crucial for cardiovascular health, however, its lasting impact on dementia remains unclear., Methods: We included 458,577 UK Biobank participants without dementia at baseline. We estimated 24-h urinary sodium (E24hUNa) using spot urinary parameters and obtained the incidence of all-cause dementia, Alzheimer's disease, and vascular dementia from multiple sources., Results: The mean E24hUNa was 3.0 g (1st-99th percentile: 1.5 g-5.1 g). Over a mean follow-up of 13.6 years, 7886 (1.7 %) participants developed all-cause dementia, including 3763 (0.8 %) Alzheimer's disease and 1851 (0.4 %) vascular dementia. In the restricted cubic spline model, we identify a potential cutoff of 3.13 g for E24hUNa, below which each 1 g decrease in E24hUNa was associated with 21 % (95 % confidence interval [CI] 1.11-1.34) higher all-cause dementia risk and 35 % (95 % CI 1.11-1.63) higher vascular dementia risk (P-value <0.001 for non-linearity). The hazard ratios were 1.15 (95 % CI, 1.07-1.24) for all-cause dementia and 1.21 (95 % CI 1.04-1.40) for vascular dementia among individuals with E24hUNa below 3.13 g compared to those with E24hUNa higher than 3.13 g., Limitations: One of the major limitations is the estimation of 24-h urinary sodium with spot urine samples., Conclusions: An E24hUNa level below 3.13 g, equivalent to 3.37 g daily sodium intake, is associated with increased risks of all-cause and vascular dementia. This exploratory study suggests a potential lower limit below which the risk of dementia increases with a lower sodium level. Future studies are necessary to validate our findings., Competing Interests: Declaration of competing interest The authors declare that they have no conflict of interest., (Copyright © 2024 The Authors. Published by Elsevier B.V. All rights reserved.)

Current evidence is inconclusive on cognitive benefits or harms of statins among stroke patients, who have high risk of dementia. This observational cohort study investigated the association between statin use and post-stroke dementia using data from the Clinical Practice Research Datalink. Patients without prior dementia who had an incident stroke but received no statins in the preceding year were followed for up to 10 years. We used inverse probability weighted marginal structural models to estimate observational analogues of intention-to-treat (ITT, statin initiation vs. no initiation) and per-protocol (PP, sustained statin use vs. no use) effects on the risk of dementia. To explore potential impact of unmeasured confounding, we examined the risks of coronary heart disease (CHD, positive control outcome), fracture and peptic ulcer (negative control outcomes). In 18,577 statin initiators and 14,613 non-initiators (mean follow-up of 4.2 years), the adjusted hazard ratio (aHR) for dementia was 0.70 (95% confidence interval [CI] 0.64-0.75) in ITT analysis and 0.55 (95% CI 0.50-0.62) in PP analysis. The corresponding aHR ITT and aHR PP were 0.87 (95% CI 0.79-0.95) and 0.70 (95% CI 0.62-0.80) for CHD, 1.03 (95% CI 0.82-1.29) and 1.09 (95% CI 0.77-1.54) for peptic ulcer, and 0.88 (95% CI 0.80-0.96) and 0.86 (95% CI 0.75-0.98) for fracture. Statin initiation after stroke was associated with lower risk of dementia, with a potentially greater benefit in patients who persisted with statins over time. The observed association of statin use with post-stroke dementia may in part be overestimated due to unmeasured confounding shared with the association between statin use and fracture., (© 2022. The Author(s).)

Background and Purpose: The roles of blood low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C) and triglycerides in the development of post-stroke dementia remain uncertain. This study was to investigate their potential associations., Methods: A retrospective cohort study was conducted using the Clinical Practice Research Datalink. Patients with first-ever stroke but no prior dementia were followed up for 10 years. Cox regression was used to examine the association of baseline LDL-C, HDL-C and triglycerides with post-stroke dementia., Results: Amongst 63,959 stroke patients, 15,879 had complete baseline data and were included in our main analysis. 10.8% developed dementia during a median of 4.6 years of follow-up. The adjusted hazard ratio of dementia for LDL-C (per log mmol/l increase) was 1.29 (95% confidence interval [CI] 1.14-1.47), with a linear increasing trend (p trend <0.001). The counterpart for triglycerides was 0.79 (95% CI 0.69-0.89), with a linear decreasing trend (p trend <0.001). For HDL-C, there was no association with dementia (adjusted hazard ratio 0.89, 95% CI 0.74-1.08) or a linear trend (p trend = 0.22)., Conclusions: Blood lipids may affect the risk of post-stroke dementia in different ways, with higher risk associated with LDL-C, lower risk associated with triglycerides, and no association with HDL-C., (© 2021 The Authors. European Journal of Neurology published by John Wiley & Sons Ltd on behalf of European Academy of Neurology.)

Background: Prior atherosclerotic cardiovascular disease (ASCVD), including coronary heart disease (CHD) and peripheral artery disease (PAD), are common among patients with stroke, a known risk factor for dementia. However, whether these conditions further increase the risk of post-stroke dementia remains uncertain., Objective: To examine whether prior ASCVD is associated with increased risk of dementia among stroke patients., Methods: A retrospective cohort study was conducted using the Clinical Practice Research Datalink with linkage to hospital data. Patients with first-ever stroke between 2006 and 2017 were followed up to 10 years. We used multi-variable Cox regression models to examine the associations of prior ASCVD with dementia and the impact of prior ASCVD onset and duration., Results: Among 63,959 patients, 7,265 cases (11.4%) developed post-stroke dementia during a median of 3.6-year follow-up. The hazard ratio (HR) of dementia adjusted for demographics and lifestyle was 1.18 (95% CI: 1.12-1.25) for ASCVD, 1.16 (1.10-1.23) for CHD, and 1.25 (1.13-1.37) for PAD. The HRs additionally adjusted for multimorbidity and medications were 1.07 (1.00-1.13), 1.04 (0.98-1.11), and 1.11 (1.00-1.22), respectively. Based on the fully adjusted estimates, there was no linear relationship between the age of ASCVD onset and post-stroke dementia (all p-trend >0.05). The adjusted risk of dementia was not increased with the duration of pre-stroke ASCVD (all p-trend >0.05)., Conclusion: Stroke patients with prior ASCVD are more likely to develop subsequent dementia. After full adjustment for confounding, however, the risk of post-stroke dementia is attenuated, with only a slight increase with prior ASCVD.

Background: Trial and observational evidence is conflicting in terms of the association of blood lipids, atherosclerosis and statin use with dementia and cognitive impairment in the general population. It is uncertain whether the associations occur in stroke patients, who are at known higher risk of cognitive decline. This systematic review was to synthesize the evidence for these associations among stroke patients., Methods: MEDLINE, EMBASE, the Cochrane Library and trial registries were searched. We included randomized controlled trials (RCTs) or observational cohort studies conducted among patients with stroke and reported on the association of blood lipids, atherosclerosis or statin use with dementia or cognitive impairment. Meta-analysis was conducted separately for crude and maximally adjusted odds ratios (ORs) and hazard ratios (HRs)., Results: Of 18,026 records retrieved, 56 studies (one RCT and 55 cohort studies) comprising 38,423 stroke patients were included. For coronary heart disease, the pooled OR of dementia and cognitive impairment was 1.32 (95%CI 1.10-1.58, n = 15 studies, I 2  = 0%) and 1.23 (95%CI 0.99-1.54, n = 14, I 2  = 26.9%), respectively. Peripheral artery disease was associated with dementia (OR 3.59, 95%CI 1.47-8.76, n = 2, I 2  = 0%) and cognitive impairment (OR 2.70, 95%CI 1.09-6.69, n = 1). For carotid stenosis, the pooled OR of dementia and cognitive impairment was 2.67 (95%CI 0.83-8.62, n = 3, I 2  = 77.9%) and 3.34 (95%CI 0.79-14.1, n = 4, I 2  = 96.6%), respectively. For post-stroke statin use, the pooled OR of dementia and cognitive impairment was 0.89 (95%CI 0.65-1.21, n = 1) and 0.56 (95%CI 0.46-0.69, n = 3, I 2  = 0%), respectively. No association was observed for hypercholesterolemia. These results were mostly consistent with adjusted ORs or HRs, which were reported from limited evidence., Conclusion: Atherosclerosis was associated with an increased risk of post-stroke dementia. Post-stroke statin use was associated with decreased risk of cognitive impairment. To confirm whether or not statins confer advantages in the post-stroke population in terms of preventing cognitive decline over and above their known effectiveness in reducing risk of further vascular events, further stroke trials including cognitive assessment and observational analyses adjusted for key confounders, focusing on key subgroups or statin use patterns are required., (Copyright © 2019 Elsevier B.V. All rights reserved.)