Abstract TP437: Asymptomatic Carotid Stenosis is Associated With Cognitive Impairment in a Chinese Community Population

Stroke ◽  
2017 ◽  
Vol 48 (suppl_1) ◽  
Author(s):  
Jiaokun Jia ◽  
Xingquan Zhao

Purpose: This study aimed to investigate the effects of aCAS on cognitive functioning in a Chinese community population who were over 40 year-old and to find the domains of cognitive impairment which were mainly affected. Methods: Information was collected on the presence of CAS, which was assessed by Color Doppler Ultrasound, from the Asymptomatic Polyvascular Abnormalities Community study, and cognitive functioning was assessed by the score of the Montreal Cognitive Assessment (MoCA). Multivariate logistic regression was used to assess the relationships between aCAS and cognitive impairment. Results: A total of 812 (61.2% men, 55% of 40-60y) patients were included in this study. After adjusting for potential confounding factors, the associations between the aCAS and cognitive impairment remained significant [odds ratio(OR)(95% confidence interval, 95%CI)=1.812(1.049-3.127)]. Also, there were significant relationships between the aCAS and the domains of cognitive function like attention, language, abstraction and recall [OR(95%CI) 2.740(1.494-5.023), 2.005(1.184-3.396), 2.841(1.594-5.065), 4.674(2.478-8.818) respectively, P < 0.05). In addition, there were no interaction effects of age and other possible risk factors on the association. Conclusion: In the over 40 year-old Chinese community population, aCAS was an independent indicator of cognitive impairment, especially affecting the function of attention, language, abstraction and recall. Table 1 Baseline demographic characteristics and cardiovascular risk factors between groups with/without cognitive impairment Values are median (interquartile range) or number (percent). Table 2 Unadjusted and Multivariate-adjusted OR (95% CI) for total and subtests of MoCA, according to groups with vs. without CAS. *P<0.05;**P<0.001 OR: odd ratio; CI: confidence interval Model 1: adjusted for age and gender. Model 2: adjusted for age, gender, BMI, education, current smoking and alcohol consumption. Model 3:adjusted for age, gender, BMI, education, current smoking, alcohol consumption hypertension, diabetes, hyperlipidemia, hs-CRP and Hcy.

2007 ◽  
Vol 107 (3) ◽  
pp. 522-529 ◽  
Author(s):  
Vibhor Krishna ◽  
Dong H. Kim

Object Studies on risk factors for subarachnoid hemorrhage (SAH) show heterogeneity. For example, hypertension has been found to be a significant risk factor in some studies but not in others. The authors hypothesized that differences in the ethnicity of the populations studied could account for these findings. Methods A metaanalysis was performed using 17 case-control and 10 cohort studies that met specified inclusion criteria. The authors used a random-effect model to calculate the pooled effect estimates for current smoking, hypertension, and alcohol consumption. A meta–regression analysis was performed using the ethnic composition of the study populations as a covariate. Studies were classified as multiethnic or monoethnic, and the pooled effect estimates were compared. Results Analysis of the cohort studies yielded a pooled effect estimate or risk ratio of 3.18 (95% confidence interval [CI] 2.37–4.26) for current smoking, 3.05 (95% CI 2.09–4.44) for hypertension, and 2.46 (95% CI 1.42–4.24) for alcohol consumption at a rate of 150 g/week or more. The results were similar for the case-control studies. For current smoking, the ethnic composition of the study population was a statistically significant predictor of heterogeneity among case-control studies (p < 0.001, even after application of the Bonferroni correction). The risk for SAH among current smokers was higher in multiethnic populations (odds ratio 3.832) than in monoethnic populations (odds ratio 2.487). Conclusions The results of this metaanalysis suggest that differences in susceptibility to the harmful health effects of smoking may be one cause of the observed differences in SAH incidence for different ethnic groups. The role of ethnicity in risk factors for SAH should be considered in future studies.


2018 ◽  
Vol 13 (6) ◽  
pp. 850-857 ◽  
Author(s):  
Matthew J. Jasinski ◽  
Mark A. Lumley ◽  
Sandeep Soman ◽  
Jerry Yee ◽  
Mark W. Ketterer

Background and objectivesThe US Centers for Medicare and Medicaid Services have mandated reducing early (30-day) hospital readmissions to improve patient care and reduce costs. Patients with ESKD have elevated early readmission rates, due in part to complex medical regimens but also cognitive impairment, literacy difficulties, low social support, and mood problems. We developed a brief family consultation intervention to address these risk factors and tested whether it would reduce early readmissions.Design, setting, participants, & measurementsOne hundred twenty hospitalized adults with ESKD (mean age=58 years; 50% men; 86% black, 14% white) were recruited from an urban, inpatient nephrology unit. Patients were randomized to the family consultation (n=60) or treatment-as-usual control (n=60) condition. Family consultations, conducted before discharge at bedside or via telephone, educated the family about the patient’s cognitive and behavioral risk factors for readmission, particularly cognitive impairment, and how to compensate for them. Blinded medical record reviews were conducted 30 days later to determine readmission status (primary outcome) and any hospital return visit (readmission, emergency department, or observation; secondary outcome). Logistic regressions tested the effects of the consultation versus control on these outcomes.ResultsPrimary analyses were intent-to-treat. The risk of a 30-day readmission after family consultation (n=12, 20%) was 0.54 compared with treatment-as-usual controls (n=19, 32%), although this effect was not statistically significant (odds ratio, 0.54; 95% confidence interval, 0.23 to 1.24; P=0.15). A similar magnitude, nonsignificant result was observed for any 30-day hospital return visit: family consultation (n=19, 32%) versus controls (n=28, 47%; odds ratio, 0.53; 95% confidence interval, 0.25 to 1.1; P=0.09). Per protocol analyses (excluding three patients who did not receive the assigned consultation) revealed similar results.ConclusionsA brief consultation with family members about the patient’s cognitive and psychosocial risk factors had no significant effect on 30-day hospital readmission in patients with ESKD.


2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
Fu-Wei Wang ◽  
Ping-I Hsu ◽  
Hung-Yi Chuang ◽  
Ming-Shium Tu ◽  
Guang-Yuan Mar ◽  
...  

Purpose. To investigate the prevalence and risk factors of hyperplastic and adenomatous colorectal polyps in a Taiwanese general population.Methods. From January 2009 to December 2011, consecutive asymptomatic subjects undergoing a routine health check-up were evaluated by colonoscopy. The colorectal polyps were assessed, and medical history and demographic data were obtained from each patient. Logistic regression analysis was conducted to search the independent risk factors for asymptomatic hyperplastic and adenomatous colorectal polyps.Results. Of the 1899 asymptomatic subjects, the prevalences of hyperplastic polyps and adenomatous polyps were 11.1% and 16.1%, respectively. Multivariate analysis revealed that high body mass index (BMI>25: OR, 1.32, 95% CI, 1.05–1.71) and current smoking (OR, 1.87, 95% CI, 1.42–2.71) were independent predictors for hyperplastic colorectal polyps. Age over 60 years old (OR, 3.49, 95% CI, 1.86–6.51), high body mass index (BMI>25: OR, 1.75, 95% CI, 1.21–2.71), heavy alcohol consumption (OR, 2.01, 95% CI, 1.02–3.99), and current smoking (OR, 1.31, 95% CI, 1.04–1.58) were independent predictors for adenomatous colorectal polyps.Conclusion. High BMI and smoking are common risk factors for both adenomatous and hyperplastic polyps. Old age and alcohol consumption are additional risk factors for the development of adenomatous polyps.


2018 ◽  
Vol 3 (2) ◽  
pp. 145-156 ◽  
Author(s):  
Stephen DJ Makin ◽  
Fergus N Doubal ◽  
Kirsten Shuler ◽  
Francesca M Chappell ◽  
Julie Staals ◽  
...  

Background Cognitive impairment can complicate minor stroke, but there is limited information on risk factors including peak cognitive ability earlier in life. Methods We recruited patients with clinically-evident lacunar or minor non-lacunar ischaemic stroke, recorded clinical features, vascular risk factors, magnetic resonance imaging-detected stroke sub-type and small vessel disease burden. At 1–3 and 12 months after stroke, we assessed educational attainment (years of education), current cognition (Addenbrooke’s Cognitive Examination–Revised), pre-morbid intelligence (National Adult Reading Test) and dependency (modified Rankin Scale). Results We recruited 157 patients (87 lacunar, 64 non-lacunar ischaemic strokes), median age 66 (inter-quartile range 56–74) years, 36/157 (23%) patients had a Addenbrooke’s Cognitive Examination–Revised score < 82 at one to three months, 29/151 (19%) had a Addenbrooke’s Cognitive Examination–Revised < 82 at one year. Lower National Adult Reading Test score (cognitive impairment per point on National Adult Reading Test odds ratio 0.91, 95% confidence interval 0.87, 0.95) and older age (per year of age odds ratio 1.04 (95% confidence interval 1.01, 1.08) predicted one-year cognitive impairment more than stroke severity (per point on National Institute of Health Stroke Scale odds ratio 0.96 (95% confidence interval 0.0.68, 1.31)) or vascular risk factors e.g. hypertension (odds ratio for diagnosis of hypertension 0.52 (95% confidence interval 0.24, 1.15). Cognitive impairment was associated with having more white matter hyper-intensities (odds ratio per point increase in Fazekas score 1.42, 95% confidence interval 1.11, 1.83). Discussion This observational study provides evidence that pre-morbid intelligence quotient and education predict cognition after stroke, and confirms the association between cognitive impairment and small vessel disease. Conclusion Pre-morbid intelligence should be considered in future studies of post-stroke cognition.


Circulation ◽  
2012 ◽  
Vol 125 (suppl_10) ◽  
Author(s):  
Moritz F Sinner ◽  
Na Wang ◽  
Joao D Fontes ◽  
Michiel Rienstra ◽  
Jared W Magnani ◽  
...  

Background: For the management of an initial episode of atrial fibrillation (AF), guidelines recommend assessment of liver function tests; nonetheless, the rationale and supporting evidence for the recommendation remain unclear. We tested the hypothesis that elevated liver transaminases, assessed by alanine transaminase (ALT) and aspartate transaminase (AST) are associated with the incidence of AF in a community-based cohort. Methods and Results: From the Framingham Heart Study Original and Offspring cohorts we investigated 3779 participants (mean age 65±10 years, 56.8% females). After up to 10 years of follow-up (29,099 person years), 383 individuals developed AF. We used Cox proportional hazards models to assess the association between liver transaminases and AF incidence, and adjusted the model for established AF risk factors and alcohol consumption. Both ALT and AST showed significant association with incident AF (Table). When we excluded participants with moderate / severe alcohol consumption, the associations for ALT and AST remained consistent (Table). Additional adjustment for C-reactive protein (inflammatory marker) only mildly lowered the effect estimates for both transaminases, but decreased the level of significance (Table). We additionally estimated the ability of transaminasess to predict AF risk. When assessed by the continuous net reclassification improvement, both ALT and AST marginally improved AF risk prediction [ALT: 0.18 (95% confidence interval, 0.07-0.29; p=0.002); AST: 0.16 (95% confidence interval, 0.04-0.28; p=0.003)]. Conclusions: Higher mean levels of ALT and AST, are associated with the incidence of AF, even when adjusted for various established AF risk factors. However, transaminases contribute only subtly towards an improvement in AF risk prediction. Pathophysiologic mechanisms explaining the association are uncertain and merit further investigation.


2019 ◽  
Vol 74 (11) ◽  
pp. 1786-1792 ◽  
Author(s):  
Carla R Schubert ◽  
Karen J Cruickshanks ◽  
Mary E Fischer ◽  
A Alex Pinto ◽  
Yanjun Chen ◽  
...  

Abstract Background Sensorineural impairments and cardiovascular risk factors (CVRF) and disease (CVD) in midlife may be important predictors of future cognitive health, but longitudinal studies that include multiple sensorineural measures in middle-aged adults are lacking. Methods Hearing, vision, and olfaction, and CVRF and CVD were measured at the Beaver Dam Offspring Study baseline (2005–2008) examination. The Mini-Mental State Examination and Trail Making Tests A and B were administered at all phases and additional cognitive function measures were obtained at 5 (2010–2013) and 10 years (2015–2017). Cox proportional hazards models were used to evaluate associations between baseline sensorineural impairments, CVRF, CVD, and 10-year cumulative incidence of cognitive impairment and decline. Results There were 2,556 participants (22–84 years) without cognitive impairment at baseline and data from at least one follow-up. In a multivariable model including age, sex, education, and head injury, visual impairment (hazard ratio = 2.59, 95% confidence interval = 1.34, 5.02), olfactory impairment (hazard ratio = 3.18, 95% confidence interval = 1.53, 6.59), CVD (hazard ratio = 2.37, 95% confidence interval = 1.24, 4.52), and not consuming alcohol in the past year (hazard ratio = 2.21, 95% confidence interval = 1.16, 4.19) were associated with the 10-year cumulative incidence of cognitive impairment. Current smoking and diabetes were associated with increased risk, and exercise with decreased risk, of 10-year decline in cognitive function. Conclusions Visual and olfactory impairments, CVRF, and CVD were associated with the 10-year cumulative incidence of cognitive impairment and decline in middle-aged adults. Identifying modifiable factors associated with cognitive decline and impairment in midlife may provide opportunities for prevention or treatment and improve cognitive health later in life.


Author(s):  
Karla Liliana Pérez-Sosa ◽  
Edgar Felipe Lares-Bayona

Alcohol is a toxic substance associated with acute and chronic disorders affecting the Central Nervous System and significantly altering brain function. Objective: To determine the relationship between cognitive impairment and alcohol consumption in university students of the Juárez University of the State of Durango. Methodology: It is a cross-sectional, descriptive, comparative, non-probabilistic study, for convenience. A database was designed on the results obtained in a clinical interview on alcohol consumption and the application of the Montreal Cognitive Assessment (MoCA) test. Contribution: The evaluation of cognitive functions show similar results, the male sex presented a better score in Attention and the female one in Orientation. More involvement was identified in the Deferred Memory functions in both groups. In relation to alcohol consumption, the cognitive functions evaluated show lower levels. The female gender was more evident cognitive impairment in relation to alcohol consumption being statistically significant (p <0.025). Alcohol consumption is a risky behavior that deserves to be recognized by the main actors about neurocognitive effects. Alcohol consumption prevention programs and cognitive diagnostic tools are appropriate strategies to reduce risk behaviors in mental health.


2020 ◽  
Vol 17 ◽  
Author(s):  
Hyung-Ji Kim ◽  
Jae-Hong Lee ◽  
E-nae Cheong ◽  
Sung-Eun Chung ◽  
Sungyang Jo ◽  
...  

Background: Amyloid PET allows for the assessment of amyloid β status in the brain, distinguishing true Alzheimer’s disease from Alzheimer’s disease-mimicking conditions. Around 15–20% of patients with clinically probable Alzheimer’s disease have been found to have no significant Alzheimer’s pathology on amyloid PET. However, a limited number of studies had been conducted this subpopulation in terms of clinical progression. Objective: We investigated the risk factors that could affect the progression to dementia in patients with amyloid-negative amnestic mild cognitive impairment (MCI). Methods: This study was a single-institutional, retrospective cohort study of patients over the age of 50 with amyloidnegative amnestic MCI who visited the memory clinic of Asan Medical Center with a follow-up period of more than 36 months. All participants underwent brain magnetic resonance imaging (MRI), detailed neuropsychological testing, and fluorine-18[F18]-florbetaben amyloid PET. Results: During the follow-up period, 39 of 107 patients progressed to dementia from amnestic MCI. In comparison with the stationary group, the progressed group had a more severe impairment in verbal and visual episodic memory function and hippocampal atrophy, which showed an Alzheimer’s disease-like pattern despite the lack of evidence for significant Alzheimer’s disease pathology. Voxel-based morphometric MRI analysis revealed that the progressed group had a reduced gray matter volume in the bilateral cerebellar cortices, right temporal cortex, and bilateral insular cortices. Conclusion: Considering the lack of evidence of amyloid pathology, clinical progression of these subpopulation may be caused by other neuropathologies such as TDP-43, abnormal tau or alpha synuclein that lead to neurodegeneration independent of amyloid-driven pathway. Further prospective studies incorporating biomarkers of Alzheimer’s diseasemimicking dementia are warranted.


Author(s):  
Victoria J. Williams ◽  
Steven E. Arnold ◽  
David H. Salat

Throughout the lifespan, common variations in systemic health and illness contribute to alterations in vasculature structure and function throughout the body, significantly increasing risk for cardiovascular and cerebrovascular disease (CVD). CVD is a prevalent cause of mortality in late life; it also promotes brain alterations, contributing to cognitive decline and, when severe, vascular dementia. Even prior to diseased states, individual variation in CVD risk is associated with structural and functional brain alterations. Yet, how cumulative asymptomatic alterations in vessel structure and function contribute to more subtle changes in brain tissue integrity and function that emerge in late life is unclear. Finally, vascular risk factors are associated with the clinical progression of neurodegenerative diseases such as Alzheimer’s disease (AD); however, recent theory posits that vascular degeneration may serve a contributory role in these conditions. This chapter reviews how lifespan changes in vascular health contribute to degenerative changes in neural tissue and the subsequent development of cognitive impairment and/or vascular dementia. It first discusses associations between vascular risk factors and cognition and also how declining vascular health may lead to cognitive impairment and dementia. Next, it identifies basic aspects of cerebrovascular anatomy and physiology sustaining tissue health and discusses how vulnerabilities of this system contribute to neurodegenerative changes. Finally, it reviews evidence of vascular contributions to AD and presents ideas for future research to better understand the full spectrum of cerebrovascular contributions to brain aging, cognitive decline, and dementia.


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