@article {1044, title = {Metabolic syndrome, endothelial dysfunction, and risk of cardiovascular events: the Northern Manhattan Study (NOMAS).}, journal = {Am Heart J}, volume = {156}, year = {2008}, month = {2008 Aug}, pages = {405-10}, abstract = {

BACKGROUND: Metabolic syndrome (MetS) predisposes to cardiovascular disease. Endothelial dysfunction is thought to be an important factor in the pathogenesis of atherosclerosis. We tested the hypothesis that both MetS and endothelial dysfunction are vascular risk factors and provide additive prognostic values in predicting cardiovascular events in a multiethnic community sample.

METHODS: The study population consisted of 819 subjects (467 female, mean age 66.5 +/- 8.8 years, 66\% Hispanic) enrolled in the NOMAS. Metabolic syndrome was defined using the revised Adult Treatment Panel III criteria. Brachial artery flow-mediated dilation (FMD) was measured using high-resolution ultrasound. Endothelial dysfunction was defined as FMD <8.44\% (lower 3 quartiles). Cox proportional hazards models were used to assess the effect of MetS and endothelial dysfunction on risk of cardiovascular events.

RESULTS: During 81 +/- 21 months of follow-up, events occurred in 84 subjects. Metabolic syndrome was independently associated with cardiovascular events in a multivariate model, including cardiovascular risk factors (adjusted hazard ratio 2.08, 95\% CI 1.27-3.40). Subjects with both MetS and endothelial dysfunction were at higher risk for cardiovascular events than those with either one of them alone (adjusted hazard ratio 2.60, 95\% CI 1.14-5.92).

CONCLUSIONS: Metabolic syndrome is associated with incident cardiovascular events. Combined use of MetS and FMD identifies those who are at higher risk of cardiovascular events. Metabolic syndrome and noninvasive FMD testing can be used concurrently for cardiovascular risk prediction.

}, keywords = {Adult, Aged, Brachial Artery, Endothelium, Vascular, Female, Humans, Kaplan-Meier Estimate, Male, Metabolic Syndrome, Middle Aged, Prognosis, Prospective Studies, Risk Factors, Stroke, Vascular Diseases}, issn = {1097-6744}, doi = {10.1016/j.ahj.2008.02.022}, author = {Suzuki, Takeki and Hirata, Kumiko and Elkind, Mitchell S V and Jin, Zhezhen and Rundek, Tanja and Miyake, Yumiko and Boden-Albala, Bernadette and Di Tullio, Marco R and Sacco, Ralph and Homma, Shunichi} } @article {1254, title = {Measures of adiposity and future risk of ischemic stroke and coronary heart disease in older men and women.}, journal = {Am J Epidemiol}, volume = {173}, year = {2011}, month = {2011 Jan 01}, pages = {10-25}, abstract = {

The relation between measures of general and central adiposity and individual cardiovascular endpoints remains understudied in older adults. This study investigated the association of measures of body size and composition with incident ischemic stroke or coronary heart disease (1989-2007) in 3,754 community-dwelling US adults aged 65-100 years. Standardized anthropometry and bioelectric impedance measurements were obtained at baseline. Body mass index at age 50 years (BMI50) was calculated on the basis of recalled weight. Although only waist/hip ratio was significantly associated with ischemic stroke in quintile analysis in women, dichotomized body mass index (BMI) (>= 30 kg/m{\texttwosuperior}) was the only significant predictor in men. For coronary heart disease, there were significant positive adjusted associations for all adiposity measures, without interaction by sex. This was true for both quintiles and conventional cutpoints for obesity, although BMI-defined overweight (25-29.9 kg/m{\texttwosuperior} was significant at midlife but not at baseline. Strengths of association for extreme quintiles (quintile 5 vs. quintile 1) were broadly comparable, but the highest effect estimates were for waist/hip ratio (hazard ratio = 1.56, 95\% confidence interval: 1.25, 1.94) and BMI50 (hazard ratio = 1.71, 95\% confidence interval: 1.37, 2.14), both of which remained significant after adjustment for mediators, BMI, or each other. Whether these differences translate to better risk prediction will require meta-analytical approaches, as will determination of prognostic cutpoints.

}, keywords = {Adiposity, Age Factors, Aged, Aged, 80 and over, Brain Ischemia, Coronary Disease, Female, Humans, Incidence, Male, Middle Aged, Obesity, Prevalence, Retrospective Studies, Risk Factors, Sex Factors, United States}, issn = {1476-6256}, doi = {10.1093/aje/kwq311}, author = {Kizer, Jorge R and Biggs, Mary L and Ix, Joachim H and Mukamal, Kenneth J and Zieman, Susan J and de Boer, Ian H and Mozaffarian, Dariush and Barzilay, Joshua I and Strotmeyer, Elsa S and Luchsinger, Jos{\'e} A and Elkind, Mitchell S V and Longstreth, W T and Kuller, Lewis H and Siscovick, David S} } @article {6668, title = {Association between left atrial abnormality on ECG and vascular brain injury on MRI in the Cardiovascular Health Study.}, journal = {Stroke}, volume = {46}, year = {2015}, month = {2015 Mar}, pages = {711-6}, abstract = {

BACKGROUND AND PURPOSE: Emerging evidence suggests that atrial disease is associated with vascular brain injury in the absence of atrial fibrillation.

METHODS: The Cardiovascular Health Study prospectively enrolled community-dwelling adults aged >=65 years. Among participants who underwent MRI, we examined associations of ECG left atrial abnormality with brain infarcts and leukoaraiosis. P-wave terminal force in lead V1 was the primary measure of left atrial abnormality; P-wave area and duration were secondary predictors. We excluded participants with atrial fibrillation before or on their index ECG. Primary outcomes were incident infarcts and worsening leukoaraiosis from initial to follow-up scan ≈5 years later. Secondary outcomes were prevalent infarcts and degree of leukoaraiosis on initial MRI. Relative risk (RR) and linear regression models were adjusted for vascular risk factors.

RESULTS: Among 3129 participants with >=1 scan, each SD increase in P-wave terminal force in lead V1 was associated with a 0.05-point (95\% confidence interval [CI], 0.0003-0.10) higher baseline white matter grade on a 10-point scale. P-wave terminal force in lead V1 was associated with prevalent infarcts of any type (RR per SD, 1.09; 95\% CI, 1.04-1.16) and more so with prevalent nonlacunar infarcts (RR per SD, 1.22; 95\% CI, 1.08-1.38). Among 1839 participants with 2 scans, P-wave terminal force in lead V1 was associated with worsening leukoaraiosis (RR per SD, 1.09; 95\% CI, 1.01-1.18), but not with incident infarcts (RR per SD, 1.06; 95\% CI, 0.93-1.20). Sensitivity analyses adjusting for incident atrial fibrillation found similar results. P-wave area and duration were not associated with outcomes.

CONCLUSIONS: ECG left atrial abnormality is associated with vascular brain injury in the absence of documented atrial fibrillation.

}, keywords = {Aged, Atrial Fibrillation, Brain, Brain Infarction, Cardiovascular Diseases, Cerebrovascular Trauma, Electrocardiography, Female, Heart Atria, Heart Diseases, Humans, Linear Models, Magnetic Resonance Imaging, Male, Middle Aged, Predictive Value of Tests, Prospective Studies, Regression Analysis, Risk Factors, Treatment Outcome}, issn = {1524-4628}, doi = {10.1161/STROKEAHA.114.007762}, author = {Kamel, Hooman and Bartz, Traci M and Longstreth, W T and Okin, Peter M and Thacker, Evan L and Patton, Kristen K and Stein, Phyllis K and Gottesman, Rebecca F and Heckbert, Susan R and Kronmal, Richard A and Elkind, Mitchell S V and Soliman, Elsayed Z} } @article {6808, title = {Intermediate and long-term risk of new-onset heart failure after hospitalization for pneumonia in elderly adults.}, journal = {Am Heart J}, volume = {170}, year = {2015}, month = {2015 Aug}, pages = {306-12}, abstract = {

BACKGROUND: Pneumonia is associated with high risk of heart failure (HF) in the short term (30 days) postinfection. Whether this association persists beyond this period is unknown.

METHODS: We studied 5,613 elderly (>=65 years) adults enrolled in the Cardiovascular Health Study between 1989 and 1994 at 4 US communities. Participants had no clinical diagnosis of HF at enrollment, and they were followed up through December 2010. Hospitalizations for pneumonia were identified using validated International Classification of Disease Ninth Revision codes. A centralized committee adjudicated new-onset HF events. Using Cox regression, we estimated adjusted hazard ratios (HRs) of new-onset HF at different time intervals after hospitalization for pneumonia.

RESULTS: A total of 652 participants hospitalized for pneumonia during follow-up were still alive and free of clinical diagnosis of HF by day 30 posthospitalization. Relative to the time of their hospitalization, new-onset HF occurred in 22 cases between 31 and 90 days (HR 6.9, 95\% CI 4.46-10.63, P < .001), 14 cases between 91 days and 6 months (HR 3.2, 95\% CI 1.88-5.50, P < .001), 20 cases between 6 months and 1 year (HR 2.6, 95\% CI 1.64-4.04, P < .001), 76 cases between 1 and 5 years (HR 1.7, 95\% CI 1.30-2.12, P < .001), and 71 cases after 5 years (HR 2.0, 95\% CI 1.56-2.58, P < .001). Results were robust to sensitivity analyses using stringent definitions of pneumonia and extreme assumptions for potential informative censoring.

CONCLUSION: Hospitalization for pneumonia is associated with increased risk of new-onset HF in the intermediate and long term. Studies should characterize the mechanisms of this association in order to prevent HF in elderly pneumonia survivors.

}, keywords = {Aged, Disease Progression, Female, Follow-Up Studies, Forecasting, Heart Failure, Hospitalization, Humans, Incidence, Inpatients, Male, Patient Readmission, Pneumonia, Proportional Hazards Models, Retrospective Studies, Risk Assessment, Risk Factors, Time Factors}, issn = {1097-6744}, doi = {10.1016/j.ahj.2015.04.028}, author = {Corrales-Medina, Vicente F and Taljaard, Monica and Yende, Sachin and Kronmal, Richard and Dwivedi, Girish and Newman, Anne B and Elkind, Mitchell S V and Lyles, Mary F and Chirinos, Julio A} } @article {6683, title = {Multiethnic genome-wide association study of cerebral white matter hyperintensities on MRI.}, journal = {Circ Cardiovasc Genet}, volume = {8}, year = {2015}, month = {2015 Apr}, pages = {398-409}, abstract = {

BACKGROUND: The burden of cerebral white matter hyperintensities (WMH) is associated with an increased risk of stroke, dementia, and death. WMH are highly heritable, but their genetic underpinnings are incompletely characterized. To identify novel genetic variants influencing WMH burden, we conducted a meta-analysis of multiethnic genome-wide association studies.

METHODS AND RESULTS: We included 21 079 middle-aged to elderly individuals from 29 population-based cohorts, who were free of dementia and stroke and were of European (n=17 936), African (n=1943), Hispanic (n=795), and Asian (n=405) descent. WMH burden was quantified on MRI either by a validated automated segmentation method or a validated visual grading scale. Genotype data in each study were imputed to the 1000 Genomes reference. Within each ethnic group, we investigated the relationship between each single-nucleotide polymorphism and WMH burden using a linear regression model adjusted for age, sex, intracranial volume, and principal components of ancestry. A meta-analysis was conducted for each ethnicity separately and for the combined sample. In the European descent samples, we confirmed a previously known locus on chr17q25 (P=2.7{\texttimes}10(-19)) and identified novel loci on chr10q24 (P=1.6{\texttimes}10(-9)) and chr2p21 (P=4.4{\texttimes}10(-8)). In the multiethnic meta-analysis, we identified 2 additional loci, on chr1q22 (P=2.0{\texttimes}10(-8)) and chr2p16 (P=1.5{\texttimes}10(-8)). The novel loci contained genes that have been implicated in Alzheimer disease (chr2p21 and chr10q24), intracerebral hemorrhage (chr1q22), neuroinflammatory diseases (chr2p21), and glioma (chr10q24 and chr2p16).

CONCLUSIONS: We identified 4 novel genetic loci that implicate inflammatory and glial proliferative pathways in the development of WMH in addition to previously proposed ischemic mechanisms.

}, keywords = {Aged, Aged, 80 and over, Chromosomes, Human, Continental Population Groups, Female, Genetic Loci, Genome-Wide Association Study, Humans, Male, Meta-Analysis as Topic, Middle Aged, Models, Genetic, Stroke, White Matter}, issn = {1942-3268}, doi = {10.1161/CIRCGENETICS.114.000858}, author = {Verhaaren, Benjamin F J and Debette, Stephanie and Bis, Joshua C and Smith, Jennifer A and Ikram, M Kamran and Adams, Hieab H and Beecham, Ashley H and Rajan, Kumar B and Lopez, Lorna M and Barral, Sandra and van Buchem, Mark A and van der Grond, Jeroen and Smith, Albert V and Hegenscheid, Katrin and Aggarwal, Neelum T and de Andrade, Mariza and Atkinson, Elizabeth J and Beekman, Marian and Beiser, Alexa S and Blanton, Susan H and Boerwinkle, Eric and Brickman, Adam M and Bryan, R Nick and Chauhan, Ganesh and Chen, Christopher P L H and Chouraki, Vincent and de Craen, Anton J M and Crivello, Fabrice and Deary, Ian J and Deelen, Joris and De Jager, Philip L and Dufouil, Carole and Elkind, Mitchell S V and Evans, Denis A and Freudenberger, Paul and Gottesman, Rebecca F and Gu{\dh}nason, Vilmundur and Habes, Mohamad and Heckbert, Susan R and Heiss, Gerardo and Hilal, Saima and Hofer, Edith and Hofman, Albert and Ibrahim-Verbaas, Carla A and Knopman, David S and Lewis, Cora E and Liao, Jiemin and Liewald, David C M and Luciano, Michelle and van der Lugt, Aad and Martinez, Oliver O and Mayeux, Richard and Mazoyer, Bernard and Nalls, Mike and Nauck, Matthias and Niessen, Wiro J and Oostra, Ben A and Psaty, Bruce M and Rice, Kenneth M and Rotter, Jerome I and von Sarnowski, Bettina and Schmidt, Helena and Schreiner, Pamela J and Schuur, Maaike and Sidney, Stephen S and Sigurdsson, Sigurdur and Slagboom, P Eline and Stott, David J M and van Swieten, John C and Teumer, Alexander and T{\"o}glhofer, Anna Maria and Traylor, Matthew and Trompet, Stella and Turner, Stephen T and Tzourio, Christophe and Uh, Hae-Won and Uitterlinden, Andr{\'e} G and Vernooij, Meike W and Wang, Jing J and Wong, Tien Y and Wardlaw, Joanna M and Windham, B Gwen and Wittfeld, Katharina and Wolf, Christiane and Wright, Clinton B and Yang, Qiong and Zhao, Wei and Zijdenbos, Alex and Jukema, J Wouter and Sacco, Ralph L and Kardia, Sharon L R and Amouyel, Philippe and Mosley, Thomas H and Longstreth, W T and DeCarli, Charles C and van Duijn, Cornelia M and Schmidt, Reinhold and Launer, Lenore J and Grabe, Hans J and Seshadri, Sudha S and Ikram, M Arfan and Fornage, Myriam} } @article {7560, title = {Disability Trajectories Before and After Stroke and Myocardial Infarction: The Cardiovascular Health Study.}, journal = {JAMA Neurol}, volume = {74}, year = {2017}, month = {2017 Dec 01}, pages = {1439-1445}, abstract = {

Importance: Ischemic strokes may accelerate long-term functional decline apart from their acute effects on neurologic function.

Objective: To test whether the increase in long-term disability is steeper after than before the event for ischemic stroke but not myocardial infarction (MI).

Design, Settings, and Participants: In the population-based, prospective cohort Cardiovascular Health Study (1989-2013), longitudinal follow-up was conducted for a mean (SD) of 13 (6.2) years. Follow-up data were used until September 1, 2013; data analysis was performed from August 1, 2013, to June 1, 2016. Models based on generalized estimating equations adjusted for baseline covariates and included a test for different slopes of disability before and after the event. Participants included 5888 Medicare-eligible individuals 65 years or older who were not institutionalized, expected to reside in the area for 3 or more years, and able to provide informed consent. Exclusions were needing a wheelchair, receiving hospice care, and undergoing radiotherapy or chemotherapy.

Exposures: Ischemic stroke and MI.

Main Outcomes and Measures: Annual assessments with a disability scale (measuring activities of daily living [ADLs] and instrumental ADLs). The number of ADLs and instrumental ADLs (range, 0-12) that the participant could not perform was analyzed continuously.

Results: The mean (SD) age of the entire cohort (n = 5888) was 72.8 (5.6) years; 2495 (42.4\%) were male. During follow-up, 382 (6.5\%) participants had ischemic stroke and 395 (6.7\%) had MI with 1 or more disability assessment after the event. There was a mean of 3.7 (2.4) visits before stroke and 3.7 (2.3) visits after stroke; there was a mean of 3.8 (2.5) visits before MI and 3.8 (2.4) visits after MI. The increase in disability near the time of the event was greater for stroke (0.88 points on the disability scale; 95\% CI, 0.57 to 1.20; P < .001) than MI (0.20 points on the disability scale; 95\% CI, 0.06 to 0.35; P = .006). The annual increase in disability before stroke (0.06 points per year; 95\% CI, 0.002 to 0.12; P = .04) more than tripled after stroke (0.15 additional points per year; 95\% CI, 0.004 to 0.30; P = .04). The annual increase in disability before MI (0.04 points per year; 95\% CI, 0.004 to 0.08; P = .03) did not change significantly after MI (0.02 additional points per year; 95\% CI, -0.07 to 0.11; P = .69).

Conclusions and Relevance: In this large, population-based study, a trajectory of increasing disability became significantly steeper after stroke but not after MI. Thus, in addition to the acute brain injury and consequent impairment, ischemic stroke may also be associated with potentially treatable long-term adverse effects on the brain that lead to accelerated functional decline.

}, keywords = {Activities of Daily Living, Aged, Brain Ischemia, Cohort Studies, Disabled Persons, Disease Progression, Female, Humans, Male, Myocardial Infarction, Prospective Studies, Stroke}, issn = {2168-6157}, doi = {10.1001/jamaneurol.2017.2802}, author = {Dhamoon, Mandip S and Longstreth, W T and Bartz, Traci M and Kaplan, Robert C and Elkind, Mitchell S V} } @article {8709, title = {Sex Differences in Cognitive Decline Among US Adults.}, journal = {JAMA Netw Open}, volume = {4}, year = {2021}, month = {2021 02 01}, pages = {e210169}, abstract = {

Importance: Sex differences in dementia risk are unclear, but some studies have found greater risk for women.

Objective: To determine associations between sex and cognitive decline in order to better understand sex differences in dementia risk.

Design, Setting, and Participants: This cohort study used pooled analysis of individual participant data from 5 cohort studies for years 1971 to 2017: Atherosclerosis Risk in Communities Study, Coronary Artery Risk Development in Young Adults Study, Cardiovascular Health Study, Framingham Offspring Study, and Northern Manhattan Study. Linear mixed-effects models were used to estimate changes in each continuous cognitive outcome over time by sex. Data analysis was completed from March 2019 to October 2020.

Exposure: Sex.

Main Outcomes and Measures: The primary outcome was change in global cognition. Secondary outcomes were change in memory and executive function. Outcomes were standardized as t scores (mean [SD], 50 [10]); a 1-point difference represents a 0.1-SD difference in cognition.

Results: Among 34 349 participants, 26 088 who self-reported Black or White race, were free of stroke and dementia, and had covariate data at or before the first cognitive assessment were included for analysis. Median (interquartile range) follow-up was 7.9 (5.3-20.5) years. There were 11 775 (44.7\%) men (median [interquartile range] age, 58 [51-66] years at first cognitive assessment; 2229 [18.9\%] Black) and 14 313 women (median [interquartile range] age, 58 [51-67] years at first cognitive assessment; 3636 [25.4\%] Black). Women had significantly higher baseline performance than men in global cognition (2.20 points higher; 95\% CI, 2.04 to 2.35 points; P < .001), executive function (2.13 points higher; 95\% CI, 1.98 to 2.29 points; P < .001), and memory (1.89 points higher; 95\% CI, 1.72 to 2.06 points; P < .001). Compared with men, women had significantly faster declines in global cognition (-0.07 points/y faster; 95\% CI, -0.08 to -0.05 points/y; P < .001) and executive function (-0.06 points/y faster; 95\% CI, -0.07 to -0.05 points/y; P < .001). Men and women had similar declines in memory (-0.004 points/y faster; 95\% CI, -0.023 to 0.014; P = .61).

Conclusions and Relevance: The results of this cohort study suggest that women may have greater cognitive reserve but faster cognitive decline than men, which could contribute to sex differences in late-life dementia.

}, keywords = {Aged, Cognitive Dysfunction, Cognitive Reserve, Cohort Studies, Executive Function, Humans, Memory, Middle Aged, Risk, Sex Factors, Time Factors, United States}, issn = {2574-3805}, doi = {10.1001/jamanetworkopen.2021.0169}, author = {Levine, Deborah A and Gross, Alden L and Brice{\~n}o, Emily M and Tilton, Nicholas and Giordani, Bruno J and Sussman, Jeremy B and Hayward, Rodney A and Burke, James F and Hingtgen, Stephanie and Elkind, Mitchell S V and Manly, Jennifer J and Gottesman, Rebecca F and Gaskin, Darrell J and Sidney, Stephen and Sacco, Ralph L and Tom, Sarah E and Wright, Clinton B and Yaffe, Kristine and Galecki, Andrzej T} } @article {9234, title = {Epilepsy, Vascular Risk Factors, and Cognitive Decline in Older Adults: The Cardiovascular Health Study.}, journal = {Neurology}, volume = {99}, year = {2022}, month = {2022 Nov 22}, pages = {e2346-e2358}, abstract = {

BACKGROUND AND OBJECTIVES: Recent studies have shown that global cognitive ability tends to decline faster over time in older adults (>=65 years) with epilepsy compared with older adults without epilepsy. Scarce data exist about the role of vascular risk factors (VRFs) on cognitive course in epilepsy. We assessed whether the associations of individual VRFs with cognitive trajectory differed depending on the presence of prevalent epilepsy.

METHODS: The Cardiovascular Health Study is a population-based longitudinal cohort study of 5,888 US adults aged >=65 years. Cognitive function was assessed annually with modified Mini-Mental State Examination (3MS; global cognitive ability) and Digit Symbol Substitution Test (DSST; information processing speed). We used linear mixed models to estimate the individual and joint associations of epilepsy and VRFs with cognitive decline by modeling epilepsy {\texttimes} VRF interactions one by one, each adjusted for all other VRFs considered, including demographics, health behaviors, clinical characteristics, and comorbid diagnoses. From these models, we estimated excess mean cognitive decline due to interaction of epilepsy with each VRF.

RESULTS: We observed excess mean decline in global cognitive ability (3MS) due to interactions of epilepsy with hypertension (6.6 points greater mean 8-year decline than expected if no interaction; 95\% CI 1.3-12.0) and with abstaining from alcohol (5.8 points greater than expected; 95\% CI 0.3-11.3). We also observed excess mean decline in information processing speed (DSST) due to interactions of epilepsy with prior stroke (18.1 points greater mean 9-year decline than expected; 95\% CI 7.6-28.5), with abstaining from alcohol (6.1 points greater than expected; 95\% CI 2.5-9.8), and with higher triglyceride levels (2.4 points greater than expected per SD; 95\% CI 0.4-4.3).

DISCUSSION: Associations of some VRFs with cognitive decline in older adults are stronger in the presence of epilepsy, suggesting a need for greater attention to vascular protection for preserving brain health in older adults with epilepsy.

}, keywords = {Aged, Cognition, Cognitive Dysfunction, Epilepsy, Humans, Longitudinal Studies, Neuropsychological Tests, Risk Factors}, issn = {1526-632X}, doi = {10.1212/WNL.0000000000201187}, author = {Choi, Hyunmi and Elkind, Mitchell S V and Longstreth, W T and Boehme, Amelia K and Hafen, Rebekah and Hoyt, Emma J and Thacker, Evan L} } @article {9291, title = {Association of Obesity With Cognitive Decline in Black and White Americans.}, journal = {Neurology}, volume = {100}, year = {2023}, month = {2023 Jan 10}, pages = {e220-e231}, abstract = {

BACKGROUND AND OBJECTIVES: There are disparities in the prevalence of obesity by race, and the relationship between obesity and cognitive decline is unclear. The objective of this study was to determine whether obesity is independently associated with cognitive decline and whether the association between obesity and cognitive decline differs in Black and White adults. We hypothesized that obesity is associated with greater cognitive decline compared with normal weight and that the effect of obesity on cognitive decline is more pronounced in Black adults compared with their White counterparts.

METHODS: We pooled data from 28,867 participants free of stroke and dementia (mean, SD: age 61 [10.7] years at the first cognitive assessment, 55\% female, 24\% Black, and 29\% obese) from 6 cohorts. The primary outcome was the annual change in global cognition. We performed linear mixed-effects models with and without time-varying cumulative mean systolic blood pressure (SBP) and fasting plasma glucose (FPG). Global cognition was set to a t-score metric (mean 50, SD 10) at a participant{\textquoteright}s first cognitive assessment; a 1-point difference represents a 0.1 SD difference in global cognition across the 6 cohorts. The median follow-up was 6.5 years (25th percentile, 75th percentile: 5.03, 20.15).

RESULTS: Obese participants had lower baseline global cognition than normal-weight participants (difference in intercepts, -0.36 [95\% CI, -0.46 to -0.17]; < 0.001). This difference in baseline global cognition was attenuated but was borderline significant after accounting for SBP and FPG (adjusted differences in intercepts, -0.19 [95\% CI, -0.39 to 0.002]; = 0.05). There was no difference in the rate of decline in global cognition between obese and normal-weight participants (difference in slope, 0.009 points/year [95\% CI, -0.009 to 0.03]; = 0.32). After accounting for SBP and FPG, obese participants had a slower decline in global cognition (adjusted difference in slope, 0.03 points/year slower [95\% CI, 0.01 to 0.05]; < 0.001). There was no evidence that race modified the association between body mass index and global cognitive decline ( = 0.34).

DISCUSSION: These results suggest that obesity is associated with lower initial cognitive scores and may potentially attenuate declines in cognition after accounting for BP and FPG.

}, keywords = {Aged, Black or African American, Cognition, Cognitive Dysfunction, Female, Humans, Male, Middle Aged, Obesity, Risk Factors, United States, White}, issn = {1526-632X}, doi = {10.1212/WNL.0000000000201367}, author = {Quaye, Emmanuel and Galecki, Andrzej T and Tilton, Nicholas and Whitney, Rachael and Brice{\~n}o, Emily M and Elkind, Mitchell S V and Fitzpatrick, Annette L and Gottesman, Rebecca F and Griswold, Michael and Gross, Alden L and Heckbert, Susan R and Hughes, Timothy M and Longstreth, W T and Sacco, Ralph L and Sidney, Stephen and Windham, B Gwen and Yaffe, Kristine and Levine, Deborah A} } @article {9972, title = {Cumulative Systolic Blood Pressure and Incident Stroke Type Variation by Race and Ethnicity.}, journal = {JAMA Netw Open}, volume = {7}, year = {2024}, month = {2024 May 01}, pages = {e248502}, abstract = {

IMPORTANCE: Stroke risk varies by systolic blood pressure (SBP), race, and ethnicity. The association between cumulative mean SBP and incident stroke type is unclear, and whether this association differs by race and ethnicity remains unknown.

OBJECTIVE: To examine the association between cumulative mean SBP and first incident stroke among 3 major stroke types-ischemic stroke (IS), intracerebral hemorrhage (ICH), and subarachnoid hemorrhage (SAH)-and explore how these associations vary by race and ethnicity.

DESIGN, SETTING, AND PARTICIPANTS: Individual participant data from 6 US longitudinal cohorts (January 1, 1971, to December 31, 2019) were pooled. The analysis was performed from January 1, 2022, to January 2, 2024. The median follow-up was 21.6 (IQR, 13.6-31.8) years.

EXPOSURE: Time-dependent cumulative mean SBP.

MAIN OUTCOMES AND MEASURES: The primary outcome was time from baseline visit to first incident stroke. Secondary outcomes consisted of time to first incident IS, ICH, and SAH.

RESULTS: Among 40 016 participants, 38 167 who were 18 years or older at baseline with no history of stroke and at least 1 SBP measurement before the first incident stroke were included in the analysis. Of these, 54.0\% were women; 25.0\% were Black, 8.9\% were Hispanic of any race, and 66.2\% were White. The mean (SD) age at baseline was 53.4 (17.0) years and the mean (SD) SBP at baseline was 136.9 (20.4) mm Hg. A 10-mm Hg higher cumulative mean SBP was associated with a higher risk of overall stroke (hazard ratio [HR], 1.20 [95\% CI, 1.18-1.23]), IS (HR, 1.20 [95\% CI, 1.17-1.22]), and ICH (HR, 1.31 [95\% CI, 1.25-1.38]) but not SAH (HR, 1.13 [95\% CI, 0.99-1.29]; P = .06). Compared with White participants, Black participants had a higher risk of IS (HR, 1.20 [95\% CI, 1.09-1.33]) and ICH (HR, 1.67 [95\% CI, 1.30-2.13]) and Hispanic participants of any race had a higher risk of SAH (HR, 3.81 [95\% CI, 1.29-11.22]). There was no consistent evidence that race and ethnicity modified the association of cumulative mean SBP with first incident stroke and stroke type.

CONCLUSIONS AND RELEVANCE: The findings of this cohort study suggest that cumulative mean SBP was associated with incident stroke type, but the associations did not differ by race and ethnicity. Culturally informed stroke prevention programs should address modifiable risk factors such as SBP along with social determinants of health and structural inequities in society.

}, keywords = {Adult, Aged, Black or African American, Blood Pressure, Cerebral Hemorrhage, Ethnicity, Female, Hispanic or Latino, Humans, Hypertension, Incidence, Ischemic Stroke, Longitudinal Studies, Male, Middle Aged, Racial Groups, Risk Factors, Stroke, Subarachnoid Hemorrhage, United States, White, White People}, issn = {2574-3805}, doi = {10.1001/jamanetworkopen.2024.8502}, author = {Johnson, Kimson E and Li, Hanyu and Zhang, Min and Springer, Mellanie V and Galecki, Andrzej T and Whitney, Rachael T and Gottesman, Rebecca F and Hayward, Rodney A and Sidney, Stephen and Elkind, Mitchell S V and Longstreth, W T and Heckbert, Susan R and Gerber, Yariv and Sullivan, Kevin J and Levine, Deborah A} }