ImportanceThe magnitude of cognitive change after incident myocardial infarction (MI) is unclear.ObjectiveTo assess whether incident MI is associated with changes in cognitive function after adjusting for pre-MI cognitive trajectories.Design, Setting, and ParticipantsThis cohort study included adults without MI, dementia, or stroke and with complete covariates from the following US population-based cohort studies conducted from 1971 to 2019: Atherosclerosis Risk in Communities Study, Coronary Artery Risk Development in Young Adults Study, Cardiovascular Health Study, Framingham Offspring Study, Multi-Ethnic Study of Atherosclerosis, and Northern Manhattan Study. Data were analyzed from July 2021 to January 2022.ExposuresIncident MI.Main Outcomes and MeasuresThe main outcome was change in global cognition. Secondary outcomes were changes in memory and executive function. Outcomes were standardized as mean (SD) T scores of 50 (10); a 1-point difference represented a 0.1-SD difference in cognition. Linear mixed-effects models estimated changes in cognition at the time of MI (change in the intercept) and the rate of cognitive change over the years after MI (change in the slope), controlling for pre-MI cognitive trajectories and participant factors, with interaction terms for race and sex.ResultsThe study included 30 465 adults (mean [SD] age, 64 [10] years; 56% female), of whom 1033 had 1 or more MI event, and 29 432 did not have an MI event. Median follow-up was 6.4 years (IQR, 4.9-19.7 years). Overall, incident MI was not associated with an acute decrease in global cognition (−0.18 points; 95% CI, −0.52 to 0.17 points), executive function (−0.17 points; 95% CI, −0.53 to 0.18 points), or memory (0.62 points; 95% CI, −0.07 to 1.31 points). However, individuals with incident MI vs those without MI demonstrated faster declines in global cognition (−0.15 points per year; 95% CI, −0.21 to −0.10 points per year), memory (−0.13 points per year; 95% CI, −0.22 to −0.04 points per year), and executive function (−0.14 points per year; 95% CI, −0.20 to −0.08 points per year) over the years after MI compared with pre-MI slopes. The interaction analysis suggested that race and sex modified the degree of change in the decline in global cognition after MI (race × post-MI slope interaction term, P = .02; sex × post-MI slope interaction term, P = .04), with a smaller change in the decline over the years after MI in Black individuals than in White individuals (difference in slope change, 0.22 points per year; 95% CI, 0.04-0.40 points per year) and in females than in males (difference in slope change, 0.12 points per year; 95% CI, 0.01-0.23 points per year).ConclusionsThis cohort study using pooled data from 6 cohort studies found that incident MI was not associated with a decrease in global cognition, memory, or executive function at the time of the event compared with no MI but was associated with faster declines in global cognition, memory, and executive function over time. These findings suggest that prevention of MI may be important for long-term brain health.
Individuals with cerebral palsy (CP) have poor skeletal and cardiovascular health. However, no studies have examined if skeletal fragility enhances cardiovascular disease (CVD) risk for this population. The purpose of this study was to determine whether adults with CP have higher 12‐month CVD incidence following a low‐trauma fracture compared with adults without CP. Data, from the Optum Clinformatics® Data Mart, were extracted from adults (18+ years) that sustained a low‐trauma fracture between 01/01/2012 and 12/31/2016. The primary outcome measure was incident CVD within 12 months following a low‐trauma fracture. Cox proportional hazards regression models were used to compare 12‐month incident CVD with adjustment for sociodemographics and chronic disease comorbidities. Mean age (SD) at baseline was 54.7 (18.9) for adults with CP (n = 1,025, 43.3% men) and 60.4 (19.7) for adults without CP (n = 460,504, 33.7% men). During the follow‐up, 121 adults with CP (11.8%, mean age [SD] = 63.9 [16.3]) and 45,330 adults without CP (9.8%, mean age [SD] = 74.5 [11.9]) developed CVD. In the fully adjusted model, adults with CP had higher 12‐month post‐fracture CVD incidence (hazard ratio [HR] = 1.63; 95% confidence interval [CI] = 1.37–1.95). When the outcome was stratified by CVD subtype, adults with CP had higher 12‐month post‐fracture incidence of ischemic heart disease (HR = 1.45; 95% CI = 1.09–1.92), heart failure (HR = 1.68; 95% CI = 1.22–2.31), and cerebrovascular disease (HR = 1.96; 95% CI = 1.54–2.50). Study findings suggest that among adults with CP, low‐trauma fracture may enhance 12‐month CVD incidence compared with adults without CP. © 2019 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 38:803‐810, 2020
ImportanceIncident stroke is associated with accelerated cognitive decline. Whether poststroke vascular risk factor levels are associated with faster cognitive decline is uncertain.ObjectiveTo evaluate associations of poststroke systolic blood pressure (SBP), glucose, and low-density lipoprotein (LDL) cholesterol levels with cognitive decline.Design, Setting, and ParticipantsIndividual participant data meta-analysis of 4 US cohort studies (conducted 1971-2019). Linear mixed-effects models estimated changes in cognition after incident stroke. Median (IQR) follow-up was 4.7 (2.6-7.9) years. Analysis began August 2021 and was completed March 2023.ExposuresTime-dependent cumulative mean poststroke SBP, glucose, and LDL cholesterol levels.Main Outcomes and MeasuresThe primary outcome was change in global cognition. Secondary outcomes were change in executive function and memory. Outcomes were standardized as t scores (mean [SD], 50 [10]); a 1-point difference represents a 0.1-SD difference in cognition.ResultsA total of 1120 eligible dementia-free individuals with incident stroke were identified; 982 (87.7%) had available covariate data and 138 (12.3%) were excluded for missing covariate data. Of the 982, 480 (48.9%) were female individuals, and 289 (29.4%) were Black individuals. The median age at incident stroke was 74.6 (IQR, 69.1-79.8; range, 44.1-96.4) years. Cumulative mean poststroke SBP and LDL cholesterol levels were not associated with any cognitive outcome. However, after accounting for cumulative mean poststroke SBP and LDL cholesterol levels, higher cumulative mean poststroke glucose level was associated with faster decline in global cognition (−0.04 points/y faster per each 10–mg/dL increase [95% CI, −0.08 to −0.001 points/y]; P = .046) but not executive function or memory. After restricting to 798 participants with apolipoprotein E4 (APOE4) data and controlling for APOE4 and APOE4 × time, higher cumulative mean poststroke glucose level was associated with a faster decline in global cognition in models without and with adjustment for cumulative mean poststroke SBP and LDL cholesterol levels (−0.05 points/y faster per 10–mg/dL increase [95% CI, −0.09 to −0.01 points/y]; P = .01; −0.07 points/y faster per 10–mg/dL increase [95% CI, −0.11 to −0.03 points/y]; P = .002) but not executive function or memory declines.Conclusions and RelevanceIn this cohort study, higher poststroke glucose levels were associated with faster global cognitive decline. We found no evidence that poststroke LDL cholesterol and SBP levels were associated with cognitive decline.
Background: Older adults with mild cognitive impairment (MCI) receive fewer guideline-concordant treatments for multiple health conditions than those with normal cognition. Reasons for this disparity are unclear. Objective: To better understand this disparity, we describe physician understanding and experience with patient MCI, particularly physician identification of MCI, ability to distinguish between MCI and dementia, and perspectives on education and training in MCI and dementia. Methods: As part of a mixed-methods study assessing the influence of patient MCI on physician recommendations for acute myocardial infraction and stroke treatments, we conducted a descriptive qualitative study using semi-structured interviews of physicians from three specialties. Key question topics included participants’ identification of MCI, impressions of MCI and dementia awareness within their practice specialty, and perspectives on training and education in MCI. Results: The study included 22 physicians (8 cardiologists, 7 neurologists, and 7 internists). We identified two primary themes: There is 1) a lack of adequate understanding of the distinction between MCI and dementia; and 2) variation in physician approaches to identifying whether an older adult has MCI. Conclusion: These findings suggest that physicians have a poor understanding of MCI. Our results suggest that interventions that improve physician knowledge of MCI are needed.
Introduction: Apart from stroke, cognitive change after incident myocardial infarction (MI) is unclear. We aim to determine associations between incident MI and acute and long-term changes in cognitive function, controlling for risk factors and pre-MI cognitive trajectories, censoring for stroke. Methods: We performed a pooled analysis of 31,377 participants, ≥18 years, free of MI and dementia, from 6 longitudinal cohort studies (1971-2017): Atherosclerosis Risk in Communities Study, Coronary Artery Risk Development in Young Adults Study, Cardiovascular Health Study, Framingham Offspring Study, Multi-Ethnic Study of Atherosclerosis, and Northern Manhattan Study. Outcomes were changes in global cognition (primary), memory, and executive function. Linear mixed-effects models were used to estimate the association between incident MI and acute cognitive decline at the time of MI (Model A), and decline in cognition over the years after MI (Model B). Results: Median study follow up was 6.4 years (IQR 4.9-19.7 years) and 1,047 participants had incident MI. Incident MI was associated with significant acute decline in global cognition and executive function, but not memory, after the MI event (Models A, Table 1). After including change in cognitive function (slope) after incident MI in the model, the effect estimates indicating acute declines in global cognition and executive function were not significant (Models B, Table 1). However, participants with incident MI demonstrated significantly faster declines in global cognition (-0.15 points/year faster [95% CI, -0.21 to -0.10]), memory (-0.13 points/year faster [95% CI, -0.23 to -0.04]), and executive function (-0.14 points/year faster [95% CI, -0.20 to -0.08]) compared to those without MI (Models B, Table 1). Conclusions: Incident MI is associated with faster declines in global cognition, memory, and executive function over years following the MI event.
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