Dementia after stroke

The Framingham study

Cristina Ivan, Sudha Seshadri, Alexa Beiser, Rhoda Au, Carlos S. Kase, Margaret Kelly-Hayes, Philip A. Wolf

Research output: Contribution to journalArticle

220 Citations (Scopus)

Abstract

Background and Purpose - Identification of risk factors for dementia after stroke is best performed in comparison with stroke-free controls, because older subjects at high risk for stroke also have a substantial risk of dementia in the absence of stroke. Previous case-control studies were hospital-based. We used a nested case-control design to prospectively evaluate these risk factors in the community-based Framingham Study cohort. Methods - We compared 212 subjects who were free of dementia in January 1982 and sustained a first stroke after this date, with 1060 age- and sex-matched, stroke- and dementia-free controls. We calculated 10-year risks of dementia (by Diagnostic and Statistical Manual of Mental Disorders, Volume IV criteria) developing in cases and controls and also estimated the hazard ratios within subgroups defined by exposure to various demographic factors (age, gender, education), stroke-related features (right or left hemisphere, stroke type, second stroke), stroke risk factors (hypertension, diabetes, atrial fibrillation, smoking) and apolipoprotein E genotype. Results - Dementia developed in 19.3% of cases and 11.0% of controls. Baseline stroke doubled the risk of dementia (hazard ratio [HR]: 2.0; 95% confidence interval [CI]: 1.5 to 3.1) and adjustment for age, sex, education, and exposure to individual stroke risk factors did not diminish the risk (HR: 2.4; 95% CI: 1.6 to 3.7). The HR was higher in younger subjects (age younger than 80 years [HR: 2.6; 95% CI: 1.5 to 4.5]), apolipoprotein E 3/3 homozygotes (HR: 3.4; 95% CI: 2.0 to 5.8), and high school graduates (HR: 2.4; 95% CI: 1.5 to 3.9). Conclusion-Stroke increases a subject's risk of dementia as compared with age- and sex-matched controls. Primary and secondary prevention of stroke should significantly decrease the risk of all dementia.

Original languageEnglish (US)
Pages (from-to)1264-1268
Number of pages5
JournalStroke
Volume35
Issue number6
DOIs
StatePublished - Jun 2004
Externally publishedYes

Fingerprint

Dementia
Stroke
Confidence Intervals
Apolipoprotein E3
Sex Education
Homozygote
Apolipoproteins E
Primary Prevention
Secondary Prevention
Diagnostic and Statistical Manual of Mental Disorders
Atrial Fibrillation
Case-Control Studies
Cohort Studies
Smoking
Odds Ratio
Genotype
Demography
Hypertension
Education

Keywords

  • Dementia
  • Epidemiology
  • Risk factors
  • Stroke
  • Vascular diseases

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Neuroscience(all)

Cite this

Ivan, C., Seshadri, S., Beiser, A., Au, R., Kase, C. S., Kelly-Hayes, M., & Wolf, P. A. (2004). Dementia after stroke: The Framingham study. Stroke, 35(6), 1264-1268. https://doi.org/10.1161/01.STR.0000127810.92616.78

Dementia after stroke : The Framingham study. / Ivan, Cristina; Seshadri, Sudha; Beiser, Alexa; Au, Rhoda; Kase, Carlos S.; Kelly-Hayes, Margaret; Wolf, Philip A.

In: Stroke, Vol. 35, No. 6, 06.2004, p. 1264-1268.

Research output: Contribution to journalArticle

Ivan, C, Seshadri, S, Beiser, A, Au, R, Kase, CS, Kelly-Hayes, M & Wolf, PA 2004, 'Dementia after stroke: The Framingham study', Stroke, vol. 35, no. 6, pp. 1264-1268. https://doi.org/10.1161/01.STR.0000127810.92616.78
Ivan C, Seshadri S, Beiser A, Au R, Kase CS, Kelly-Hayes M et al. Dementia after stroke: The Framingham study. Stroke. 2004 Jun;35(6):1264-1268. https://doi.org/10.1161/01.STR.0000127810.92616.78
Ivan, Cristina ; Seshadri, Sudha ; Beiser, Alexa ; Au, Rhoda ; Kase, Carlos S. ; Kelly-Hayes, Margaret ; Wolf, Philip A. / Dementia after stroke : The Framingham study. In: Stroke. 2004 ; Vol. 35, No. 6. pp. 1264-1268.
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N2 - Background and Purpose - Identification of risk factors for dementia after stroke is best performed in comparison with stroke-free controls, because older subjects at high risk for stroke also have a substantial risk of dementia in the absence of stroke. Previous case-control studies were hospital-based. We used a nested case-control design to prospectively evaluate these risk factors in the community-based Framingham Study cohort. Methods - We compared 212 subjects who were free of dementia in January 1982 and sustained a first stroke after this date, with 1060 age- and sex-matched, stroke- and dementia-free controls. We calculated 10-year risks of dementia (by Diagnostic and Statistical Manual of Mental Disorders, Volume IV criteria) developing in cases and controls and also estimated the hazard ratios within subgroups defined by exposure to various demographic factors (age, gender, education), stroke-related features (right or left hemisphere, stroke type, second stroke), stroke risk factors (hypertension, diabetes, atrial fibrillation, smoking) and apolipoprotein E genotype. Results - Dementia developed in 19.3% of cases and 11.0% of controls. Baseline stroke doubled the risk of dementia (hazard ratio [HR]: 2.0; 95% confidence interval [CI]: 1.5 to 3.1) and adjustment for age, sex, education, and exposure to individual stroke risk factors did not diminish the risk (HR: 2.4; 95% CI: 1.6 to 3.7). The HR was higher in younger subjects (age younger than 80 years [HR: 2.6; 95% CI: 1.5 to 4.5]), apolipoprotein E 3/3 homozygotes (HR: 3.4; 95% CI: 2.0 to 5.8), and high school graduates (HR: 2.4; 95% CI: 1.5 to 3.9). Conclusion-Stroke increases a subject's risk of dementia as compared with age- and sex-matched controls. Primary and secondary prevention of stroke should significantly decrease the risk of all dementia.

AB - Background and Purpose - Identification of risk factors for dementia after stroke is best performed in comparison with stroke-free controls, because older subjects at high risk for stroke also have a substantial risk of dementia in the absence of stroke. Previous case-control studies were hospital-based. We used a nested case-control design to prospectively evaluate these risk factors in the community-based Framingham Study cohort. Methods - We compared 212 subjects who were free of dementia in January 1982 and sustained a first stroke after this date, with 1060 age- and sex-matched, stroke- and dementia-free controls. We calculated 10-year risks of dementia (by Diagnostic and Statistical Manual of Mental Disorders, Volume IV criteria) developing in cases and controls and also estimated the hazard ratios within subgroups defined by exposure to various demographic factors (age, gender, education), stroke-related features (right or left hemisphere, stroke type, second stroke), stroke risk factors (hypertension, diabetes, atrial fibrillation, smoking) and apolipoprotein E genotype. Results - Dementia developed in 19.3% of cases and 11.0% of controls. Baseline stroke doubled the risk of dementia (hazard ratio [HR]: 2.0; 95% confidence interval [CI]: 1.5 to 3.1) and adjustment for age, sex, education, and exposure to individual stroke risk factors did not diminish the risk (HR: 2.4; 95% CI: 1.6 to 3.7). The HR was higher in younger subjects (age younger than 80 years [HR: 2.6; 95% CI: 1.5 to 4.5]), apolipoprotein E 3/3 homozygotes (HR: 3.4; 95% CI: 2.0 to 5.8), and high school graduates (HR: 2.4; 95% CI: 1.5 to 3.9). Conclusion-Stroke increases a subject's risk of dementia as compared with age- and sex-matched controls. Primary and secondary prevention of stroke should significantly decrease the risk of all dementia.

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