Background: Although research has demonstrated that depressive symptoms predict stroke incidence, depressive symptoms are dynamic. It is unclear whether stroke risk persists if depressive symptoms remit. Methods and Results: Health and Retirement Study participants (n=16 178, stroke free and noninstitutionalized at baseline) were interviewed biennially from 1998 to 2010. Stroke and depressive symptoms were assessed through self-report of doctors’ diagnoses and a modified Center for Epidemiologic Studies - Depression scale (high was ≥3 symptoms), respectively. We examined whether depressive symptom patterns, characterized across 2 successive interviews (stable low/no, onset, remitted, or stable high depressive symptoms) predicted incident stroke (1192 events) during the subsequent 2 years. We used marginal structural Cox proportional hazards models adjusted for demographics, health behaviors, chronic conditions, and attrition. We also estimated effects stratified by age (≥65 years), race or ethnicity (non-Hispanic white, non-Hispanic black, Hispanic), and sex. Stroke hazard was elevated among participants with stable high (adjusted hazard ratio 2.14, 95% CI 1.69 to 2.71) or remitted (adjusted hazard ratio 1.66, 95% CI 1.22 to 2.26) depressive symptoms compared with participants with stable low/no depressive symptoms. Stable high depressive symptom predicted stroke among all subgroups. Remitted depressive symptoms predicted increased stroke hazard among women (adjusted hazard ratio 1.86, 95% CI 1.30 to 2.66) and non-Hispanic white participants (adjusted hazard ratio 1.66, 95% CI 1.18 to 2.33) and was marginally associated among Hispanics (adjusted hazard ratio 2.36, 95% CI 0.98 to 5.67). Conclusions: In this cohort, persistently high depressive symptoms were associated with increased stroke risk. Risk remained elevated even if depressive symptoms remitted over a 2-year period, suggesting cumulative etiologic mechanisms linking depression and stroke.
|Original language||English (US)|
|Journal||Journal of the American Heart Association|
|State||Published - May 2015|
Bibliographical noteFunding Information:
The HRS (Health and Retirement Study) is supported by the National Institute on Aging (NIA U01AG009740) and is conducted by the University of Michigan. The authors gratefully acknowledge financial support from the Eunice Kennedy Shriver National Institute for Child Health and Human Development at NIH (R24HD041023 to Capistrant); the National Institute of Neurological Disorders and Stroke at NIH (T32 NS048005 to Marden); the National Heart, Lung, and Blood Institute at NIH (1F31HL112613 to Gilsanz); the National Institute of Mental Health at NIH (1RC4 MH092707 to Walter, Kubzansky, and Glymour); the Initiative for Maximizing Student Development (5R25GM055353 to Gilsanz); the National Institute on Aging (R21 AG03438502 to Glymour); the American Heart Association (grant 10SDG2640243 to Glymour and Gilsanz and 09PRE2080078 to Capistrant) and National Institute of Allergy and Infectious Diseases at NIH (grants AI113251 and AI104459 to Tchetgen Tchetgen) and National Institute of Environmental Health Science (grant AI113251 to Tchetgen Tchetgen). The content is solely the responsibility of the authors and does not represent the official views of the funders. The study funders had no role in the design, execution or interpretation of these analyses.
© 2015 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley Blackwell.
- longitudinal cohort study
- marginal structural model