Literature DB >> 19211494

Reproductive history, oral contraceptive use, and the risk of ischemic and hemorrhagic stoke in a cohort study of middle-aged Swedish women.

Ling Yang1, Hannah Kuper, Sven Sandin, Karen L Margolis, Zhengming Chen, Hans-Olov Adami, Elisabete Weiderpass.   

Abstract

BACKGROUND AND
PURPOSE: Controversy persists as to whether oral contraceptive (OC) use and reproductive history play a role in the etiology of stroke, particularly ischemic stroke. Our aim was to investigate this question in a cohort of middle-aged Swedish women.
METHODS: The Women's Lifestyle and Health Cohort Study included 49259 Swedish women, aged 30 to 49 years at baseline (1991 to 1992). Participants completed an extensive questionnaire and were traced through linkages to national registries until the end of 2004.
RESULTS: Among the 45699 women included in these analyses, there were 285 cases of incident stroke during follow-up (193 ischemic stroke, 72 hemorrhagic stroke, and 20 of unknown origin). Neither ischemic nor hemorrhagic stroke risk was related to OC use, duration, or type of OC use, even among women who were smokers or hypertensive. Though not statistically significant, risk of hemorrhagic stroke was elevated in women who started using OCs after the age of 30 (Hazard Ratio [HR] 2.3, 95% CI=0.8 to 6.8) and women recommended by a doctor to stop using OC for medical reasons (2.1, 0.9 to 5.0) compared with never users. Compared with nulliparous women, parous women had a statistically significant lower risk of hemorrhagic stroke (0.5, 0.2 to 0.8), but similar association was not found for ischemic stroke (0.9, 0.5 to 1.4).
CONCLUSIONS: There was no significant association of OC use with ischemic or hemorrhagic stroke, and the parity was associated with reduced risk of hemorrhagic stroke but not with ischemic stroke.

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Year:  2009        PMID: 19211494     DOI: 10.1161/STROKEAHA.108.531913

Source DB:  PubMed          Journal:  Stroke        ISSN: 0039-2499            Impact factor:   7.914


  20 in total

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10.  PPARγ activation rescues mitochondrial function from inhibition of complex I and loss of PINK1.

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