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Stroke. 2003;34:1771-1776
Published online before print May 29, 2003, doi: 10.1161/01.STR.0000077015.90334.A7
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(Stroke. 2003;34:1771.)
© 2003 American Heart Association, Inc.


Original Contributions

Triggers of Subarachnoid Hemorrhage

Role of Physical Exertion, Smoking, and Alcohol in the Australasian Cooperative Research on Subarachnoid Hemorrhage Study (ACROSS)

Craig Anderson, PhD, FAFPHM, FRACP; Cliona Ni Mhurchu, BSc(Hons), PhD; David Scott, BA(Hons), PhD; Derrick Bennett, MSc, PhD; Konrad Jamrozik, DPhil, FAFPHM Graeme Hankey, MD, FRCP, FRACP for the Australasian Cooperative Research on Subarachnoid Hemorrhage Study Group

From the Clinical Trials Research Unit (C.A., C.N.M., D.B.) and Department of Statistics (D.S.), University of Auckland, Auckland, New Zealand; Department of Primary Health Care and General Practice, Imperial College of Science, Technology and Medicine, London, and Department of Public Health, University of Western Australia, Crawley, Australia (K.J.); and Stroke Unit, Royal Perth Hospital, Perth, Australia (G.H.).

Correspondence to Professor Craig Anderson, Clinical Trials Research Unit, University of Auckland, Private Bag 92019, Auckland, New Zealand. E-mail c.anderson{at}ctru.auckland.ad.nz

Background and Purpose— Unaccustomed strenuous physical exertion can trigger myocardial infarction, but little is known about the mechanisms precipitating subarachnoid hemorrhage (SAH).

Methods— We identified all cases of first-ever SAH among the combined populations (2.8 million) of 4 urban centers in Australia and New Zealand. Information on the type, time, and intensity of exposures in the 26 hours before the onset of SAH was ascertained by structured interviews. We used the case-crossover technique to assess the risk of SAH associated with transient exposures of moderate to extreme physical exertion, heavy cigarette smoking, and binge alcohol consumption.

Results— We registered 432 first-ever cases of SAH (62% women; mean age, 56.5 years). A definite time of onset of SAH was established for 393 patients (91%), and information on the levels of physical activity in the preceding 26 hours was obtained in 338 (78%). Of these patients, 19% engaged in moderate to extreme exertion (>=5 metabolic equivalents) in the 2 hours before SAH, which was associated with a tripling in the risk of SAH (odds ratio [OR], 2.7; 95% CI, 1.6 to 4.6). There was no evidence of any association between heavy cigarette smoking or binge drinking and risk of SAH in the subsequent 2 hours (OR, 1.1; 95% CI, 0.4 to 3.7; and OR, 0.41; 95% CI, -{infty} to 5.3). Habitual exercise did not appear to alter the risk of SAH associated with moderate to extreme exertion.

Conclusions— Moderate to extreme physical exertion tripled the risk of SAH, but there was no association between transient heavy smoking or binge drinking and risk of SAH. These data suggest that heavy physical activity may trigger SAH.


Key Words: crossover studies • epidemiology • physical activity • risk factors • subarachnoid hemorrhage




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