This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Juvela, S. Articles by Moomaw, C. Search for Related Content PubMed PubMed Citation Articles by Juvela, S. Articles by Moomaw, C.

(Stroke. 2002;33:2152.)
© 2002 American Heart Association, Inc.

Letters to the Editor

Risk Factors for Aneurysmal Subarachnoid Hemorrhage

Seppo Juvela, MD, PhD

Department of Neurosurgery, Helsinki University Central Hospital, Helsinki, Finland

An extract of the first 250 words of the full text is provided, because this article has no abstract.

To the Editor:

I read with interest a recent article concerning risk factors for subarachnoid hemorrhage (SAH).¹ The results of this study confirm the results of previous studies that showed for the first time that cigarette smoking is an independent risk factor for SAH irrespective of alcohol consumption, hypertension, or use of nonsteroidal anti-inflammatory drugs or narcotics.^2,3 Cigarette smoking seems even today to be the most important risk factor with a similar attributable risk for SAH despite a well-known decreased prevalence in smoking in Western countries during the past 10 to 15 years. In addition, cigarette smoking increases the risk for SAH in a dose-response manner. Particularly, those smoking more than 20 cigarettes per day have an increased risk.^2,3 The mechanism behind this increased risk is likely that cigarette smoking increases risk for rupture of an existing aneurysm by increasing its growth rate and, to a lesser degree, by causing aneurysm formation.⁴

Alcohol consumption seems to have a relatively short-term risk for SAH given that recent alcohol intake during the few days before SAH is a more important risk factor than long-term heavy consumption, likely because of alcohol-induced transient changes in blood pressure or other mechanisms, and because alcohol consumption seems not to cause aneurysm formation or to increase the growth rate of an existing aneurysm.^3–5

Recently, family history of intracranial aneurysms has been offered as evidence for genetic causality of cerebral aneurysms.^6,7 In the present study, cigarette smoking was for the first time analyzed as a confounding factor for this association. This . . . [Full Text of this Article]

Brett Kissela, MD; Daniel Woo, MD; Laura Sauerbeck, RN Joseph Broderick, MD

Department of Neurology

Rakesh Shukla, PhD

Department of Environmental Health

Charles Moomaw, PhD

Institute for Health Policy and Health Services Research, University of Cincinnati College of Medicine, Cincinnati, Ohio