Dose-response relationship between cigarette smoking and risk of ischemic stroke in young women

Department of Neurology, Room 12-006, University of Maryland, Baltimore, 655 W. Baltimore St, Baltimore, MD 21201, USA.
Stroke (Impact Factor: 6.02). 09/2008; 39(9):2439-43. DOI: 10.1161/STROKEAHA.107.510073
Source: PubMed

ABSTRACT Although cigarette smoking is known to be a risk factor for ischemic stroke, there are few data on the dose-response relationship between smoking and stroke risk in a young ethnically diverse population.
We used data from the Stroke Prevention in Young Women Study, a population-based case-control study of risk factors for ischemic stroke in women aged 15 to 49 years to examine the relationship between cigarette smoking and ischemic stroke. Historical data, including smoking history, was obtained through standardized interviews. Odds ratios (OR) were estimated using logistic regression. Cases (n=466) were women with stroke in the greater Baltimore-Washington area, and controls (n=604) were women free of a stroke history identified by random digit dialing.
After multivariable adjustment, the OR comparing current smokers to never smokers was 2.6 (P<0.0001); no difference in stroke risk was observed between former smokers and never smokers. Adjusted OR increased with increasing number of cigarettes smoked per day (OR=2.2 for 1 to 10 cigs/d; 2.5 for 11 to 20 cigs/d; 4.3 for 21 to 39 cigs/d; 9.1 for 40 or more cigs/d).
These results suggest a strong dose-response relationship between cigarette smoking and ischemic stroke risk in young women and reinforce the need for aggressive smoking cessation efforts in young adults.

Download full-text


Available from: John Sorkin, Jun 22, 2015
  • [Show abstract] [Hide abstract]
    ABSTRACT: Cerebrovascular accidents (strokes) are a challenge to modern health care throughout the world because they contribute greatly to morbidity, disability, and mortality rates. Ischemic stroke constitutes the majority of cases of cerebrovascular accidents. It is a complex multifactorial polygenic disease, i.e., it develops under the influence of conventional risk factors and the genetic component. The latter is formed by the joint contribution of many independent or interacting polymorphic genes. Current studies of the genetic susceptibility to ischemic stroke use two approaches based on the analysis of the association between polymorphic sites of the genome and the disease, including the candidate-gene approach and genome-wide association studies, followed by a meta-analysis of the results. This review considers the published data on genetic susceptibility to ischemic stroke, which may be a starting point for the investigation of molecular mechanisms that determine the pathophysiology of ischemic stroke. Although some progress has been made in this field, the problem of identifying genetic risk factors that could be used as markers for predicting individual susceptibility to ischemic stroke is still far from a complete solution. The main obstacle to this is the low replication of the results. It can be overcome by investigating ethnically uniform populations and clinically distinct IS forms.
    Molecular Biology 03/2015; 49(2):195-216. DOI:10.1134/S0026893315020120 · 0.74 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Cystic kidneys and vascular aneurysms are clinical manifestations seen in patients with polycystic kidney disease (PKD), a cilia-associated pathology (ciliopathy). Survivin overexpression is associated with cancer, but the clinical pathology associated with survivin down-regulation or knockout has never been studied before. The present studies aim to examine if and how cilia function (Pkd1 or Pkd2) and structure (Tg737) play a role in cystic kidney and aneurysm through survivin down-regulation. Cysts and aneurysms from PKD patients, Pkd mouse and zebrafish models are characterized by chromosome instability and low survivin expression. This triggers cytokinesis defects and formation of nuclear polyploidy or aneuploidy. In vivo conditional mouse and zebrafish models confirm that survivin gene deletion in the kidneys results in a cystic phenotype. As in hypertensive Pkd1, Pkd2 and Tg737 deletion, aneurysm formation can also be induced in vascular-specific normotensive survivin mice. Survivinknockout also contributes to abnormal oriented cell division in both kidney and vasculature. Furthermore, survivin expression and ciliary localization are regulated by flow-induced cilia activation through PKC, Akt and NF-κB. Circumventing ciliary function by re-expressing survivin can rescue PKD phenotypes. For the first time, our studies offer a unifying mechanism that explains both renal and vascular phenotypes in PKD. Although primary cilia dysfunction accounts for aneurysm formation and hypertension, hypertension itself does not cause aneurysm. Furthermore, aneurysm and cyst formation share a common cellular and molecular pathway involving cilia function or structure, survivin expression, cytokinesis, cell ploidy, symmetrical cell division and tissue architecture orientation.
    Circulation 11/2013; 129(6). DOI:10.1161/CIRCULATIONAHA.113.005746 · 14.95 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: BACKGROUND: The hazardous effects of smoking and the favorable influence of physical activity on the progression of atherosclerosis have been well studied, but little is known about the interactions of these 2 factors. METHODS: A total of 1090 subjects who were screened for brain disease (at annual medical checkups) between April 2007 and March 2008 were studied to clarify the effects of smoking on maximum carotid intima-media thickness (IMT) in patients with different grades of physical activity. Univariate and multivariate analyses were performed to investigate relationships between maximum IMT and independent variables, such as smoking status, age, gender, coexisting disease, physical activity, alcohol drinking, family history, subjective symptoms, body mass index, systolic blood pressure, diastolic blood pressure, blood sugar, total cholesterol, high-density lipoprotein cholesterol, and triglycerides. RESULTS: Univariate analysis revealed only the low physical activity group to have a significant relationship between smoking and maximum IMT. When the subjects were divided into 3 age groups (≤49, 50-59, and ≤60 years of age, respectively), the same association was noted for high and moderate physical activity groups ≤49 years of age. Multivariate analysis further revealed smoking status to be a significant predictor of maximum IMT in the young low and moderate activity groups. CONCLUSIONS: In physically inactive young people, smoking might have detrimental effects on maximum IMT, while high physical activity may be protective.
    Journal of stroke and cerebrovascular diseases: the official journal of National Stroke Association 11/2011; 22(2). DOI:10.1016/j.jstrokecerebrovasdis.2011.07.009 · 1.99 Impact Factor