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      Cigarette Smoke Exposure Promotes Arterial Thrombosis and Vessel Remodeling after Vascular Injury in Apolipoprotein E-Deficient Mice

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          Background: Cigarette smoking is a major risk factor for the development of cardiovascular disease. However, in terms of the vessel wall, the underlying pathomechanisms of cigarette smoking are incompletely understood, partly due to a lack of adequate in vivo models. Methods: Apolipoprotein E-deficient mice were exposed to filtered air (sham) or to cigarette mainstream smoke at a total particulate matter (TPM) concentration of 600 µg/l for 1, 2, 3, or 4 h, for 5 days/week. After exposure for 10 ± 1 weeks, arterial thrombosis and neointima formation at the carotid artery were induced using 10% ferric chloride. Results: Mice exposed to mainstream smoke exhibited shortened time to thrombotic occlusion (p < 0.01) and lower vascular patency rates (p < 0.001). Morphometric and immunohistochemical analysis of neointimal lesions demonstrated that mainstream smoke exposure increased the amount of α-actin-positive smooth muscle cells (p < 0.05) and dose-dependently increased the intima-to-media ratio (p < 0.05). Additional analysis of smooth muscle cellsin vitro suggested that 10 µg TPM/ml increased cell proliferation without affecting viability or apoptosis, whereas higher concentrations (100 and 500 µg TPM/ml) appeared to be cytotoxic. Conclusions: Taken together, these findings suggest that cigarette smoking promotes arterial thrombosis and modulates the size and composition of neointimal lesions after arterial injury in apolipoprotein E-deficient mice.

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          Most cited references 29

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            Role of smoking in global and regional cardiovascular mortality.

             S. Henley,  M Thun,  D. López (2005)
            Smoking is a major cause of cardiovascular disease mortality. There is little information on how it contributes to global and regional cause-specific mortality from cardiovascular diseases for which background risk varies because of other risks. We used data from the American Cancer Society's Cancer Prevention Study II (CPS II) and the World Health Organization Global Burden of Disease mortality database to estimate smoking-attributable deaths from ischemic heart disease, cerebrovascular disease, and a cluster of other cardiovascular diseases for 14 epidemiological subregions of the world by age and sex. We used lung cancer mortality as an indirect marker for accumulated smoking hazard. CPS-II hazards were adjusted for important covariates. In the year 2000, an estimated 1.62 (95% CI, 1.27 to 2.04) million cardiovascular deaths in the world, 11% of total global cardiovascular deaths, were due to smoking. Of these, 1.17 million deaths were among men and 450,000 among women. There were 670,000 (95% CI, 440,000 to 920,000) smoking-attributable cardiovascular deaths in the developing world and 960,000 (95% CI, 770,000 to 1,200,000) in industrialized regions. Ischemic heart disease accounted for 54% of smoking-attributable cardiovascular mortality, followed by cerebrovascular disease (25%). There was variability across regions in the role of smoking as a cause of various cardiovascular diseases. More than 1 in every 10 cardiovascular deaths in the world in the year 2000 were attributable to smoking, demonstrating that it is an important preventable cause of cardiovascular mortality.
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              Cigarette smoking as a risk factor for stroke. The Framingham Study.

              The impact of cigarette smoking on stroke incidence was assessed in the Framingham Heart Study cohort of 4255 men and women who were aged 36 to 68 years and free of stroke and transient ischemic attacks. During 26 years of follow-up, 459 strokes occurred. Regardless of smoking status and in each sex, hypertensive subjects had twice the incidence of stroke. Using the Cox proportional hazard regression method, smoking was significantly related to stroke after age and hypertension were taken into account. Even after pertinent cardiovascular disease risk factors were added to the Cox model, cigarette smoking continued to make a significant independent contribution to the risk of stroke generally and brain infarction specifically. The risk of stroke increased as the number of cigarettes smoked increased. The relative risk of stroke in heavy smokers (greater than 40 cigarettes per day) was twice that of light smokers (fewer than ten cigarettes per day). Lapsed smokers developed stroke at the same level as nonsmokers soon after stopping. Stroke risk decreased significantly by two years and was at the level of nonsmokers by five years after cessation of cigarette smoking.

                Author and article information

                J Vasc Res
                Journal of Vascular Research
                S. Karger AG
                October 2008
                23 April 2008
                : 45
                : 6
                : 480-492
                aDepartment of Cardiology and Pulmonary Medicine, Georg August University of Göttingen, Göttingen, and bPhilip Morris Research Laboratories GmbH, Cologne, Germany; cPhilip Morris Research Laboratories bvba, Leuven, Belgium; dPhilip Morris International, Neuchâtel, Switzerland; ePhilip Morris USA, Richmond, Va., USA
                127439 J Vasc Res 2008;45:480–492
                © 2008 S. Karger AG, Basel

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                Page count
                Figures: 6, Tables: 3, References: 47, Pages: 13
                Research Paper


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