الفهرس 
INTRODUCTION & RATIONALEOnly 14 pages are availabe for public view
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Abstract
The cardiovascular risk attributable to cigarette smoking increases sharply at low levels of cigarette consumption and with exposure to secondhand smoke. The risk then tends to plateau at higher levels of smoking. This finding indicates a low threshold for effect and a nonlinear dose-response relationship. Some of the nonlinearity of the relationship between the number of cigarettes smoked per day and CVD risk may be due to impreciseness of this measure of actual exposure to smoke. However, the data on risk associated with exposure to secondhand smoke indicate a true nonlinear relationship between exposure and CVD risk. Cardiovascular risk is not reduced by smoking cigarettes of lower machine-delivered yields of nicotine or tar.
The constituents of tobacco smoke believed to be responsible for cardiovascular disease include oxidizing chemicals, nicotine, CO, and particulate matter. Oxidizing chemicals, including oxides of nitrogen and many free radicals, increase lipid peroxidation and contribute to several potential mechanisms of CVD, including inflammation, endothelial dysfunction, oxidation of LDL, and platelet activation.
Nicotine is a sympathomimetic drug that increases heart rate and cardiac contractility, transiently increasing blood pressure and constricting coronary arteries. Nicotine may also contribute to endothelial dysfunction, insulin resistance, and lipid abnormalities. However, international epidemiologic evidence and data from clinical trials of nicotine patches suggest that chemicals other than nicotine contribute to an elevated risk of death from MI and stroke.
Smoking causes acute cardiovascular events such as MI and sudden deathby adversely affecting the balance of myocardial demand