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Smoking and Cardiovascular Disease

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Smoking is a major cause of cardiovascular disease (CVD) and causes approximately one of every four deaths from CVD, according to the 2014 Surgeon General’s Report on smoking and health. CVD is the single largest cause of death in the United States, killing more than 800,000 people a year. More than 16 million Americans have heart disease. Almost 8 million have had a heart attack and 7 million have had a stroke. Even people who smoke fewer than five cigarettes a day may show signs of early CVD. The risk of CVD increases with the number of cigarettes smoked per day, and when smoking continues for many years.

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Smoking and Cardiovascular Disease (CVD) Smoking is a deadly habit to keep, literally. Smoking along with other contributing factors such as high blood pressure and cholesterol can cause chronic diseases. One disease that has been the number one killer of men and women in the U.S. is cardiovascular disease. Cardiovascular disease has many contributors, but smoking itself is a high risk to contract the disease. Non-smokers also have to pay attention to the air they are breathing because the smoke around you can kill you! What is heart disease? Many of us at a young age believe that heart disease can only happen to “older” people.If oxygen doesn't arrive the tissue or organ will die (healingnutrition.com). And how does this affect people who smoke? Smokers have twice the risk of heart attack as nonsmokers. Smoking attributes to One-fifth of the annual 1,000,000 deaths from CVD. Surveillance data indicate that an estimated 1,000,000 young people become "regular" smokers each year. Smoking and CVD Smoking adds to the artery-clogged process. It is know that smoking is a contributing factor to CVD, but why? What does smoking actually do to help in CVD? First of all, smoking overworks the heart and reduces its oxygen supply. It also makes clots more likely to form in blood vessels and increases the risk of potentially fatal changes in the heartbeat (Better Health Channel, 2004). Other damages that smoking contributes to CVD is: Causes immediate and long term increases in blood pressure and heart rate, as well as changes the properties of blood vessels and blood cells—allowing cholesterol and other fatty substances to build up (Holy Name Health Manual). Second-Hand Smoke So you say you your safe because you don’t smoke. Not always true. Many of us know of someone who smokes and may be living with that person or even just eating at a restaurant with them. Second-hand smoke is basically the air that non-smokers breathe in while in the same areas of smokers.

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Law and Wald (2003), who conducted a meta-analysis of five large studies of smoking and CHD, demonstrated a nonlinear dose-response relationship between the number of cigarettes smoked per day and the RR of disease (Figure 6.3). The researchers suggested that the effect of cigarette smoking on risk of CHD may have a low threshold and that the dose-response characteristics of the risk relationship are less steep at higher doses. This hypothesis was used to explain the seeming anomaly of a high RR of CHD associated with relatively low exposure to secondhand smoke. By using serum levels of cotinine (a metabolite of nicotine) as biomarkers of exposure, Whincup and colleagues (2004) explored the dose response relationship between exposure to cigarette smoke and CHD in persons involuntarily exposed to cigarette smoke. More than 2,000 men who said they did not smoke had blood levels of cotinine measured in 1978–1980 and then had follow-up for 20 years. Nicotine exposure was examined by quartiles of blood cotinine as follows: less than or equal to 0.7 nanograms per milliliter (ng/mL), 0 to 1.4, 1.5 to 2.7, and 2.8 to 14.0. Hazard ratios for CHD, which included deaths and non- fatal MIs, were significantly increased at all upper quartiles (hazard ratios, 1.43 to 1.57) compared with the lowest exposure quartile, after adjustment for established CHD risk factors. Hazard ratios were also higher at the first and second five-year follow-ups (3.73 to 10.58 and 1.95 to 2.48, respectively) than those at later follow-ups. The substantial cardiovascular risk attributable to involuntary exposure to cigarette smoke (USDHHS 2006) and the practice in most CVD studies of not excluding from the control group persons who had secondhand smoke exposure have resulted in underestimation, in many research reports, of the effects of active smoking compared with no exposure to cigarette smoke.

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Ultimately, the main methods considered in this promotion plan are as follows, detect the problem, prevent it, consider and treat the risks. The main directions of the plan are to develop several policies in the relation to the problem, create some training opportunities, enhance some data for monitoring the problem, etc. Thus, it may be concluded that to make people understand that smoking influences thy health and crates additional risks for heart attacks a number of actions should be provided, like the assessment of the problem, health promotion, policy development and provide assurance that the society has an access to the relevant information and help.

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Whincup PH, Gilg JA, Emberson JR, Jarvis MJ, Feyerabend C, Bryant A, Walker M, Cook DG. Passive smoking and risk of coronary heart disease and stroke: prospective study with cotinine measurement. BMJ (British Medical Journal). 2004;329(7459):200–5.

Law MR, Wald NJ. Environmental tobacco smoke and ischemic heart disease. Progress in Cardiovascular Diseases. 2003;46(1):31–8.

Rosengren A, Wilhelmsen L, Wedel H. Coronary heart disease, cancer and mortality in male middle-aged light smokers. Journal of Internal Medicine. 1992;231(4):357–62.

Prescott E, Scharling H, Osler M, Schnohr P. Importance of light smoking and inhalation habits on risk of myocardial infarction and all cause mortality: a 22 year follow up of 12,149 men and women in the Copenhagen City Heart Study. Journal of Epidemiology and Community Health. 2002;56(9):702–6.

Bjartveit K, Tverdal A. Health consequences of smoking 1–4 cigarettes per day. Tobacco Control. 2005;14(5):315–20.

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