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Author Norman M Kaplan, MD Section Editors George L Bakris, MD Mark S Gold, MD James K Stoller, MS, MD Deputy Editor John P Forman, MD, MSc
Last literature review version 19.1: January 2011 | This topic last updated: April 25, 2008 (More)
SMOKING AND HYPERTENSION — Tobacco use is the most common cause of avoidable cardiovascular mortality worldwide . There are now 1.3 billion cigarette smokers, 82 percent in developing countries, and if current practices continue, there will be an estimated one billion tobacco-related deaths during the 21st century. The immediate noxious effects of smoking are related to sympathetic nervous overactivity, which increases myocardial oxygen consumption through a rise in blood pressure, heart rate, and myocardial contractility .
Chronically, cigarette smoking induces arterial stiffness which may persist for a decade after smoking cessation . The incidence of hypertension is increased among those who smoke 15 or more cigarettes per day , and the coexistence of hypertension and smoking decreases left ventricular function in asymptomatic people .
With each cigarette, the blood pressure rises transiently and the pressor effect may be missed if the blood pressure is measured 30 minutes after the last smoke. The transient rise in blood pressure may be most prominent with the first cigarette of the day even in habitual smokers. In one study of normotensive smokers, there was an average elevation in systolic pressure of 20 mmHg after the first cigarette (figure 1) . Furthermore, ambulatory blood pressure monitoring suggests an interactive effect between smoking and coffee drinking in patients with mild essential hypertension, resulting in a mean elevation in daytime systolic pressure of approximately 6.0 mmHg .
First cigarette raises blood pressure
Change in systolic blood pressure over 15 minutes after smoking the first cigarette of the day (blue squares) or during sham smoking (red circles) in 10 normotensive smokers. Smoking was associated with a 15 to 20 mmHg rise in systolic pressure that began to dissipate at 15 minutes. Data from Gropelli, A, Giorgi, DM, Omboni, S, et al, J Hypertens 1992; 10:495.
However, habitual smokers generally have lower blood pressures than nonsmokers as observed in most [8,9], but not all , studies. The mild reduction in BP in smokers is related to decreased body weight . Support for this observation is the higher body weight and increased blood pressure among former smokers versus that observed among never-smokers . A vasodilator effect of cotinine, the major metabolite of nicotine, also may contribute to the lower blood pressure .
Despite these observations, smoking should be avoided in any hypertensive patient because it can markedly increase the risk of secondary cardiovascular complications and enhance the progression of
renal insufficiency [14,15]. An example of the latter effect was observed in one prospective study (with a mean follow-up of 35 months) that examined the factors associated with alterations in renal function among 53 hypertensive patients in whom the serum creatinine concentration rose from 1.5 to 1.9 mg/dL (133 to 168 µmol/L) despite a significant reduction in the target mean blood pressure (127 to 97 mmHg) . Smoking was the most significant independent factor underlying progressive renal disease (serum creatinine 1.5 and 2.1 mg/dL [133 and 186 µmol/L] at the beginning and end of the study for smokers, respectively, versus 1.25 and 1.32 mg/dL [110 and 117 µmol/L] for nonsmokers, respectively). The mechanism underlying this adverse effect is unclear but may be related to the transient increase in systemic blood pressure with smoking being transmitted to the glomerulus, resulting in glomerular hypertension.
Cessation of smoking can rapidly lower the risk of coronary heart disease by 35 to 40 percent; this benefit is independent of the duration of smoking. It is unclear whether cessation of smoking has a similar benefit in helping preserve renal function. (See "Cardiovascular risk of smoking and benefits of smoking cessation".)
INFORMATION FOR PATIENTS — Educational materials on this topic are available for patients. (See "Patient information: Quitting smoking".) We encourage you to print or e-mail this topic review, or to refer patients to our public web site, www.uptodate.com/patients, which includes this and other topics.
Use of UpToDate is subject to the Subscription and License Agreement REFERENCES 1. Teo KK, Ounpuu S, Hawken S, et al. Tobacco use and risk of myocardial infarction in 52 countries in the INTERHEART study: a case-control study. Lancet 2006; 368:647. 2. Najem B, Houssière A, Pathak A, et al. Acute cardiovascular and sympathetic effects of nicotine replacement therapy. Hypertension 2006; 47:1162. 3. Jatoi NA, Jerrard-Dunne P, Feely J, Mahmud A. Impact of smoking and smoking cessation on arterial stiffness and aortic wave reflection in hypertension. Hypertension 2007; 49:981. 4. Bowman TS, Gaziano JM, Buring JE, Sesso HD. A prospective study of cigarette smoking and risk of incident hypertension in women. J Am Coll Cardiol 2007; 50:2085. 5. Rosen BD, Saad MF, Shea S, et al. Hypertension and smoking are associated with reduced regional left ventricular function in asymptomatic: individuals the Multi-Ethnic Study of Atherosclerosis. J Am Coll Cardiol 2006; 47:1150.
320:898. Smoking and the kidney.6. Persistent blood pressure increase induced by heavy smoking. J Hypertens 1992. J Hypertens 1995. Blood pressure in smokers and nonsmokers: epidemiologic findings. if present. 15. Yang S. 111:932. Regalado M. 14. 80:1309. 13:1663. Poulter NR. Independent effects of smoking on risk of hypertension: small. Marks BL. et al. Sharp DS. Hypertension Ambulatory Recording VEnetia STudy. Am J Kidney Dis 2000. J Hypertens 2002. Smoking related to 24-h ambulatory blood pressure and heart rate: a study in 352 normotensive Danish subjects. Cigarette smoking is associated with augmented progression of renal insufficiency in severe essential hypertension. HARVEST Study Group (Italy). Groppelli A. Green MS. 13:965. Jucha E. Falaschetti E. Benowitz NL. Epstein LH. Høegholm A. et al. Circulation 1989. Am J Hypertens 1997. 10. et al. 12. Luz Y. Omboni S. MD . 10:495. Narkiewicz K. N Engl J Med 1989. 37:187. Wesson DE. Inverse relation between serum cotinine concentration and blood pressure in cigarette smokers. Gupta S. Primatesta P. 20:171. 7. Hypertension 2001. Wiinberg N. Giorgi DM. Association between smoking and blood pressure: evidence from the health survey for England. 35:687. Perkins KA. Cardiovascular risk of smoking and benefits of smoking cessation Authors Melvyn Rubenfire. Biasion T. Interactive effect of cigarettes and coffee on daytime systolic blood pressure in patients with mild essential hypertension. Am Heart J 1986. Maraglino G. MD. Orth SR. 13. et al. 10:483. The effect of nicotine on energy expenditure during light physical activity. MPH Section Editors Christopher P Cannon. Mikkelsen KL. J Am Soc Nephrol 2002. et al. 11. 8. 9. MD Elizabeth Jackson.
2010 (More) INTRODUCTION — The facts regarding the risk of cigarette smoking and cardiovascular disease are well known to both the medical profession and the public [1-3]. The importance of smoking cessation in diabetic patients is discussed separately. MD Deputy Editor Brian C Downey. where estimates are as high as 50 percent or greater for male smokers.Mark S Gold. even those who smoked more than 40 cigarettes per day.6]. the majority of whom reside in developing countries. (See "Smoking and cardiovascular risk in diabetes mellitus". an estimated 22 percent of men and 17. for example. Smoking rates are higher among men and women with lower educational and income levels. with the most common age being 14 to 15 years. MD. the following observations have been made regarding a major role for smoking: . over 60 percent of 737 current smokers. the effects of smoking on the atherosclerosis process. Trends towards increasing tobacco consumption among the young have also been observed in other countries besides the US [4.3 billion people smoke. (See "Overview of the risk factors for cardiovascular disease".5 percent of women in the United States smoke . and the beneficial effects of smoking cessation will be reviewed here . did not believe that they were at an increased risk for a myocardial infarction (MI) .) SMOKING AND CARDIOVASCULAR DISEASE — With respect to coronary heart disease (CHD).) The relationship between smoking and coronary heart disease. Adolescents from Mexican subgroups have the highest rates of smoking followed by non-Hispanic blacks and non-Hispanic whites . In one study. FACC Last literature review version 19. The majority of smokers start smoking before the age of 18. Currently. Many smokers do not believe that smoking is harmful for them.1: January 2011 | This topic last updated: September 8. Globally. an estimated 1.
cardiac death (relative risk 1. including sudden cardiac death [14. (See "Secondhand smoke exposure: Effects in adults".Smoking status before coronary artery bypass graft (CABG) surgery does not affect survival after surgery. . Secondhand smoke — The impact of secondhand smoke on the cardiovascular system is discussed separately. smoking accounted for 36 percent of the populationattributable risk of a first MI .41) compared to those who stopped smoking for at least one year .08) compared to nonsmokers. and subjects who smoke four or more cigars per day are exposed to an amount of smoke equivalent to 10 cigarettes.Patients who continue to smoke in the presence of established CHD have an increased risk of reinfarction and an increased risk of death.49. In one study. lungs. Those who persisted in smoking cessation had no increased risk of death compared to nonsmokers.75).Smoking is an independent major risk factor for CHD. respectively) when compared to those who quit smoking *17+. the adjusted hazard ratio for 35 year all-cause and cardiovascular mortality was 1.2 and 1.15].774 men followed for 14 years found that.63.39) .)After percutaneous coronary intervention. smoking significantly increased all-cause mortality (relative risk 1.62 and 1. cigars are generally perceived as being safer than cigarettes. persistent smokers have a greater relative risk of death (1. and gastrointestinal tract and the risk of chronic obstructive lung disease.41 compared to exsmokers or never smokers) and the incidence of death.76) and Q wave myocardial infarction (2.44 and 1. for current smokers compared to nonsmokers . even those who do not inhale are exposed to their own environmental smoke.13]. and a higher relative risk of total and cardiac mortality (relative risk 1. or myocardial infarction (relative risk 1. there was a dose-response relationship and the relative risk for those who smoke less than or greater than 5 cigars per day were 1. respectively.56.Cigarette smoking increases all-cause and cardiovascular mortality [12.10]. section on 'Cardiovascular disease'.The incidence of a MI is increased sixfold in women and threefold in men who smoke at least 20 cigarettes per day compared to subjects who never smoked [9.68).Among patients with left ventricular dysfunction (left ventricular ejection fraction ≤35 percent) in the SOLVD trial. In the worldwide INTERHEART study of patients from 52 countries. and total atherosclerotic cardiovascular disease . cerebrovascular disease. (See "Long-term outcome after coronary artery bypass graft surgery". respectively . One cohort study of 17. and need for repeat revascularization (relative risk 1. Cigar smoke contains the same toxic and carcinogenic compounds that are found in cigarette smoke. data about the role of cigar smoking and the risk of cardiovascular disease are limited. those who smoked cigars were at a greater risk for developing coronary heart disease (relative risk 1. Cigar smoking may result in endothelial dysfunction .) Cigar smoking — Although there is an established association between cigar smoking and cancer of the upper respiratory. compared to nonsmokers.27). Moreover. recurrent heart failure requiring hospitalization. but persistent smokers after CABG have a greater relative risk of all-cause mortality (relative risk 1.
3). Current smoking was associated with a 50 percent increase in the progression of atherosclerosis versus nonsmokers during the study period. In contrast. with a first-time MI and 687 matched controls found no difference in the incidence of MI between nonsmoking regular snuff users compared to those who never used any tobacco products (adjusted odds ratio 0. particularly among adolescents and young adults.914 patients in whom intima-medial thickness of the carotid artery was measured by ultrasound over a three-year period. a much larger study of over 135.An American Cancer Society study of 121. aged 24 to 64. This study consisted of 10. Smokeless tobacco — The use of snuff and other types of smokeless tobacco is increasing. the cardiovascular health hazards of smokeless tobacco are not well established .278 men ≥30 years of age found that current cigar smokers ≤75 years of age had an increased risk of death from coronary heart disease (adjusted rate ratio 1. the relative risk was 2.4 for smokeless tobacco users . found that the age-adjusted relative risk of cardiovascular mortality was 1. One population based study of 687 men.1.96) . including over 6000 smokeless tobacco users. SMOKING AND ATHEROSCLEROSIS — The direct effect of smoking on the development of atherosclerosis was assessed in the ARIC (Atherosclerosis Risk in Communities) study .000 male construction industry employees from Sweden. For men aged 35 through 54 at the start of followup. however. Passive cigarette smoke exposure increases the progression of atherosclerosis . there was no increased risk in those >75 years of age or former cigar smokers of any age . and patients with environmental tobacco smoke exposure had a 20 percent greater rate of atherosclerosis progression compared to patients without environmental tobacco smoke exposure (figure 1).
GL. N: nonsmoker. et al. C: current smoker. -E: without exposure to enviornmental smoke. P: past smoker. for the ARIC Investigators.In the ARIC study of 10. Smoking has also been correlated with increases in atherosclerotic disease of the thoracic aorta  and the carotid arteries . JAMA 1998. suggesting that some of the adverse effects of cigarette smoking may be cumulative and irreversible. Burke. Another study of patients with preexisting coronary disease found that smoking accelerates the progression of lesion size and new lesion formation as assessed by serial coronary angiography . Data from Howard. +E: with exposure to environmental smoke.914 subjects followed for three years. 279:119. . Although more pack-years of exposure was independently associated with faster progression. the progression rates of current and previous smokers did not differ. G. current smoking and passive smoke exposure in nonsmokers or past smokers were associated with a statistically significant increase in the progression of intimal-medial thickness of the carotid artery as assessed by ultrasound. Wagenknecht. LE.
and cutaneous and perhaps coronary vasoconstriction [36-38].51-53]. in whom levels are less than 1 percent. platelet aggregation. (See "Screening for cardiovascular risk with C-reactive protein" and "C-reactive protein in cardiovascular disease". the mechanism by which it occurs is incompletely understood. even when passive. section on 'Lipoproteins and atherosclerosis'. resulting in stiffening of and trauma to the wall . elevated whole blood viscosity due to secondary polycythemia. or serum C-reactive .55]. in patients with advanced lung disease.) This effect can be detected clinically by measuring carboxyhemoglobin levels which average 5 to 10 percent higher in smokers than nonsmokers. carbon monoxide administration. These findings suggest that smoking contributes to the inflammatory response that is a factor in the pathogenesis of atherosclerosis. does not affect blood pressure. concentrations of soluble adhesion molecules are higher in smokers than nonsmokers [53. possibly leading to impaired prostacyclin production and enhanced platelet-vessel wall interactions . increased platelet activity (possibly due to enhanced sympathetic activity) . specifically oxidized low-density lipoprotein cholesterol [32-34]. In addition. A similar effect is seen with acute secondhand smoke exposure . Multiple factors may be involved since smoking has a variety of effects that may contribute to atherogenesis .Smoking has been correlated with elevated levels of C-reactive protein and fibrinogen [54. In addition. The effect on endothelial function results from oxidative stress with enhanced oxidation of LDL and from reduced generation of nitric oxide [46. resulting in the formation of proatherogenic oxidized particles.) Role of carbon monoxide — Carbon monoxide is inhaled in cigarette smoke. impairs endothelium-dependent vasodilation of normal coronary arteries and reduces coronary flow reserve [45-50]. under conditions similar to cigarette smoking. producing an increase in heart rate and blood pressure.49. elevation in the blood fibrinogen concentration . This can reduce the elastic properties of the aorta. and. increased expression of tissue factor . free radicals in cigarette smoke damage lipids. which is thought to induce vascular injury by multiple mechanisms .Pathogenesis — Although the relationship between CHD and smoking. metabolism. Smoking can also potentiate the endothelial dysfunction induced by hypercholesterolemia [33. even when passive.47]. (See "Overview of homocysteine".)Smoking has been correlated with elevations in serum homocysteine. In healthy subjects. and role in atherosclerosis". reducing the amount of hemoglobin available to carry oxygen and impeding oxygen release by hemoglobin that is not directly bound to carbon monoxide. (See "Smoke inhalation". Smoking is associated with an adverse effect on serum lipids (elevated low-density lipoproteins and triglycerides and reduced high-density lipoproteins)  and with insulin resistance [30. appears clear.55]. (See "Lipoprotein classification. It binds more avidly than oxygen to hemoglobin.)Cigarette smoking activates the sympathetic nervous system. plasma catecholamines.31].Smoking.Smoking can damage the vascular wall.Smoking enhances the prothrombotic state via inhibition of tissue plasminogen activator release from the endothelium .
In humans. an effect that was mitigated by the addition of antioxidants . A study in human coronary artery endothelial cells found significantly lower nitric-oxide production with exposure to smokers' serum than nonsmokers' serum. antioxidant therapy improves endothelial dysfunction in smokers . and beta-carotene does not appear to improve long-term outcomes with the possible exception of specific patient subsets. carbon monoxide exposure in patients with CHD results in severe adverse effects. Role of oxidative stress — Free radical-mediated oxidative stress may play a pivotal role in the development of atherosclerosis.protein . Nicotine has been reported to have variable effects on nitric oxide [59.) SMOKING AND OUTCOME AFTER REPERFUSION THERAPIES — The relative outcomes of smokers compared to nonsmokers after reperfusion therapies have been evaluated across the spectrum of coronary artery disease. In comparison. Since these parameters are changed with smoking. ventricular dysfunction. and increased number and complexity of ventricular arrhythmias [57.) It is not clear if nicotine plays a direct role in the development of atherosclerosis. Myocardial infarction . (See "Nutritional antioxidants in coronary heart disease".) Free radicals are present in both the gas and "tar" phases of cigarette smoke  and may also be generated from endogenous sources in response to smoking . Role of nicotine — Nicotine in cigarette smoke plays a major role in the transient smoking-related increases in cardiac output. chronic administration of antioxidants such as vitamin C. However.58]. heart rate. (See "Cardiovascular effects of nicotine".60]. vitamin E. but does not appear to increase lipid deposition in the vascular wall . These include exercise-induced ischemia at a lower level of work. the observations suggest that some factor other than carbon monoxide is responsible. section on 'Pathophysiology'. and blood pressure. Nicotine may contribute to acute endothelial dysfunction in smokers . (See "Nutritional antioxidants in coronary heart disease".
7) and 30 day mortality (10. which involved 2366 nonsmokers." (see "Fibrinolytic (thrombolytic) agents in acute ST elevation myocardial infarction: Therapeutic use"). and severe coronary disease than nonsmokers [67-74]. previous infarction.75].117 exsmokers. This could explain the angiographic finding that the mechanism of infarction in smokers is more often thrombosis of a less critical atherosclerotic lesion than in nonsmokers . 2244 exsmokers. GUSTO I was largest trial to evaluate the impact of cigarette smoking on outcome as it included 11. 11.69]. smokers are more likely to have an inferior rather than anterior wall infarction [70. the International Tissue Plasminogen Activator/Streptokinase Mortality trial.After fibrinolytic therapy — Despite the important role of cigarette smoking in the development of atherosclerosis. and 3649 active smokers. several studies have reported that smokers who receive a fibrinolytic agent for an acute MI have a better outcome than nonsmokers [67-74].72] but not all  studies reported that smoking history was of not an independent prognostic factor (figure 2). This phenomenon is called the "smoker's paradox.9 versus 3.71. and 17.507 current smokers .975 nonsmokers. for unclear reasons. resulting in smokers having a higher patency rate and being more likely to have TIMI-3 flow in the infarct artery after fibrinolysis [70. some [69.71. had a higher incidence of in-hospital complications including shock.3 versus 4. found that nonsmokers. .Smokers have an otherwise better risk profile than nonsmokers. compared to the other two groups.70.71]. they tend to be significantly younger (mean 11 years in GUSTO I) and have a lower incidence of diabetes. Also. As an example. suggesting a hypercoagulable state [70. Nonsmokers also had a higher in-hospital and six-month mortality than exsmokers or active smokers. Nonsmokers had a significantly higher rate of in-hospital complications and a higher in-hospital (9. and bleeding . stroke.74]. Similar findings were noted in TIMI II and GUSTO I [68. More active thrombogenic mechanisms may lead to a larger thrombus component that is more susceptible to fibrinolytic therapy. hypertension. After adjustment for these clinical factors. The reason for the surprisingly better outcomes after fibrinolysis in smokers may be related to the following factors: Smokers have a higher hematocrit and baseline level of fibrinogen.0 percent).
5 percent.0 and 1. et al. Boyko. for the Israeli Thrombolytic Survey Group. J Am Coll Cardiol 1996. D. the difference was no longer evident after adjusting for baseline and clinical variables (bottom panel). The apparent difference may be explained by smokers being younger and having a more favorable risk profile than nonsmokers.) Unstable angina — The smoker's paradox appears not to apply to patients presenting with unstable angina. . section on 'Abciximab'. 28:1506. intensive care unit mortality was lower for smokers than for exsmokers or nonsmokers (0. V. In a multicenter registry that included almost 8000 patients with unstable angina. Zahger. After primary percutaneous coronary intervention — In a post hoc analysis of patients with ST-elevation MI in the CADILLAC trial. Data from Gottlieb. However.Smokers have a higher rate of survival after myocardial infarction because of a more favorable risk profile A review of 999 patients with an acute myocardial infarction found that smokers appeared to have a higher survival rate after a myocardial infarction compared to nonsmokers (top panel). S. there was no significant difference in survival at one year after correction for baseline differences such as age and other cardiovascular risk factors .7 versus 1. (See "Clinical trials of platelet glycoprotein IIb/IIIa receptor inhibitors in coronary heart disease: Intravenous agents".
82-86]. At the time of the infarction. However.62 at 0 to <6 months. The cardiac risks associated with cigarette smoking diminish relatively soon after smoking cessation and continue to fall with increasing length of time since quitting . smokers who undergo percutaneous coronary intervention may also have better short-term outcomes than nonsmokers. Acute coronary syndromes — Smoking cessation improves outcomes in patients who have had an acute coronary syndrome [15. the reduction in cardiac event rate associated with smoking cessation ranges from 7 to 47 percent .17) and significantly increased for active smokers (RR 1.58-0. angioplasty. CABG.48 for 18 to <36 months.60 from 6 to <18 months. Stable coronary artery disease — Among patients with stable coronary artery disease. when corrected for age and other cardiovascular risk factors. of whom 5659 ceased smoking and 6944 continued to smoke . index cardiac event. The range of benefits can be illustrated by the following findings: The mortality benefit of smoking cessation was assessed in a meta-analysis of 20 prospective cohort studies with at least two years follow-up including 12. with an adjusted relative risk of 0. The relative risk of mortality for smokers who quit compared with those who continued to smoke was 0. population-based cohort study of 2619 patients who survived to hospital discharge after a first myocardial infarction .71).88) after adjustment for baseline clinical and angiographic differences . In an observational study evaluating 5682 patients treated with PCI in 9 clinical trials.02 for ≥36 months). or known CHD. Using the nonsmokers as the reference group. and current smokers (56 percent of whom quit smoking). target lesion revascularization was significantly lower in smokers.respectively) .603 smokers.64 (95% CI 0. 90 .69 (95% CI 0. This was illustrated in a randomized trial in which 209 hospitalized patients. The efficacy and cardiovascular benefits of smoking cessation vary importantly with the method used to attain smoking cessation. and 1. CARDIOVASCULAR BENEFITS OF SMOKING CESSATION — The benefits of quitting cigarette smoking are also firmly established but perhaps less well known and accepted. smoking history was not an independent predictor.The effect of smoking cessation on recurrent coronary events was evaluated in a retrospective. roughly equal percentages were nonsmokers. The benefit was not affected by age.51). Among subjects without known CHD. sex. Among those who permanently quit smoking. or the year in which the study began. 1. former smokers. the risk ratio progressively and significantly decreased with longer duration of cessation (RR 1. All patients had had an MI.54-0. the multivariable risk ratio (RR) for recurrent coronary events was nonsignificantly increased in former smokers (RR 1. 1. country.
the mortality after sixyear follow-up was significantly higher among patients who continued to smoke compared to those who stopped (relative risk 1. relative risk reduction 0. The early benefit may result from improved coagulation parameters or reversal of endothelial dysfunction. 95% CI 0.16-0. The benefits were equivalent in those aged 55 to 64 and over age 65 and were the same as observed among comparable patients aged 34 to 54. while the late benefit may reflect slowing or even reversal of the atherosclerosis process. After 24 months.63). These improved outcomes were associated with a significantly higher rate of continuous abstinence from smoking (33 versus 9 percent).8 versus 12. Effect of age — The relative benefits of smoking cessation are equivalent in young and old patients [82. for example. patients in the intensive smoking cessation group had significantly lower rates of allcause mortality (2.27-0. 95% CI 0. In one series of middle-aged women. Stroke — The risk of ischemic stroke also decreases over time after smoking cessation. In one study of 1893 patients with CHD who were older than 55 years.0 percent. The continued decline in risk over time after smoking cessation suggests that more than one mechanism may be involved.7) .77. by race and gender (United States. Approximately 70 percent of cigarette smokers state that they would like to quit smoking. were randomly assigned to 12 weeks of behavior modification counseling and individualized pharmacotherapy (nicotine replacement therapy and/or bupropion) at no cost or to usual care (in-hospital counseling and printed educational material) . in both sexes smoking rates are higher in less educated and poorer segments of the population. Prevalence of cigarette smoking in adults. 1965 . Despite these facts. relative risk reduction 0.percent of whom had an acute coronary syndrome.93) and hospitalization (23 versus 41 percent.44.84]. the excess risk among former smokers largely disappeared two to four years after cessation .2000) . approximately 25 percent of the adult United States population continues to smoke and there has been little change in the prevalence of smoking since 1990 (figure 3) . Nearly equal numbers of men and women smoke.
antidepressant therapy. smoking impairs endothelium-dependent vasodilation of normal coronary arteries and reduces coronary flow reserve [45. The impact of smoking cessation on endothelial function was studied prospectively in over 1500 smokers. NCHS. Despite gaining an average of 5 kg.48]. while endothelial function did not improve from baseline in those who continued to smoke. or a return to smoking.4 kg for men and 5.Many smokers. especially women. an independent . While the depression associated with cessation is usually mild. Smokers who quit were significantly more likely to gain weight than life-long nonsmokers. Possible deleterious effects — There are no convincing reasons not to quit smoking although several issues have been raised: Nicotine withdrawal and depression can occur as a result of quitting.Data are age adjusted to the 2000 standard population. cite weight gain as a reason not to quit smoking.0 kg for women. it may be sufficiently severe to require counseling. however. after one year. 36 percent had successfully quit smoking . smokers who quit had significantly improved endothelial function compared to baseline. Despite this weight gain. CDC Improvement in endothelial function — As mentioned above. This issue was studied in the third National Health and Nutrition Survey conducted from 1988 through 1991 . National Health Interview Survey NHIS. The long-term weight gain for smokers who quit compared to smokers who continued to smoke was 4. This improvement in endothelial function likely contributes to the reduction in mortality and other benefits associated with smoking cessation. Survey redesigned in 1997 and data for 1998 and subsequent years may not be directly comparable to earlier years.
Behavioral therapy. can markedly improve his or her health. Methods of smoking cessation — Physicians often fail to intervene against smoking .and significant improvement in endothelial function has been prospectively observed which may offset any deleterious effects of modest weight gain . long lives should be the goal of modern society. by quitting smoking. and nicotine is now being evaluated as a therapeutic agent in this condition. nicotine replacement therapy.)Cessation has been associated with exacerbations of ulcerative colitis . (See "Management of smoking cessation in adults". From a public health standpoint it can be argued that any other effective measure for prevention of cigarette use may also increase health care costs in the long run. An analysis of the health care costs of smoking cessation revealed short-term savings. and the use of certain medications may each improve the quit rate.) Smoking cessation for the primary care clinician . but the promotion of healthy. but increased health care costs in the long run since former smokers lived longer and used greater amounts of terminal health care . (See 'Improvement in endothelial function' above. This observation has no relevance to the individual who. The lack of economic incentives for physicians to promote smoking cessation and pessimism among physicians regarding the effects of these interventions may explain these findings . There are a number of ways that physicians can and should actively intervene against smoking in virtually all smokers (table 1).
Clinical Practice Guideline Number 18.S. or to refer patients to our public web site. which includes this and other topics. compared to those who do not. (See 'Smoking and cardiovascular disease' above. MC. 96-0692. Bailey WC. Public Health Service. U. Smoking Cessation. MD: Agency for Health Care Policy and Research. Cohen. Similarly. Given the high number of smokers who first start smoking during adolescence. (See "Patient information: Quitting smoking". INFORMATION FOR PATIENTS — Educational materials on this topic are available for patients. 1996.com/patients. the risk of a recurrent event is increased among those who continue to smoke. et al.) We encourage you to print or e-mail this topic review. SUMMARY — Smoking is a leading preventable risk factor for cardiovascular disease. www. assessment and education regarding smoking is recommended for all adolescents in addition to adults.uptodate. among those patients with established cardiovascular disease. Rockville. Department of Health and Human Services. AHCPR Publication No. JJ.Modified from Fiore.) .
Heart disease and stroke statistics--2009 update: a report from the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Ambrose JA. Lung. Jacob B.) Use of UpToDate is subject to the Subscription and License Agreement REFERENCES 1. Jha P. patients are more likely to attempt to quit if advised to do so by healthcare providers. et al. Ayanian JZ. 281:1019. 5. (See 'Smoking and outcome after reperfusion therapies' above and 'Cardiovascular benefits of smoking cessation' above. 358:1137. and Blood Institute. 2. Lloyd-Jones. et al. Carnethon. (See "Management of smoking cessation in adults". Perceived risks of heart disease and cancer among cigarette smokers. JAMA 1999. AHA.) Many providers fail to counsel patients regarding smoking cession. . 119:e182. 6. Gajalakshmi V. J Am Coll Cardiol 2006. (See 'Cigar smoking' above and 'Smokeless tobacco' above. However. 4. Thom T. 7.Available evidence suggests that cigar smoking increases the risk of the development of cardiovascular disease. the cardiovascular health hazards of smokeless tobacco are not well established. A nationally representative case-control study of smoking and death in India. M. Barua RS. D. American Heart Association Task Force on Risk Reduction. et al. and stroke: a statement for healthcare professionals from the American Heart Association. 43:1731. Cigarette smoking. R. 47:2130. However. Circulation 1997. Cleary PD. J Am Coll Cardiol 2004. Adams. Heart disease and stroke statistics--2006 update: a report from the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. 3. Rosamond W. Miller NH. N Engl J Med 2008. Haase N. Ockene IS. The pathophysiology of cigarette smoking and cardiovascular disease: an update. et al. 96:3243. Lung. 113:e85. cardiovascular disease. National Heart.) The benefits of smoking cessation have been demonstrated in a broad range of patients with cardiovascular disease. and Blood Institute. Circulation 2006. AHA/ACC guidelines for secondary prevention for patients with coronary and other atherosclerotic vascular disease: 2006 update endorsed by the National Heart. ACC. Circulation 2009.
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45. et al. Am Heart J 1987. Biochemical evidence of a chronic abnormality in platelet and vascular function in healthy individuals who smoke cigarettes. Endothelial dysfunction. et al. Circulation 2001. Circulation 1993. Nowak J. et al. Deficiency in nitric oxide bioactivity in epicardial coronary arteries of cigarette smokers. et al. 49. Eales-Reynolds LJ. Dysfunctional endothelial nitric oxide biosynthesis in healthy smokers with impaired endothelium-dependent vasodilatation. 76:6. Circulation 2000. Goto S. Ambrose JA. Oates JA. FitzGerald GA. D'Agostino RB. 48. Matetzky S. Celermajer DS. Belanger AJ. 98:528. Hausberg M. Tani S. 95:31. Piper ME. Circulation 1986. et al. 93:271. Effects of smoking and smoking cessation on endothelial function: 1-year outcomes from a randomized clinical trial. 41. Sumida H. Unfavorable effect of smoking on the elastic properties of the human aorta. Georgakopoulos D. Smoking increases tissue factor expression in atherosclerotic plaques: implications for plaque thrombogenicity. 44. Gossett LK. Kangavari S. 42. J Am Coll Cardiol 1996. 28:1161. et al. Fibrinogen. Passive smoking and impaired endotheliumdependent arterial dilatation in healthy young adults. et al. Tsiamis E. Stefanadis C. 73:662. 50. Circulation 1999. Fusegawa Y. Wheelan KR. Circulation 1997. . Circulation 2000. 88:2149. 102:602. and cigarette smoking: a mechanism for arterial thrombosis and myocardial infarction. 46. Coronary heart disease in smokers: vitamin C restores coronary microcirculatory function. Smoking-induced coronary vasoconstriction in patients with atherosclerotic coronary artery disease: evidence for adrenergically mediated alterations in coronary artery tone. Handa S.37. Adams MR. Cigarette smoking is associated with doserelated and potentially reversible impairment of endothelium-dependent dilation in healthy young adults. Wright RA. Winniford MD. van de Borne PJ. 334:150. 39. Kugiyama K. et al. 40. 55:1988. Kaufmann PA. 99:1411. Thromb Res 1999. Vlachopoulos C. and risk of cardiovascular disease: insights from the Framingham Study. Barua RS. Ohgushi M. J Am Coll Cardiol 2010. cigarette smoking. Yasue H. Cigarette smoking increases sympathetic outflow in humans. Kremers MS. Gnecchi-Ruscone T. Murray JJ. Platelet spontaneous aggregation in platelet-rich plasma is increased in habitual smokers. et al. 51. 38. et al. et al. 31:811. Watanabe H. 43. Narkiewicz K. Johnson HM. 113:1006. Labinjoh C. di Terlizzi M. Kugiyama K. et al. Celermajer DS. Clarkson P. N Engl J Med 1996. Circulation 1998. et al. Does passive smoking impair endothelium-dependent coronary artery dilation in women? J Am Coll Cardiol 1998. 104:1905. Circulation 1987. 102:1233. Kannel WB. 47. Newby DE. Sorensen KE. impaired endogenous fibrinolysis.
Buring JE. Cigarette smoking and hypertension influence nitric oxide release and plasma levels of adhesion molecules. 62. Endogenous free radical generating sources are involved in smoking-mediated dysfunction of nitric oxide biosynthesis in human coronary artery endothelial cells: an in vitro demonstration. Aronow WS. Haramaki N. 55. Circulation 1996. Chronic nicotine administration does not affect peripheral vascular reactivity in the rat. 57. Ann Intern Med 2003. 63. Pryor WA. 38:1633. Barua. 107:2342. Saha.52. 41 Suppl A:306A. et al. Sharpe GM. 64. 54. Bleecker ER. et al. et al. N Engl J Med 1989. Am J Cardiol 2002. 65. 50:340. Effect of cigarette smoking and breathing carbon monoxide on cardiovascular hemodynamics in anginal patients. et al. Neunteufl T. . 53. et al. Mayhan WG. Circulation 1974. Reactive oxygen species are involved in smoking-induced dysfunction of nitric oxide biosynthesis and upregulation of endothelial nitric oxide synthase: an in vitro demonstration in human coronary artery endothelial cells. Radicals. Ann N Y Acad Sci 1993. Vangrow JS. Relationship between cigarette smoking and novel risk factors for cardiovascular disease in the United States. Bermudez EA. Münzel T. 138:891. 94:3109. Long-term smoking impairs platelet-derived nitric oxide release. 104:810. Clin Chem Lab Med 2001. 321:1426. Stone K. 39:822. and peroxynitrite. 61. He J. Chronic exposure to nicotine alters endothelium-dependent arteriolar dilatation: effect of superoxide dismutase. Allred EN. J Am Coll Cardiol 2002. Short-term effects of carbon monoxide exposure on the exercise performance of subjects with coronary artery disease. et al. 60. et al. Just H. et al. Relation between markers of systemic vascular inflammation and smoking in women. Rifai N. Saunders S. 271:1135. Circulation 2003. Heitzer T. Browne AE. Circulation 1996. Cassidy J. Sun YP. J Am Coll Cardiol 2001. Contribution of nicotine to acute endothelial dysfunction in long-term smokers. Ambrose JA. 58. Kostner K. Heher S. hydrogen peroxide. et al. 89:1117. Cusa C. et al. Barua RS. Bazzano LA. peroxynitrate. 686:12. SK. 39:251. Mazzucchelli I. Muntner P. Antioxidant vitamin C improves endothelial dysfunction in chronic smokers. et al. Zevin S. Zhu BQ. Srivastava S. Li Z. Chaitman BR. 66. Ikeda H. 86:1126. J Am Coll Cardiol 2003. Mazzone A. J Pharmacol Exp Ther 1994. Buchholz JN. Nicotine does not influence arterial lipid deposits in rabbits exposed to second-hand smoke. 94:6. Cardiovascular effects of carbon monoxide and cigarette smoking. 59. et al. J Appl Physiol 1999. Svrivastava. Circulation 2001. Barrios V. Gourlay SG. DC. Ichiki K. RS. 56. Oxidants in cigarette smoke.
Mueller HS. 75. Reiner J. et al. JAMA 1982. Rose G. Second Multicenter Thrombolytic Trials of Eminase in Acute Myocardial Infarction. 76. 27:1662. White HD. . Burke AP. Cohen DJ. phase II. 150:358. 73. et al. et al. 26:1222. Paradoxical effect of smoking in the Spanish population with acute myocardial infarction or unstable angina: results of the ARIAM Register. Risk factor changes and mortality results. Boyko V. Ruiz-Bailén M. Doucet M. TEAM-2 Investigators. Experience gleaned from the International Tissue Plasminogen Activator/Streptokinase Mortality Trial. 36:102. Sato H. Am Heart J 1997. Circulation 1992. Analyses of patient subgroups in the Thrombolysis in Myocardial Infarction (TIMI) trial. Riff P. Zahger D. et al. et al. 72:373. A randomised controlled trial of anti-smoking advice: 10-year results. Malcom GT. Predictors of early morbidity and mortality after thrombolytic therapy of acute myocardial infarction. Multiple risk factor intervention trial. Farb A. Braunwald E. de Chillou C. J Am Coll Cardiol 1996. Effect of cigarette smoking on coronary patency after thrombolytic therapy for myocardial infarction. Influence of cigarette smoking on rate of reopening of the infarct-related coronary artery after myocardial infarction: a multivariate analysis. Cutlip DE. Barbash GI. 74. 69. et al. Allen A. 85:1254. Ishihara M.67. 68. Significance of smoking in patients receiving thrombolytic therapy for acute myocardial infarction. White HD. et al. 77. J Am Coll Cardiol 1996. Global Utilization of Streptokinase and Tissue-Plasminogen Activator for Occluded Coronary Arteries. 79. Reina-Toral A. 336:1276. Sadoul N. Shipley MJ. Coronary risk factors and plaque morphology in men with coronary disease who died suddenly. Evaluation of paradoxic beneficial effects of smoking in patients receiving thrombolytic therapy for acute myocardial infarction: mechanism of the "smoker's paradox" from the GUSTO-I trial. Gottlieb S. 248:1465. Weisz G. Colwell L. N Engl J Med 1997. J Epidemiol Community Health 1982. Multiple Risk Factor Intervention Trial Research Group. Garcia E. 78. Tateishi H. 134:955. et al. Smoking and prognosis after acute myocardial infarction in the thrombolytic era (Israeli Thrombolytic National Survey). Impact of smoking status on outcomes of primary coronary intervention for acute myocardial infarction--the smoker's paradox revisited. J Am Coll Cardiol 1995. 87:53. Anderson JL. 72. with angiographic insights. 70. Impact of smoking on clinical and angiographic restenosis after percutaneous coronary intervention: another smoker's paradox? Circulation 2001. Hamilton PJ. Clinical implications of cigarette smoking in acute myocardial infarction: acute angiographic findings and long-term prognosis. Karagounis LA. Chest 2004. 28:1506. Cox DA. Gomez MA. Circulation 1993. de Hoyos EA. et al. Am Heart J 2005. Barbash GI. 71. Cohen LS. Am J Cardiol 1993. Modan M. 104:773. 125:831. et al.
86. Motley RJ. 2000. 319:1365. et al. 85. Holme I. Lancet 1981. 84. Results from the CASS registry. 81. Bonneux L.S. The health benefits of smoking cessation. Mooss AN. Smoking cessation and decreased risk of stroke in women. Stampfer MJ. Gersh BJ. 266:3139. Predictors of physician's smoking cessation advice. Troiano RP. Pamuk ER. et al. Survey data. Frank E. 87. Behaviorial Risk Factor Surveillance System. Kronmal RA. et al.80. Gibson N.gov/brfss/ (Accessed 3/7/05). 92. Report from the Oslo Study Group of a randomised trial in healthy men. 137:494. 1990 DHHS Publication (CDC) 90-8416. N Engl J Med 1995. 290:86. 37:125. Intensive smoking cessation intervention reduces mortality in high-risk smokers with cardiovascular disease. Kaplan RC. 131:446. Hunter CB. Access at: www. 82. Department of Health and Human Services. JAMA 1991. Colditz GA. 160:939. A report of the Surgeon General. JAMA 2003. 337:1052. Hermanson B. et al.cdc. Ford GA. 2:1303. Washington. Leren P. Chest 2007. Willan A. 83. 90. Capewell S. Wilson K. Heckbert SR. Rea TD. 91. N Engl J Med 1988. Digestion 1987. Rhodes J. et al. 88. Winkleby MA. Barendregt JJ. N Engl J Med 1997. Smoking status and risk for recurrent coronary events after myocardial infarction. Ann Intern Med 2002. 333:1165. Effect of diet and smoking intervention on the incidence of coronary heart disease. Centers for Disease Control and Prevention. Kawachi I. 89. 269:232. Beneficial six-year outcome of smoking cessation in older men and women with coronary artery disease. Cook D. Velve Byre K. van der Maas PJ. Critchley JA. Hjermann I. Arch Intern Med 2000. Mohiuddin SM. et al. The influence of smoking cessation on the prevalence of overweight in the United States. Altman DG. . Flegal KM. DC: U. Time relationships between cessation of smoking and onset of ulcerative colitis. Omenn GS. JAMA 1993. Effect of smoking cessation on mortality after myocardial infarction: meta-analysis of cohort studies. Mortality risk reduction associated with smoking cessation in patients with coronary heart disease: a systematic review. The health care costs of smoking.
MD. The earlier you quit. MPH Last literature review version 19. peptic ulcer disease. and pregnancy complications. More than 400. BENEFITS OF QUITTING SMOKING — Smoking cessation has major and immediate health benefits for men and women of all ages. and the difficulties of relapse for those who try to quit. Quitting and staying away from cigarettes is difficult. as compared to those who . MD Deputy Editor Pracha Eamranond. FACP Stephen I Rennard.Patient information: Quitting smoking Authors Joyce A Sackey.000 deaths occur each year as a result of cigarette smoking . This topic review discusses the benefits of stopping smoking. People who quit smoking before age 50 reduce their risk of dying over the next 15 years by one-half. In addition. impotence. MD. but not impossible.1: January 2011 | This topic last updated: May 4.000 deaths each year from heart disease. skin wrinkling. the greater the benefits. 2009 (More) INTRODUCTION — Cigarette smoking is a major cause of disease in the United States. Smoking is a major cause of non-fatal diseases including osteoporosis. treatments that can aid in the process of quitting. MD Section Editor Mark S Gold. exposure to secondhand smoke is estimated to cause 40.
In some studies. the risk of dying from coronary heart disease is reduced by about one-half and continues to decline over time. including emphysema". and smoking cessation can rapidly reduce this risk. While much of the lung damage caused by smoking is not reversible. Smoking cessation is also important to those who do not smoke since being exposed to second-hand cigarette smoke is responsible for a number of serious health conditions. and diagnosis". stopping smoking can reduce further damage to the lungs. pancreas. Peptic ulcer disease — Cigarette smoking increases the risk of developing peptic ulcer disease. Smoking cessation reduces the risk of lung cancer within five years of stopping. Pulmonary disease — Smoking increases the risk of long-term lung diseases such as chronic obstructive pulmonary disease. and bladder. esophagus. (See "Patient information: Lung cancer risks.continue to smoke. Cancer — Cigarette smoking is responsible for almost 90 percent of cases of lung cancer. One year after stopping smoking. since it reduces the risk of getting a second cancer and may improve the chance of survival from the first cancer. the risk of heart attack was reduced to the rate of nonsmokers within two years of quitting smoking.) . if ulcers have developed. although former smokers still have a higher risk of lung cancer than people who have never smoked. Stopping smoking is beneficial even after one of these cancers is diagnosed. Smoking cessation decreases that risk and increases the rate of ulcer healing. (See "Patient information: Chronic obstructive pulmonary disease (COPD). such as cancers of the head and neck.) Stopping smoking may also reduce the risk of other cancers. Cigarette smoking makes it more difficult to treat asthma. and many smokers with a chronic cough and sputum (phlegm coughed up from the lungs) note an improvement in these symptoms during the first year after stopping smoking. (See "Patient information: Peptic ulcer disease". Cardiovascular disease — Cigarette smoking doubles the risk of developing coronary heart disease.) Asthma and sudden infant death syndrome (SIDS) are more common among children exposed to smoke. symptoms.
or other signs of depression should be discussed with a healthcare provider. Increased bone loss has also been noted in male smokers. Stopping smoking probably reduces the risk of these conditions. or by drinking alcohol. Some people who stop smoking experience depression. followed by an additional four to seven pounds over the next four to five months. by stress. which can be intense. difficulty concentrating. Depression may also be a side effect of some medications taken to help quit smoking. anxiety. Smoking causes premature skin wrinkling and increases the risk of sexual problems (eg. These cravings are a common time for ex-smokers to relapse. The average weight gain is eight to 10 pounds. pregnant women who smoke have an increased risk of birth defects and of having an underweight baby. . RISKS OF QUITTING SMOKING — Generally. any risks of smoking cessation are far outweighed by the benefits.) Other diseases — Smoking also causes or worsens many other conditions. Symptoms of sleeplessness. The cravings will go away if ignored. it is reasonable to prepare for the discomforts of stopping smoking: Symptoms of withdrawal are common while attempting to stop smoking. people gain two to five pounds in the first two weeks. Typically. irritability.Osteoporosis — Smoking increases bone loss and increases the risk of hip fracture in women. (See "Patient information: Bone density testing". this can be severe enough that it requires counseling or antidepressant medication and it can cause the person to start smoking again. although it is not clear how much a man's risk of fracture is increased by smoking. difficulty concentrating. may persist for many months. Nevertheless. Stopping smoking begins to reverse this risk after about 10 years. Symptoms generally peak in the first three days and decrease over the next three to four weeks. sadness. and restlessness. impotence). Cravings may be brought on by situations associated with smoking. (See "Patient information: Depression treatment options for adults". As an example.) Weight gain can occur while stopping smoking because people tend to eat more after quitting. frustration or anger. Episodic cravings for cigarettes. irritability. Withdrawal symptoms can include difficulty sleeping.
and coworkers about the plan to quit. or holiday) is another option.Avoid smoking in the home and car and other places where you spend a lot of time. can differ markedly in the way in which they smoke. A few may not be addicted to smoking. Withdrawal symptoms usually become manageable within a few weeks of stopping completely. the first step is usually to set a quit date. anniversary. frustration.An exercise program and eating a reasonable diet can minimize weight gain.Review other quit attempts.Talk with a healthcare provider about ways to quit smoking. however. although choosing a special date (eg. birthday. depression. .) PREPARING TO QUIT — Smoking is recognized as a chronic addictive disease. Recalling previous quit attempts may help anticipate these symptoms. and ask for their support. low tar and low nicotine cigarettes have no known benefits and are not recommended. You are more likely to quit if you use both methods together. Discuss any prior attempts to quit with a healthcare provider to improve your chances of successfully quitting. Changing behaviors and taking a medication are the two main methods of quitting smoking. A vacation from work may be an easier time to quit. including anxiety. (See "Patient information: Exercise". and factors that may lead to relapse can differ markedly. After deciding to quit smoking. although it is estimated that 85 percents of smokers in the United States are addicted. friends. success in quitting. The benefits of quitting smoking are much greater than the risk of gaining weight. Smokers. Ideally. Even among those who are addicted. this date should be in the next two weeks. stressful situations. particularly if you smoke during work breaks. Examples include having smokers in the household or workplace. and intense cravings to smoke. Other steps that may help in preparing to quit include the following: Tell family. This is the day when you will completely quit smoking. symptoms that occur when you try to quit. but this frequently causes the person to inhale more often or more deeply.Prepare to deal with things that trigger smoking. and drinking alcohol. What worked? What did not work? What contributed to relapse?Prepare to deal with nicotine withdrawal symptoms. Some people switch to a brand of cigarettes that is lower in tar and nicotine before quitting.
a telephone hotline. Using behavioral changes with a medication increases your chances of success. or prolonged withdrawal symptoms. They typically include lectures. one cigarette typically leads to many more.Recognize that cravings frequently lead to relapse. it is important to identify situations or activities that increase your risk of smoking or relapse. some people who have failed with other techniques feel these treatments were helpful. lack of support from family and friends. a tapering method leading to a "quit day." development of coping skills. information from a healthcare provider. the internet. a healthcare provider. a counselor. you may need to develop new coping skills. sunflower seeds.BEHAVIORAL CHANGES TO HELP YOU QUIT — You can make changes in your behavior to help you quit smoking on your own or you can participate in individual or group sessions. such as starting an exercise program or learning relaxation techniques. or audio tapes. booklets. etc.) Problem solving/skills training — When preparing to quit. This may include one or more of the following: Make lifestyle changes to reduce stress and improve quality of life. such as depression. group meeting. Support — Support can be very helpful in quitting smoking and staying off cigarettes. Vigorous exercise can enhance the ability to stop smoking and avoid relapse. Keep oral substitutes (such as sugarless gum. it is important to have someone to discuss any problems that develop while trying to quit. and suggestions for preventing relapse. The cost can vary from nothing to several hundred dollars. . Although scientific support for these two methods is weak. After identifying these situations. Support can come from family and friends.Avoid thoughts like "having one cigarette will not hurt". Group counseling — Group programs are offered by a number of organizations.) handy for when cravings develop. videos. a telephone hotline. and support groups can be helpful.Have as much information as possible about what to expect during a quit attempt and how to cope during this time. Hypnosis and acupuncture — Hypnosis and acupuncture are popular stop-smoking methods. a counselor. Cravings will subside. carrots. weight gain. People who live with smokers can consider negotiating with them to stop smoking at home or in the car. Cravings can be prevented to some degree by avoiding situations associated with smoking. or support groups. Self-help materials such as pamphlets. by minimizing stress and by avoiding alcohol. (See 'Medications for quitting' below.Minimize time with smokers. Some medical centers have patient resources or learning centers with self-help materials (see 'Where to get more information' below). and also helps to minimize or avoid weight gain. In addition to getting encouragement.
or inhaler) are probably more effective than use of one form alone. Gum — Nicotine gum contains nicotine that is slowly released with chewing. anger. difficulty concentrating. frustration. but will not prevent symptoms completely. most people develop withdrawal symptoms. Smokers who smoke more than 25 cigarettes per day can use the 4 mg dose. in the United States. restlessness. anxiety. Many smokers are able to quit without using nicotine replacement therapy. even in people with known heart disease. smokers can become chronic gum users. or inhaler. Gum is available in 2 mg and 4 mg pieces. Other options include nicotine replacement therapy and bupropion (Zyban®. although nicotine is available to virtually anyone who desires it. lozenges. nasal spray. Nicotine replacement therapy appears to be safe. individual smokers may find one form particularly effective. patch. However. These include depression. Any of these medications can have side effects. Nicotine is available in several forms: as a gum or lozenge. Wellbutrin®). One of the most effective treatments is varenicline (Chantix®). irritability. and all appear similarly effective . . However.MEDICATIONS FOR QUITTING — There are several medications that may help you stop smoking. However. nasal spray. using nicotine replacement along with smoking is not recommended. some of these are available without a prescription while others require a prescription. but the intensity of the symptoms may be reduced. difficulty falling or staying asleep. this produces blood levels of nicotine 40 percent lower than smoking. None of these forms is significantly superior to another. a prescription medication. Nicotine replacement therapy is designed to reduce the intensity of these symptoms. Combinations of these therapies (usually a patch plus gum. and nicotine craving. People who smoke 25 cigarettes per day or less can use 2 mg of nicotine gum when needed. Withdrawal symptoms are not prevented by gum use. Nicotine replacement therapy — Without nicotine.
There are disadvantages of using nicotine gum. occurring in 94 percent of people . Withdrawal symptoms are reduced in intensity. causing vivid dreams. To be effective. On the other hand. Nasal spray — Nicotine nasal spray delivers a liquid solution of nicotine to the nose. but not eliminated. Lozenges — Nicotine lozenges slowly release nicotine into the saliva in the mouth. Treatment with nicotine patches is generally recommended at "full dose" for four to six weeks. Skin patches — Nicotine patches deliver nicotine to the blood through a skin patch.When used with an intensive behavioral program. similar to what happens when you smoke. Use of nicotine at night may interfere with sleep. Several doses are available. The combination of an intensive behavioral program and nicotine patches can double your chances of quitting. There is a low risk of addiction with nicotine patches. Longer use of nicotine patches does not generally improve the chance of quitting. Without a behavioral program. nicotine gum can double your chances of quitting. they may be easier for some people to use. Because the lozenges do not require chewing. which may help prevent difficult early morning withdrawal symptoms. quit rates with gum are usually lower. Swallowed nicotine can cause stomach upset and is not very effective for treating nicotine withdrawal. use of nicotine patches at night increases morning blood nicotine levels. Compared to the patch and gum. The nicotine works similarly to the gum. nasal irritation is common. The highest dose patch (21 to 22 mg/patch) delivers nicotine at a rate about half as high as that of a thirty cigarette per day smoker. as it must be absorbed in the mouth and not swallowed. However. Some brands of patches include a tapering period of several additional weeks. Gum use is generally recommended for three to six months. the nasal spray produces a relatively rapid rise in nicotine levels in the blood. Some people have a low oral pH (acidity) that reduces the absorption of nicotine. the nicotine must be absorbed through the cheek or gums rather than swallowed.
5 mg tablet twice daily for the next four daysOne 1 mg tablet twice daily starting at day seven . Varenicline — Varenicline (Chantix®) is a prescription medication that works in the brain to reduce nicotine withdrawal symptoms and cigarette cravings. Because most of the nicotine is deposited in the mouth. It should be taken after eating with a full glass of water as follows: One 0. However. it was more effective than both bupropion and placebo (a look-alike substitute that contains no medication) [3-5]. which may be worn to provide a constant low level of nicotine. Irritation of the mouth or throat is common. Nasal sprays are safe. Nicotine is released when you inhale through the device. but are one of the most expensive types of nicotine replacement. Inhaler — The nicotine inhaler is made up of a mouthpiece and a plastic cartridge that contains nicotine. Nicotine inhalers are available by prescription in the United States. People with asthma or chronic cough may not be able to use the inhaler due to throat irritation.during the first two days of use. nicotine is absorbed slowly. Examples of combination treatment include a nicotine patch. and continuing in many after three weeks of treatment. However. use of these combinations should be supervised by a knowledgeable healthcare provider.5 mg tablet daily for three daysOne 0. which may be used as needed for cigarette cravings. particularly in the beginning. which may make it less effective for treating cravings. Combinations of nicotine replacement — Using a combination of two nicotine replacement products may be more effective than using one form alone. and nicotine gum. sprays can prolong nicotine addiction more than other forms of nicotine replacement. In several studies.
head trauma. if you develop agitation. and combining the two may be even more effective. Common side effects of varenicline include nausea and abnormal dreams. If you have a past history of mood or behavior problems. unusual behavior changes. discuss this with your healthcare provider before taking varenicline. Although some of these thoughts and behaviors may have been due to quitting smoking rather than varenicline. you should stop varenicline and call your healthcare provider. It is usually taken once daily for three days. . you should stop bupropion and call your healthcare provider. Smoking is a "relapsing" condition. the better. If you have not quit after taking varenicline for 12 weeks. The drug is not recommended for those who have a seizure disorder. you may continue taking it for an additional 12 weeks. Bupropion — Bupropion (Zyban®. You should continue it for 12 weeks before determining if it is working. the report states that not all such patients had discontinued smoking. Each quit should be regarded a victory. Options include working harder to make behavioral changes and continuing varenicline or switching to another treatment. Wellbutrin®) is an antidepressant that can be used to help you stop smoking. If you develop agitation. or thoughts of suicide. anorexia nervosa. talk to your healthcare provider about the next step. depression. it is typically continued for seven to 12 weeks. Similarly. or bulimia. Similar to varenicline. and the longer it lasts. RELAPSE — Most smokers make many attempts to quit before they are able to quit completely. Bupropion is generally well tolerated. if you successfully quit at 12 weeks. or who drink alcohol excessively. if you have a past history of mood or behavior problems. but it may cause dry mouth and difficulty sleeping. depression. and relapse should not be thought of as failures. In 2007. Bupropion may be more effective than nicotine replacement therapy.You should try to quit smoking one week after starting varenicline. or thoughts of suicide. unusual behavior changes. the US Food and Drug Administration informed healthcare providers of a small number of people who developed suicidal thoughts and aggressive and erratic behavior during treatment with varenicline . discuss this with your healthcare provider before taking bupropion. then increased to twice daily starting two weeks before the quit date.
Consider trying different methods or combinations of methods. This article will be updated as needed every four months on our web site (www. Later relapses often occur during stressful situations or with social situations that are associated with smoking. when withdrawal symptoms are strongest. or a special dinner. a movie. a new outfit. (See "Patient information: Depression treatment options for adults". if relapse occurs. counseling) correctly. Consider rewards for not smoking. If you have success for a while. WHERE TO GET MORE INFORMATION — Your healthcare provider is the best source of information for questions and concerns related to your medical problem. such as depression or alcohol or drug dependency. and determine if you used the methods (medication. consider getting professional help from a healthcare provider or counselor. Being aware of these high risk situations may help. you can learn what helped and what did not and try again.Start varenicline or bupropion one week before your quit date or start nicotine replacement on the day you quit. . Then explore solutions to use next time.Pick a date to quit smoking. friends) during this critical time.uptodate. Behavior changes should usually be combined with a medication (eg. Keep this in mind when attempting to quit for the first time.Begin making changes in your behavior — avoid situations that lead you to smoke. If other problems. Consult support groups for more tips on coping with withdrawal. Try to mobilize support resources (eg. often combined with drinking alcohol. family.However.Deal with withdrawal symptoms as they develop. or bupropion). Do not "smoke just one" to get through a rough day. it is important to understand why so that your next attempt will be more successful. Tell friends and family about your plan. Try to figure out the reasons that led to start smoking again. use the money saved on cigarettes for a special treat such as a massage. varenicline.) WHERE DO I START? — The following steps are recommended to start the process of quitting smoking: Talk to your healthcare provider about the method you plan to use to quit.com/patients). Most relapses occur in the first week after quitting. nicotine replacement therapy. make it more difficult to quit.
Some of the most relevant are listed below. . Patient Level Information: Patient information: Chronic obstructive pulmonary disease (COPD). as well as selected articles written for healthcare professionals.Related topics for patients. including emphysema Patient information: Lung cancer risks. symptoms. and diagnosis Patient information: Peptic ulcer disease Patient information: Bone density testing Patient information: Depression treatment options for adults Patient information: Exercise Professional Level Information: Cardiovascular risk of smoking and benefits of smoking cessation Cigarette smoking and other risk factors for lung cancer Management of smoking cessation in adults Smoking and cardiovascular risk in diabetes mellitus Smoking and pregnancy Smoking cessation counseling strategies in primary care Strategies to reduce postoperative pulmonary complications The following organizations also provide reliable health information. are also available.
quitnet.trytostop.html) National Heart.gov/medlineplus/healthtopics.National Library of Medicine (www.lungusa.nlm.gov/) American Lung Association (www.nih.nih.org) . Lung and Blood Institute (www.com) Quitworks (www.org) QuitNet (www.americanheart.nhlbi.org/) American Heart Association (www.
296:56. Cochrane Database Syst Rev 2007. BMJ 2000. 2. Jorenby DE. Silagy C. an alpha4beta2 nicotinic acetylcholine receptor partial agonist. Efficacy of varenicline. 296:47. Stead L. Sowden A.ahrq.gov/cder/drug/early_comm/varenicline. JAMA 2006. 3. Nicotine receptor partial agonists for smoking cessation. Cahill K. Effectiveness of interventions to help people stop smoking: findings from the Cochrane Library. Lancaster T. Varenicline. Lancaster T. 321:355. J Natl Cancer Inst 1999. vs placebo or sustained-release bupropion for smoking cessation: a randomized controlled trial. Cigarette smoking. Rigotti NA. Nides M.fda. et al.Agency for Health Care Research and Quality (www. Caporaso N. 5. et al. 2007). vs sustained-release bupropion and placebo for smoking cessation: a randomized controlled trial. Hays JT. Gonzales D. an alpha4beta2 nicotinic acetylcholine receptor partial agonist. www. 4.htm (Accessed on November 26. Rennard SI. . 6. Stead LF. Bergen AW.gov/consumer/tobacco/) [1-6] Use of UpToDate is subject to the Subscription and License Agreement REFERENCES 1. :CD006103. JAMA 2006. 91:1365.
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