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The Cardiologist’s Guide to the Cardiovascular Consequences of Smoking and the Benefits of Cessation Overview Coronary artery disease Cardiovascular benefits of smoking cessation Peripheral vascular disease Abdominal aortic aneurysm Stroke Cardiovascular disease and environmental tobacco smoke Smoking and Coronary Artery Disease (CAD) Smoking: Role in the Pathogenesis of Cardiovascular Events Endothelial dysfunction Enhanced inflammatory response Oxidative modification Increased hematologic thrombogenicity Atherosclerotic Disease Right Coronary Artery Lavi et al. Circulation. 2007;115:2621-2627; http://www.texasheartinstitute.org/HIC/Topics/Diag/diangio.cfm. Accessed June 14, 2007. Smoking: Increased Thrombogenicity Tissue factor (TF) is highly expressed in atherosclerotic plaques and may play a role in thrombosis TF was assessed by adding factor Xa (FXa) Current smokers have significantly higher levels of circulating TF activity than nonsmokers 400 Factor Xa (FXa) pmol/L/min 300 P=.003 283 217 200 100 0 Current Current Smokers Prior Smokers After to Smoking 2 Smoking 2 Cigarettes Cigarettes Sambola et al. Circulation. 2003;107:973-977. Smoking: Impaired Endothelial Vasodilator Function Angiographically normal nonsmokers Flow-dependent dilation was significantly blunted in current smokers compared with nonsmokers Angiographically irregular nonsmokers Angiographically normal smokers Angiographically irregular smokers P<.01 Flow-Dependent Dilation (%) P<.001 60 P<.01 P<.01 50 40 P<.01 30 20 10 0 –10 Nonsmokers Zeiher et al. Circulation. 1995;92:1094-1100. Current Smokers Smoking: Epicardial Endothelial Dysfunction Current smokers are more likely to have epicardial endothelial Endothelial Dysfunction (%) dysfunction than nonsmokers 60 P=.03 46% 45 35% 34% Nonsmokers Ex-smokers 30 15 0 Lavi et al. Circulation. 2007;115:2621-2627. Current Smokers Smoking: Elevated White Blood Cell Count Elevated white blood cell (WBC) count has been associated with a greater risk of cardiovascular events Current smokers have significantly increased WBC counts compared with nonsmokers P<.0001 Nonsmokers Cell Counts (109/L) 8 Ex-smokers Current Smokers 6 P=.03 4 P<.0001 2 P<.0001 0 WBC Neutrophils Lymphocytes Monocytes Lavi et al. Circulation. 2007;115:2621-2627; Stewart et al. Circulation. 2005;111:1756-1762 640 560 480 400 320 240 160 80 Nonsmokers aF -isoprostane 2 Current Smokers Esterified F2-Isoprostanesa (pmol/L) Free F2-Isoprostanesa (pmol/L) Smoking: Increased Oxidative Modification 1000 900 800 700 600 500 400 300 Nonsmokers Current Smokers level is an index of lipid peroxidation in vivo. The dots representing subjects who smoked are each connected to a dot representing a nonsmoker matched to the subject for age and sex. Adapted from Morrow et al. N Engl J Med. 1995;332(18):1198-1203. NO Concentration (nmol/L) Smoking: Reduced Nitric Oxide (NO) Biosynthesis 5000 4000 P<.0001 3613 3000 2000 1266 1000 0 Nonsmokers Barua et al. Circulation. 2001;104:1905-1910. Current Smokers Smoking: Multiplicative Risk Factor for Coronary Artery Disease 250 189 Rates per 1000a 200 150 103 100 92 54 50 0 23 No Risk Factors Smoking, Elevated Smoking Plus Elevated Cholesterol, or Elevated Cholesterol Cholesterol Plus Hypertension Alone or Hypertension Hypertension All 3 Risk Factors Present Risk Factor Status at Entry Into the Study a All rates were age-adjusted by 10-year age groups to the US white male population in 1980. Hypercholesterolemia defined as cholesterol 250 mg/dL. Hypertension defined as a diastolic blood pressure 90 mm Hg. Burns. Prog Cardiovasc Dis. 2003;46(1): 11-29; Source: Pooling Project Research Group, 1978. Smoking: Increased Coronary Artery Disease (CAD) Mortality Relative Risk (95% CI)a 12 10 8 5.4 6 3.7 4 2 1.7 1.0 0 Nonsmokers 1-14/Day Fatal CAD a The 15-24/Day 25/Day Cigarettes/Day Current Smokers probability of an event (developing a disease) occurring in exposed people compared with the probability of the event in nonexposed people. Adjusted for age. Willett et al. N Engl J Med. 1987;317(21):1303-1309. Smoking: Effect on Coronary Artery Disease Progression of Existing Lesions 60 57 37 30 20 40 20 10 0 0 Current Smokers Waters et al. Circulation. 1996;94:614-621. 36 30 10 Nonsmokers P=.007 50 Patients (%) Patients (%) 60 P=.002 50 40 Formation of New Lesions 20 Nonsmokers Current Smokers Smoking: Increased Risk of Angina Relative Risk (95% CI)a 5 4 3 2.6 2.0 2 1.6 1.0 1 0 Nonsmokers 1-14/Day 15-24/Day 25/Day Cigarettes/Day Current Smokers aThe probability of an event (developing a disease) occurring in exposed people compared with the probability of the event in nonexposed people. Adjusted for age. Willett et al. N Engl J Med. 1987;317(1):1303-1309. Smoking: Increased Risk of Acute Nonfatal Myocardial Infarction Current smoking was associated with a 3-fold increase in odds of a Odds Ratio (95% CI)a nonfatal acute myocardial infarction compared with nonsmokers 10 9 8 7 6 5 4 3 2 1 0 Age <40 y Age 40-49 y Nonsmokers aThe Age 50-59 y Ex-smokers Age 60-69 y 1-19 Age >70 y 20 ratio of the odds of development of disease in exposed persons to the odds of development of disease in nonexposed persons. Teo. Lancet. 2006;368:647-658. Smoking: Increased Risk of Sudden Cardiac Death Relative Risk (95% CI)a 4.0 3.0 2.3 2.0 1.0 1.0 0.0 Nonsmokers aThe Current Smokers probability of an event (developing a disease) occurring in exposed people compared with the probability of the event in nonexposed people. Adjusted for age. Wannamethee et al. Circulation. 1995;91:1749-1756. Smoking: Increased Risk of Q-Wave MI After Percutaneous Coronary Revascularization Relative Risk (95% CI)a 4.0 3.0 2.08 2.0 1.28 1.0 1.0 0.0 Nonsmokers Ex-smokers Current Smokers Q-wave Myocardial Infarction (MI) aThe probability of an event (developing a disease) occurring in exposed people compared with the probability of the event in nonexposed people. Adjusted for the baseline variables significantly associated with each end point. Hasdai et al. N Engl J Med. 1997;336:755-761. Summary: Smoking and Coronary Artery Disease (CAD) Smoking plays a role in the development of CAD via: – – – – – Endothelial dysfunction Increased thrombogenicity Elevated WBC counts Increased oxidative stress Reduced NO biosynthesis Smoking acts as a multiplicative risk factor for development of CAD Smoking is associated with an increased – – – – – Rate of progression of CAD Risk of angina Risk of acute myocardial infarction Risk of sudden cardiac death Risk of Q-wave myocardial infarction after Percutaneous Coronary Revascularization Smoking and Peripheral Vascular Disease Peripheral Vascular Disease (PVD) PVD affects approximately 20% of adults older than age 55 Approximately half of patients with PVD are asymptomatic 5% to 10% of asymptomatic patients will progress to symptomatic PVD over 5 years Build-up of atherosclerotic plaque in arterial wall Patients with symptomatic PVD are at higher risk for other cardiovascular disease and mortality Hankey et al. JAMA. 2006;295:547-553; Hooi et al. Am J Epidemiol. 2001;153:666-672; Hooi et al. Br J Gen Pract. 1999;49:49-55; Hooi et al. Scand J Prim Health Care. 1998;16:177-182; http://healthguide.howstuffworks.com/peripheral-artery-disease-and-intermittent-claudication-in-depth.htm. Accessed October 8, 2007. Asymptomatic Peripheral Vascular Disease: Increased Risk Odds Ratio (95% CI)a 4.0 2.8 3.0 2.0 1.6 1.0 1.0 0.0 Nonsmokers aThe Ex-smokers Current Smokers ratio of the odds of development of disease in exposed persons to the odds of development of disease in nonexposed persons. Adjusted for other cardiovascular risk factors. Hooi et al. Scand J Prim Health Care. 1998;16:177-182. Intermittent Claudication (IC): Increased Risk Rate of development of IC is approximately 4 times as great in current smokers than in nonsmokers (OR 4.1[2.3-7.9]) Risk tends to increase with the intensity of smoking The 5-year mortality for patients with IC who continue to smoke is 40% to 50% Stenosis of the Left Iliac Artery Hooi et al. Scand J Prim Health Care. 1998;16:177-182; Kannel et al. Geriatrics. 1973;28:61-68; http://www.radiologyassistant.nl/en/42c2527422d06. Risk of Peripheral Vascular Disease vs Coronary Artery Disease For smokers, the risk of peripheral vascular disease (PVD) is greater than the risk of coronary artery disease (CAD) Relative Risk (95% CI)a 8 PVD CAD 6 3.94 4 1.87 2 1.59 1.66 0 Moderate Smokers aThe Heavy Smokers probability of an event (developing a disease) occurring in exposed people compared with the probability of the event in nonexposed people. Adjusted for age and sex. Price et al. Eur Heart J. 1999;20(5):344-353. Peripheral Vascular Disease: Progression Smoking is the most important risk factor for the progression of peripheral vascular disease (PVD) Symptoms of PVD occur approximately a decade earlier in smokers than nonsmokers Smokers with PVD have twice the amputation rate of nonsmokers MyFootShop Peripheral VascularDisease. http://www.myfootshop.com/detail.asp?Condition=Peripheral%20Vascular%20Disease. Accessed October 19, 2007; Bendermacher et al. J Thromb Haem. 2005;3:1628-37; Dormandy et al. J Vasc Surg. 2000;31(1 pt 2):S1-296. Lower Extremity Bypass Grafts: Increased Risk of Graft Failure Peto ORa 95% CI Prospective Patency Studies Wray Greenhalgh Herring Provan Rutherford Ameli Wiseman Powell Cheshire Giswold Subtotal (95% CI) Peto ORa 95% CI Weight % 1.26 1.77 1.29 2.76 10.22 3.79 5.57 2.95 1.86 5.72 37.19 6.46 14.55 1.98 4.38 1.96 3.89 2.90 2.36 5.18 3.04 3.09 (1.42, 29.30) (4.06, 52.14) (0.44, 8.85) (1.58, 12.19) (1.15, 3.34) (1.62, 9.30) (1.41, 5.95) (0.88, 6.35) (1.49, 17.95) (1.50, 6.19) (2.34, 4.08) 0.2 0.5 1 2 5 10 Favors Treatment Favors Control aAn approximation to the exact OR that is used when doing a meta-analysis using the Peto method. Willigendael et al. J Vasc Surg. 2005;42:67-74. Smoking: Increased Mortality After Vascular Surgery In order to provide very late survival data, Kazmers et al evaluated 310 patients undergoing elective vascular surgery Follow-up was 6.644.62 years Age, diabetes, smoking, and low ejection fraction were independently associated with overall mortality postoperatively Kazmers et al. J Surg Res. 2002;105:109-114. Summary: Smoking and Peripheral Vascular Disease (PVD) Smoking is associated with an increased risk of – – – – – – Asymptomatic PVD Intermittent claudication Progression of PVD Amputation due to complications of PVD Femoral-popliteal bypass graft failure Mortality after vascular surgery Symptoms of PVD occur approximately a decade earlier in smokers than in nonsmokers Current smokers are at greater risk for developing PVD than coronary artery disease Smoking and Abdominal Aortic Aneurysm (AAA) AAA: Greater Risk in Smokers Than CAD or Cerebrovascular Disease The association between smoking and aortic aneurysm is substantially Pooled Estimates of Ratio of Current Smokers’ RRa stronger than the association between smoking and coronary or cerebrovascular disease 8 7 6 P<.00001 5 4 3 2 4.7 3.0 1.0 1 0 Never Smokers Aortic Aneurysm to CAD Aortic Aneurysm to Cerebrovascular Disease AAA= Abdominal Aortic Aneurysm; CAD=Coronary Artery Disease aThe probability of an event (developing a disease) occurring in exposed people compared with the probability of the event in nonexposed people. Lederle et al. J Vasc Surg. 2003(2);38:329-334. Smoking and AAA: Increased Risk Odds Ratio (95% CI)a 12.0 9.0 5.5 6.0 3.0 2.9 10 to 19 20 to 24 3.0 1.0 0.7 0.0 Nonsmokers 1 to 9 Cigarettes/Day Current Smokers 25 AAA= Abdominal Aortic Aneurysm aThe ratio of the odds of development of disease in exposed persons to the odds of development of disease in nonexposed persons. Adjusted for age and sex. Vardulaki et al. Br J Surg. 2000;87(2):195-200. Relative Risk (95% CI)a Smoking: Increased Progression of Aortic Atherosclerosis 3 2.30 2.00 2 1.40 1.00 1 0 Never Smokers 1 to 9 10 to 19 20 Cigarettes/Day Current Smokers aThe probability of an event (developing a disease) occurring in exposed people compared with the probability of the event in nonexposed people. Adjusted for age, systolic blood pressure, serum total cholesterol, Quetelet index, diabetes mellitus, menopausal status, alcohol consumption, use of replacement estrogens, and duration of follow-up. Witteman et al. Circulation. 1993;88(part 1):2156-2162. Smoking: Effect on AAA Expansion Average Linear Growth Rate (mm/year) P<.001 2.83 3.0 2.53 2.5 2.0 1.5 1.0 0.5 0.0 Nonsmokers AAA= Abdominal Aortic Aneurysm Brady. Circulation. 2004;110:16-21. Current Smokers Summary: Smoking and Abdominal Aortic Aneurysm (AAA) Current smokers have a higher risk of developing an AAA than either coronary artery disease or cerebrovascular disease Smoking is associated with an increased risk of – Formation of AAA – Progression of aortic atherosclerosis – Expansion of AAA Smoking and Stroke Smoking and Stroke Smoking contributes to 12% to 14% of all stroke deaths Smoking may potentiate the effects of other stroke risk factors Smoking increases stroke risk – Acutely: effects on thrombus formation – Chronically: increased burden of atherosclerotic disease MRI of Brain With an Acute Ischemic Stroke Goldstein et al. Stroke. 2006;37:1583-1633; http://www.ucihs.uci.edu/stroke/whatisastroke.shtml. Accessed October 19, 2007. Smoking: Increased Progression of Carotid Atherosclerosis Both active smoking and environmental tobacco smoke exposure are Progression of Intima-Medial Thickness, µm/3 y (95% CI)a associated with increased progression of carotid atherosclerosis. 50 43.0 38.8 40 30 20 aAdjusted 31.6 32.8 Nonsmokers Nonsmokers without with b Exposure Exposureb Ex-smokers without Exposureb 25.9 Ex-smokers with Exposureb Current Smokers for demographic characteristics, cardiovascular risk factors, and lifestyle variables (risk factor model and Keys score, education, leisure activity, body mass index, and alcohol use). bTo environmental tobacco smoke. Howard et al. JAMA. 1998;279(2):119-124. Smoking: Increased Risk of Fatal and Nonfatal Stroke in Women Relative Risk (95% CI)a 6 5 3.8 4 3 2.5 2.9 2 1.0 1 0 Nonsmokers 1-14 15-24 ≥25 Cigarettes/Day Current Smokers aThe probability of an event (developing a disease) occurring in exposed people compared with the probability of the event in nonexposed people. Adjusted for age, follow-up period, history of diabetes, hypertension, high cholesterol levels, and relative weight (in 5 categories). Colditz et al. N Engl J Med. 1988;318(15):937-941. Smoking: Increased Risk of Hemorrhagic Stroke Relative Risk (95% CI)a 12 <15 Cigarettes/day (n=1914) 15 Cigarettes/day (n=3265) 10 8 6 4 2.06 3.43 1.74 2.39 4.04 2.89 2 0 aThe Nonsmokers (n=20,339) Total Hemorrhagic Stroke Intracerebral Hemorrhage Subarachnoid Hemorrhage probability of an event (developing a disease) occurring in exposed people compared with the probability of the event in nonexposed people. Adjusted for age, exercise, alcohol consumption, body mass index, history of hypertension, and history of diabetes. Kurth et al. Stroke. 2003;34:2792-2795. Smoking: Increased Stroke Mortality Cigarette smoking increases the risk of mortality from stroke in men 60 50.6 Mortality Ratea 50 39.0 40 30.9 30 20 10 0 1-15 15-24 Cigarettes/Day Current Smokers aTwenty-year age-adjusted mortality per 10,000 person-years for men. P<.014 for trend. Hart et al. Stroke. 1999;30:1999-2007. ≥25 Summary: Smoking and Stroke Smoking contributes to 12% to 14% of all stroke deaths Increased risk of – – – – – Progression of carotid atherosclerosis Stroke Hemorrhagic stroke Intracerebral hemorrhage Subarachnoid hemorrhage Increased stroke-related mortality Cardiovascular Disease (CVD) and Environmental Tobacco Smoke Effects of Environmental Tobacco Smoke on Cardiovascular Disease Effects of environmental tobacco smoke – risk of heart disease – platelet and endothelial function – arterial stiffness – atherosclerosis – oxidative stress – inflammation – ↓ heart rate variability – energy metabolism – infarct size American Heart Association. Scientific Position, Risk Factors and Coronary Heart Disease, 2005. http://americanheart.org. Accessed February 2007; Barnoya et al. Circulation. 2005; 111:2684-2698; http://www.istockphoto.com/file_closeup/abuse/smoking/tobacco_products/3383715_cigarette_burning.php?id=3 383715. Accessed October 11, 2007. Environmental Tobacco Smoke: Prevalence of Heart Disease Exposure to environmental tobacco smoke increases the risk of Proportion With Major CAD heart disease among nonsmokers by 30% 0.20 Light activea 0.15 Heavy passiveb 0.10 0.05 Light passivec 0 0 5 10 Years of Follow up 15 20 Adjusted for age, systolic blood pressure, diastolic blood pressure, total cholesterol, HDL cholesterol, FEV, height, preexisting CAD, body mass index, triglycerides, white cell count, diabetes, physical activity, alcohol intake, and social class. aLight active refers to men smoking 1-9 cigarettes a day. bHeavy passive refers to upper three quarters of cotinine concentration combined (0.8 to 14.0 ng/mL). cLight passive refers to lowest quarter of cotinine concentration among nonsmokers (0-0.07 ng/mL). Whincup et al. BMJ. 2004;329:200-205. Environmental Tobacco Smoke: Platelet Activation Nonsmokers 11-dehydro-thromboxane B2 34.8 32.8 pg/mLa ns ns ns 30.8 28.8 26.8 Min/10° Plateletsa 36.8 Current Smokers 5.6 Malondialdehyde 5.2 4.4 22.8 2.5 3 4 Day 5 12 ns ns ns ns ns ns 3.6 3.2 2 ns ns 4.0 24.8 1 ns 4.8 1 2 3 4 5 12 Day ns=not significant. a Unless marked as “ns,” differences for each value between groups were statistically significant at a level of P<.05. Schmid et al. Thromb Res. 1996;81:451-460. ns Environmental Tobacco Smoke: Vascular Endothelial Dysfunction Acute exposure to environmental tobacco smoke significantly reduces mean coronary flow velocity reserve (CFVR) in nonsmokers CFVR (Mean ±SD) 5.5 Current Smokers Nonsmokers 5.0 4.5 P<.001 4.0 3.5 3.0 2.5 2.0 Before Acute Exposure After Acute Exposure CFVR is a measure of endothelial function in the coronary circulation. Otsuka et al. JAMA. 2001;286:436-441. Environmental Tobacco Smoke: Risk of Acute Myocardial Infarction (MI) Exposure to environmental tobacco smoke increased the risk of non-fatal acute MI in a graded manner Odds Ratio (95% CI)a 4 Nonsmokers 2 1 0.75 aThe Never 1-7 8-14 15-21 22 Environmental Tobacco Smoke Exposure (Hours per Week) ratio of the odds of development of disease in exposed persons to the odds of development of disease in nonexposed persons. Adjusted for age, sex, region, physical activity, and consumption of fruits, vegetables, and alcohol. Adapted from Teo et al. Lancet. 2006;368:647-658. Summary: Cardiovascular Disease and Environmental Tobacco Smoke Exposure to environmental tobacco smoke increases risk of – Heart disease, by 30% – Acute myocardial infarction (MI) Environmental tobacco smoke affects multiple factors associated with the development of coronary artery disease, including – Platelet activation – Vascular endothelial dysfunction Cardiovascular Benefits of Smoking Cessation Cardiovascular Benefits of Cessation: Fibrinogen After 2 weeks of cessation by formerly chronic smokers, both fibrinogen concentration and the rate of fibrinogen synthesis are reduced 3.0 P<.001 3.06 2.49 2.5 P<.001 30 2.0 1.5 1.0 0.5 0.0 Fibrinogen ASR mg/kg Plasma Fibrinogen Concentration (g/L) 3.5 24.1 25 20 16.1 15 10 5 0 Smoking Abstentiona Smoking ASR=absolute rate of fibrinogen synthesis. aAbstention period of 2 weeks. Hunter et al. Clin Sci (Lond). 2001;100(4):459-465. Abstentiona White Blood Cells (×109/l) Cardiovascular Benefits of Cessation: White Blood Cells 8 7.0 7 P<.026 6.1 6 5 4 3 2 1 0 Smoking aAbstention period of 17 weeks. Eliasson et al. Nicotine Tob Res. 2001;3(3):249-255. Abstentiona Cardiovascular Benefits of Cessation: Improved Lipid Profile P<.015 5.0 2.5 P<.001 2.0 1.5 1.32 1.16 1.0 LDL (mmol/L) HDL (mmol/L) 3.0 3.78 4.0 3.52 3.0 2.0 1.0 0.5 0.0 0.0 Abstentiona Smoking Smoking HDL/LDL Ratio 1.0 0.8 P<.001 0.6 0.42 0.4 0.33 0.2 0.0 Smoking Abstentiona HDL=high-density lipoprotein; LDL=low-density lipoprotein. aAbstention period of 17 weeks. Eliasson et al. Nicotine Tob Res. 2001;3(3):249-255. Abstentiona Cardiovascular Benefits of Cessation: Hemodynamic Profile Smoking cessation is associated with an improvement in 120 100 120 P<.05 90 87 80 60 40 20 P<.05 100 80 76 72 60 40 20 0 0 Smoking a Abstention Heart Rate (Beats/min) Mean Arterial Pressure (mm Hg) hemodynamic parameters. Abstentiona period of 6 months. Oren et al. Angiology. 2006;57(5):564-568. Smoking Abstentiona Cardiovascular Benefits of Cessation: Hemodynamic Profile (cont’d) Smoking cessation is associated with an improvement in arterial compliance 8 6.3 6 5.1 4 2 0 Smoking aProvides 90 P<.01 Abstentionc Augmentation Index (%)b Oscillatory Compliance (mL/mm Hg × 100)a 10 80 70 P<.05 63.1 60 50.6 50 40 30 20 10 0 Smoking Abstentionc an assessment of small arteriolar compliance. bThe amplitude of the reflected wave depends on the stiffness of the small vessels and large arteries and thus provides a measure of systolic arterial stiffness.cAbstention period of 6 months. Oren et al. Angiology. 2006;57(5):564-568. Cardiovascular Benefits of Cessation: Platelet Effects Smoking is associated with reduced platelet volume and enhanced platelet cAMPc response to stimulation of adenylate cyclase with prostaglandin E1 Nonsmoking/ Nonchewing Smoking Nicotine Chewing Gum P=.02 Nonsmoking/ Nonchewing P<.001 12 9.0 MPV (fL) (95% CI)b cAMP After PGE (nmol/L) (95% CI)a Smoking Nicotine Chewing Gum 10 8 6 4 0 1 2 1 4 8 9 1 4 8 9 12 Weeks aPGE=prostaglandin 8.8 8.6 8.4 8.2 0 1 2 1 4 8 9 1 4 8 9 12 Weeks E1; bMPV=mean platelet volume; ccAMP= cyclic adenosine monophosphate. Terres et al. Am J Med. 1994;97:242-249. Cardiovascular Benefits of Cessation: Platelet Effects (cont’d) Smoking abstinence is associated with reduced platelet aggregability ADP=5.0 µmol/L Platelet Aggregation (%) 100 80 Group Aa NS P<.01 NS 60 Group Bb P<.01 NS 40 20 0 0 aQuit 7 14 Time (Days) smoking for 28 days. bResumed smoking after quitting for 14 days. ADP=adenosine diphosphate. ADP is a platelet aggregation agonist. Morita et al. J Am Coll Cardiol. 2005;45:589-594. 21 28 Cardiovascular Benefits of Cessation: Reduced Risk of Arrhythmic Death Cessation of cigarette smoking is associated with a reduction in arrhythmic death for patients with post-myocardial infarction left ventricular dysfunction 100 P=.040 Survival (%) 80 60 40 Smokers Ex-smokers 20 0 0 1 2 Survival in Years Peters et al. J Am Coll Cardiol. 1995;26(5):1287-1292. 3 Cardiovascular Benefits of Cessation: Reduced Risk of Acute Myocardial Infarction (MI) Odds Ratio (95% CI)a 4 P<.0001 2 1 Current >1-3 >3-5 >5-10 >10-15 >15-20 20 Ex-smokers (Years Since Cessation) aThe ratio of the odds of development of disease in exposed persons to the odds of development of disease in nonexposed persons. Adjusted for sex, region, diet, alcohol, physical activity, consumption of fruits, vegetables, and alcohol. Adapted from Teo. Lancet. 2006;368:647-658. Cardiovascular Benefits of Citywide SmokeFree Ordinance: Reduced Incidence of Acute MI 27% reduction in the incidence of acute myocardial infarction (MI) after implementation of a smoke-free ordinance in Pueblo City, Colorado AMI Counts per 100,000 Person-Years 300 257 P<.001 Preordinance 250 200 Postordinance 187 150 119 116 100 50 0 Pueblo City Bartecchi et al. Circulation. 2006;114:1490-1496. El Paso County Cardiovascular Benefits of Cessation: Reduced Risk of Recurrent Cardiac Arrest Occurrence at 3 Years (%) The risk for recurrent cardiac arrest is lower among those who quit smoking than among continuing smokers P=.038 30 27 25 19 20 15 10 5 0 Current Smokers Ex-smokersa Recurrent Cardiac Arrest aAbstention period of 3 years. Hallstrom et al. N Engl J Med. 1986;314:271-275. Cardiovascular Benefits of Cessation: Reduced Mortality After Percutaneous Coronary Revascularization Current smokers had a significantly greater risk of overall mortality after percutaneous coronary revascularization 100 Survival (%) 80 60 40 Quitters Persistent Smokers 20 0 0 2 3 4 5 6 7 8 9 Years After Index Procedure Hasdai. N Engl J Med. 1997;336(11):755-761. 10 11 12 Cardiovascular Benefits of Cessation: Reduced Mortality After Coronary Artery Bypass Graft Estimated survival benefit associated with smoking cessation increased from 3% at 5 years to 10% at 10 years and 15% at 15 years Probability of Survival (%) 100 80 60 P<.0001 (Ex-smokers vs Current Smokers) Quitters 40 Nonsmokers Persistent Smokers 20 0 0 5 10 Years Adapted from van Domburg et al. J Am Coll Cardiol. 2000;36(3):878-883. 15 20 Cardiovascular Benefits of Cessation: Reduced Progression of Peripheral Vascular Disease Rest Pain, Cumulative (%) 30 Smoking Abstention 20 P=.049 10 0 1 2 3 4 Years Jonason et al. Acta Med Scand. 1987;221:253-260. 5 6 7 Cardiovascular Benefits of Cessation: Reduced Risk of Stroke Relative Risk (95% CI)a 4 2.5 2.0 2 1.0 1.2 1 0 aThe P for trend <.0001 3 Nonsmokers Ex-smokers Current Smokers (<20 cig/d) Current Smokers (≥20 cig/d) probability of an event (developing a disease) occurring in exposed people compared with the probability of the event in nonexposed people. Adjusted for age and treatment assignment. Robbins et al. Ann Intern Med. 1994;120(6):458-462. Cardiovascular Benefits of Smoking Cessation Short-term Benefits fibrinogen concentration rate of fibrinogen synthesis WBCs Improved HDL/LDL ratio risk of stroke HDL; decreased LDL arterial pressure HR Improved arterial compliance risk of arrhythmic death after MI platelet volume Enhanced platelet cAMP response to stimulation of ADP with prostaglandin E1 smoking-induced platelet aggregability Long-term Benefits Reduced risk of – Stroke – Repeat CABG – Recurrent coronary events after MI – Arrhythmic death after MI – Secondary CVD events – Revascularization procedure after CABG Reduced – Mortality after CABG – Mortality after PTCA – Levels of inflammatory markers associated with progression of CVD (C-reactive protein, WBC, and fibrinogen) Twardella et al. Eur Heart J. 2004;25:2101-2108; Morita et al. J Am Coll Cardiol. 2005;45:589-594; Oren et al. Angiology. 2006;57:564-568; Terres et al. Am J Med. 1994; 97:242-249; Nilsson et al. J Int Med. 1996; 240:189-194; Peters et al. J Am Coll Cardiol. 1995;26:1287-1292; Rea et al. Ann Intern Med. 2002;137: 494-500; Hasdai et al. N Engl J Med. 1997;336:755-761; van Domburg et al. J Am Coll Cardiol. 2000; 36:878-883; Bakhru et al. PLoS Med. 2005;2:e160; Eliasson et al. Nicotine Tob Res. 2001;3 :249-255; Hunter et al . Clin Sci. 2001;100 :459-465; Wannamethee et al. JAMA. 1995;274:155-160.