Download Cardiovascular Benefits of Cessation

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 6.644.62 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.