.

Many Diseases Are Directly Caused By Smoking

Cardiovascular Cancer
Lung Oral cavity/pharynx Laryngeal Esophageal Stomach Pancreatic Kidney Bladder Cervical Leukemia Ischemic heart disease Stroke Vascular dementia2 Peripheral vascular disease3 Abdominal aortic aneurysm

Respiratory
COPD Pneumonia Poor asthma control

Active Smoking
Reproductive
Other
Adverse surgical outcomes/ wound healing Hip fractures Low bone density Cataract Peptic ulcer disease Low birthweight Pregnancy complications Reduced fertility SIDS

In patients who are Helicobacter pylori positive. COPD = chronic obstructive pulmonary disease; SIDS = sudden infant death syndrome. 1. Surgeon Generals Report. 2004. 2. Roman GC. Cerebrovasc Dis. 2005;20(Suppl 2):91-100. 3. Willigendael EM et al. J Vasc Surg. 2004;40:1158-1165.

Introduction
Smoking is a leading risk factor for all CVD. Coronary heart diseases, stroke, and peripheral artery diseases are all increased in smokers compared to non-smokers. IHD account for the largest number of deaths from CVD caused by smoking(64% in men, 60% in women).

Continued ,,,
CHD, including AMI, IHD, and angina pectoris, risk increase continuously with the daily cigarette smoking. The fact that the risk is highest in young people highlights the particular relevance of smoking cessation among this group. Compared to non-smokers, smokers have a higher risk of sudden death, recurrent ischemia, and re-occlusion after and AMI.

Current data
An estimated, 20.8% of all adults smoke cigarettes in the United States. Cigarette smoking estimates by age are as follows: 1824 years (23.9%), 2544 years (23.5%), 4564 years (21.8%), and 65 years or older (10.2%). Cigarette smoking is more common among men (23.9%) than women (18.0%). Cigarette smoking is more common among adults who live below the poverty level (30.6%) than among those living at or above the poverty level (20.4%).
(Adult Cigarette Smoking in the United States: Current Estimates (updated November 2007)

10

20

30

40

50

60

70

Percentage

Downward trend

0 Men Women

19 48 19 52 19 56 19 60 19 64 19 68 19 72 19 76 19 80 19 84 19 88 19 92 19 96

What's in a Cigarette?

Cigarette smoke contains over 4,700 chemical compounds including 60 known carcinogens.

Carcinogenic: Polycyclic Aromatic Hydrocarbons (e.g.: Benzopyrene): N-nitrosaminous compounds (VNA and TSNA) Aromatic Amines (bladder cancer carcinogen) Trace metals (promoters in conjunction with carcinogens)

Polycyclic aromatic hydrocarbons, oxidizing agents, particulate matter, and acrolein are more likely the agents that affect the CVS.

Diseases attributed to smoking

Lung cancer Heart attack Heart disease Hypertension Stroke Oral cancer Bladder cancer Pancreatic cancer Cervical cancer Pregnancy complications Low birth weight babies Early menopause Lower estrogen level for women

Effects of smoking on the CVS

Active and passive smoking affects the CVS through the same mechanisms.

Nicotine is the agent in tobacco that has been most widely researched. Even though it is responsible for the addiction, it is not the major agent acting on the CVS.

The mechanisms of the effects of smoking

The mechanisms of the effects of smoking are not fully elucidated but are believed to include:
1. 2. 3. 4. 5. 6. Hemodynamic stress Endothelial injury and dysfunction Development of an atherogenic lipid profile Enhanced coagulability Arrhythmogenesis Relative hypoxemia because of the effects of carbon monoxide 7. Cigarette smoking also induces a chronic inflammatory state.

1. Platelet activation:

Scanning electron micrograph of platelets in the early stages of aggregation.

1. Platelet activation:
A key factor in AMI and sudden death is thrombosis caused by platelet activation.

Tobacco smoke activates platelets through several mechanisms. These mechanisms include: Endothelial dysfunction, oxidative stress, decreased platelet derived nitric oxide (NO) production, and increased fibrinogen and thromboxane.

1. Platelet activation:
Platelet activation exposure. occurs soon after

Platelet activation has been observed after smoking for 5 minutes, and 20 minutes of breathing second hand smoking.
Despite the much lower dose of tobacco smoke inhaled by passive smokers, the effects of platelet activation is 96% of that observed in active smokers.

1. Platelet activation:
The increased platelet agreeability resulting from smoking is an ameliorated as nearly as 2 weeks after smoking cessation, suggesting that the effects of tobacco smoke on platelet agreeability are transient and partially reversible.

2. Endothelial dysfunction:

Oxidative Stress: Endothelial Dysfunction and CAD Risk Factors

Hypertension

Diabetes

Smoking

LDL

Homocysteine

Estrogen deficiency

O2 Endothelial Cells and H2O2 Vascular Smooth Muscle

Endothelial Dysfunction
Apoptosis Leukocyte adhesion

Lipid deposition
Vasoconstriction

VSMC growth

Thrombosis

Endothelial Dysfunction and CAD Risk Factors

Endothelial dysfunction is strongly and independently associated with cardiovascular events. Endothelial Dysfunction results in atherosclerosis, plaque rupture, and decreases blood flow owing to thrombosis and vasospasm.

Endothelial Dysfunction and CAD Risk Factors

Tobacco smoke exposure leads to endothelial dysfunction, which is manifest clinically in 15 to 30 minutes. NO, secreted by the endothelium and responsible for vasodilatation, is decreased in active and passive smokers.

3. Atherosclerosis:

Atherosclerotic plaque leads to narrowing of the artery

Normal coronary artery

Lipid profile in smokers

Lipid levels are altered in smokers and passive smokers.

Tobacco smoke increase LDL and decreases HDL.

In addition to altering lipid levels, cigarette smoking renders LDL more prone to oxidation.

Lipid profile in smokers

Active and passive smoking have higher levels of products of lipid peroxidation and oxidation LDL. Oxidation LDL is rapidly ingested by macrophages which, in turn, forms foam cells in atherosclerotic lesions.

Inflammatory markers
Active and Passive smokers also show evidence of increased inflammatory markers. Inflammation is now recognized as a key step in the atherosclerosis process .(e.g.: leukocyte count, acute phase reactants, IL-6, and TNF) This Inflammatory state is reduced after smoking cessation.

4. Increased oxidative stress:

Smokers and passive smokers have increased markers of oxidative stress.

Under normal conditions, oxidative stress results from free radicals generated during the respiratory process.
The body uses anti-oxidants such as folate, Vitamin C, and B-Carotene.

4. Increased oxidative stress:

Smokers and passive smokers have been found to have lower levels of anti-oxidants.

Therefore, the harmful effect of tobacco smoke are two-fold. First, tobacco smoke is a source of free radicals. Second, it leads to a decrease in anti-oxidant levels that normally protect the body against oxidative damage.

5. Other Effects:
Smoking leads to higher levels of epinephrine and norepinephrine. These changes increase myocardial oxygen demand.

In addition tobacco smoke has also been found to have arrythmogenic potential. Arterial stiffness is also increased in smokers and passive smokers.

Or

Effects of smoking cessation on survival

Cessation at age 35-44
100
Stopped smoking

Cessation at age 55-64

100
Stopped smoking

% survival from age 40 years

80
Cigarette smokers Non smokers

% survival from age 60 years

80
Cigarette smokers

60

60

Non smokers

40

40

20

20

40

50

60

70

80

90 100 years

40

50

60

70

80

90 100 years

Smoking cessation is always associated with a benefit but an early cessation is associated with a greater benefit
Doll R, Peto R et al. BMJ 2004; 328: 1519-28

Reduction in CHD mortality

Primary prevention in England and Wales between 1981 and 2000

For a 35% reduction of smoking prevalence - 4.2% reduction of hypercholesterolemia - 7.7% reduction of high blood pressure in the general population
Slide courtesy of D Thomas Adapted from Unal B, Critchley JA, Capewell S. BMJ 2005;331;614-19

Summary
Tobacco related deaths continue to increase1 Smoking confers significant excess risk to patients with, and without, existing cardiovascular disease2,3
The majority of men and women under 50 years old who have an AMI, smoke4 A reduction in smoking reduces the risk of acute coronary events and CHD mortality5,6
1. WHO. PLoS Med. 2006; 3: e442 2. Qiao Q et al. Eur Heart J 2000; 21: 1621-6 3. Van Werkhoven JMF et al. Eur Heart J 2011; 32: 365370 4. Thomas D et al. Poster presented at French Society of Cardiology. January 2007 5. D F Mackay, et al Heart 2010; 96: 1525-1530 6. INTERHEART study. Lancet 2006; 368: 64758

References:
Eric J. Topol, Textbook of Cardiovascular medicine, third ed. Chapter 8; Smoking. Goldman L, Ausiello D. Cecil Textbook of Medicine. 22nd ed. Philadelphia, Pa:Saunders, 2003. Kumar & Clark: Clinical Medicine 6ed. Cardiology. World Health Organization, WHO Global InfoBase Online, Country Comparable Data. Centers for Disease Control and Prevention (CDC). http://www.emedicine.com/med/topic1642.htm American Heart Association

Cardiovascular Benefits of Cessation: Reduced Risk of Acute Myocardial Infarction (MI)

4 Odds Ratio (95% CI)a

P<.0001

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 Cessation: Reduced Risk of Arrhythmic Death

100 80 Survival (%)

P=.040

60
40

Smokers
Ex-smokers

20 0
0

1 Survival in Years

Peters et al. J Am Coll Cardiol. 1995;26(5):1287-1292.

Cardiovascular Benefits of Cessation: Reduced Mortality After Percutaneous Coronary Revascularization

100

80
Survival (%) 60

40 20
0 0

Quitters
Persistent Smokers

4 5 6 7 8 9 Years After Index Procedure

10

11

12

Hasdai et al N Engl J Med. 1997;336(11):755-761

Cardiovascular Benefits of Cessation: Reduced Mortality After Coronary Artery Bypass Graft
100 Probability of Survival (%)

80
60 P<.0001 (Ex-smokers vs Current Smokers) Quitters Nonsmokers

40 20
0

Persistent Smokers

10 Years

15

20

Adapted from van Domburg et al. J Am Coll Cardiol. 2000;36(3):878-883

Cardiovascular Benefits of Cessation: Reduced Risk of Stroke

4
Relative Risk (95% CI)a

P for trend <.0001

2,5 2,0

2 1,0 1 1,2

Nonsmokers

Ex-smokers

Current Smokers (<20 cig/d)

Current Smokers (20 cig/d)

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 and treatment assignment. Robbins et al. Ann Intern Med. 1994;120(6):458-462.

Cardiovascular Benefits of Cessation: Reduced Progression of Peripheral Vascular Disease

30 Rest Pain, Cumulative (%)

Smoking Abstention 20 P=.049

10

3 Years

Jonason et al. Acta Med Scand. 1987;221:253-260.

Fiore MC. Treating tobacco use and dependence. Resp Care 2000;45:1200 West R. Smoking cessation guidelines for health professionals: an update. Thorax 2000;55:987 Simon JA. Smoking cessation counseling (intensive vs minimal). Am J Med 2003;114(7):555

 : 4000 , 250

1. National Toxicology Program. 11th Report on Carcinogens; 2005. : http://ntpserver.niehs.nih.gov. 2. Mackay J, Eriksen M. The Tobacco Atlas. World Health Organization; 2006. 3. Harvard Health Letter. May 2005. 4. Surgeon Generals Report. The Health Consequences of Smoking; 2004.

Anti-Smoking support after a CV event

EUROASPIRE III
100 90 80

90.7

70
Percentage (%) 60 50 40 30 20 10 0 Verbal advice

1. 2. 3. 4. 5. 6. 7. 8. 9.

Belgium Bulgaria Croatia Cyprus Czech Rep. Finland France Germany Greece

10. 11. 12. 13. 14. 15. 16. 17. 18.

Hungary 19. Spain Ireland 20. The Netherlands Italy 21. Turkey Latvia 22. United Kingdom Lithuania Poland Romania Russian Federation Slovenia

34.6

n = 13,935 Smokers 1/3

14.3

Written advice

Seek professional help or prescribed pharmacological support

Slide courtesy of E Lopez de S

Adapted from Kotseva K et al. Eur J Cardiovasc Prev Rehabil. 2009;16:121-37.

 Fagerstrm

0-2 3-6 7-10

.
(Clair C, Rigotti NA, Porneala B, et al. JAMA 2013;309:1014-21

The process of stopping smoking

US PHS Guideline Treating Tobacco Use and Dependence: 2008 Update

Ask

- Ask about tobacco use at every visit

Advise

- Advise to quit in a clear, strong, and personalised manner

Assess

A A

Assess willingness to make a quit attempt

A
Arrange follow-up through personal and telephone contact and continue supporting, encouraging, and treating the patient

Assist

- Assist in quit attempt with counselling, pharmacotherapy, and social support

Arrange

Tobacco Dependence Support: ABC

The 2007 New Zealand Smoking Cessation Guidelines recommend a modified version of the 5 As1

Ask about
tobacco use at every visit

Brief advice
to stop smoking

Cessation support
to help with the quit attempt
1. McRobbie H, et al. N Z Med J. 2008;121:57-70.

Support should use evidence-based techniques

Patient Barriers to Treatment Initiation May Be Overcome With Effective Physician-Patient Dialogue

Patient Barriers
Poor understanding of their condition1 Managing multiple comorbid conditions Lack of perceived benefit from treatment1,2 Deficient knowledge about treatment options3 Lack of self-confidence in managing their condition4 Fears of side effects5
Effective communication may help overcome barriers and improve health outcomes1,4

1. 2. 3. 4. 5.

Nelson M, et al. Am J Med. 2007;120:S28-S32 George J et al, Chest. 2005;128:3198-3204 Moffat M, et al. Fam Pract. 2007;24:65-70 Naik AD, et al. Circulation. 2008;117:1361-1368 Horne R. Chest. 2006;130:65S-72S.

3 Essential Skills for Effective and Efficient Physician-Patient Dialogue1,2

Management Goals
1. Assess motivation and

Understand your patients

current perspective

readiness to change
2. Share information

Overcome communication
barriers and provide advice tailored to your patients needs

meaningfully and demonstrate empathy

3. Jointly develop a

Encourage patients to participate

in shared treatment decisions that may optimise outcomes3

treatment plan and build a partnership

1. 2. 3.

Makoul G, et al. Acad Med. 2001;76:390-393 Duffy et al. Acad Med. 2004;79:495-507 Heisler et al. J Gen Intern Med. 2003; 18: 893-902.