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Η σημασία του καπνίσματος στην παθογένεση των καρδιαγγειακών παθήσεων Βασιλική Ν. Γιαννακοπούλου MD, Phds, FESC, FEAS Διευθ. ΕΣΥ Θριάσιο Νοσοκομείο Συνεργάτης.

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Παρουσίαση με θέμα: "Η σημασία του καπνίσματος στην παθογένεση των καρδιαγγειακών παθήσεων Βασιλική Ν. Γιαννακοπούλου MD, Phds, FESC, FEAS Διευθ. ΕΣΥ Θριάσιο Νοσοκομείο Συνεργάτης."— Μεταγράφημα παρουσίασης:

1 Η σημασία του καπνίσματος στην παθογένεση των καρδιαγγειακών παθήσεων Βασιλική Ν. Γιαννακοπούλου MD, Phds, FESC, FEAS Διευθ. ΕΣΥ Θριάσιο Νοσοκομείο Συνεργάτης Λιπιδαιμικού Ιατρείου ΩΚΚ

2 Rodrigo de Jerez was one of the Spanish crewmen who sailed to the Americas on the Santa Maria as part of Christopher Columbus's first voyage across the Atlantic Ocean in He is credited being the 1 st European smoker Rodrigo de JerezSpanishSanta MariaChristopher ColumbusAtlantic Ocean The Spanish introduced tobacco to Europeans in about 1518 Nicot, french ambassador in Lisbon, sent samples to Paris in 1559 ("sacred herb“referred by French, Spanish, & Portuguese ) in 1604 Stuart King James I wrote a famous polemic titled “A Counterblaste to Tobacco” Nazi Germany saw the first modern anti-smoking campaign and in 1941 tobacco was banned in various public places as a health hazard History

3 $206 billion, originally between the four largest original participating manufacturers of United States tobacco companies (Philip Morris Inc., R. J. Reynolds, Brown & Williamson and Lorillard) and the Attorneys General of 46 States. This caused an enormous growth in the tobacco industry until the scientific revelations discovering health consequences of smoking, and tobacco companies adding chemical additives were revealed in the mid-20th century, as the Big Tobacco corporate crime and corruption expose revealed, leading to the landmark corporate criminal case Tobacco Master Settlement Agreement (MSA) of 1998 for $206 billion, originally between the four largest original participating manufacturers of United States tobacco companies (Philip Morris Inc., R. J. Reynolds, Brown & Williamson and Lorillard) and the Attorneys General of 46 States.

4 † In patients who are Helicobacter pylori positive. COPD = chronic obstructive pulmonary disease; SIDS = sudden infant death syndrome. 1. Surgeon General’s Report Roman GC. Cerebrovasc Dis. 2005;20(Suppl 2): Willigendael EM et al. J Vasc Surg. 2004;40: Cancer Lung Oral cavity/pharynx Laryngeal Esophageal Stomach Pancreatic Kidney Bladder Cervical Leukemia Cardiovascular Ischemic heart disease Stroke – Vascular dementia 2 Peripheral vascular disease 3 Abdominal aortic aneurysm Respiratory COPD Pneumonia Poor asthma control Reproductive Low birthweight Pregnancy complications Reduced fertility SIDS Other Adverse surgical outcomes/ wound healing Hip fractures Low bone density Cataract Peptic ulcer disease † Active Smoking Many Diseases Are Directly Caused By Smoking

5 Tobacco atlas 4 th Edition 2011 World Lung Foundation, American Cancer Society

6 Tobacco Kills More Americans/year Than Alcohol, Cocaine, Crack, Heroin, Homicide, Suicide, Car Accidents, Fires & AIDS combined:

7 Cardiovascular diseases linked with smoking Over 1/5 of deaths due to smoking-related illness are caused by heart disease

8 European Cardiovascular Disease Statistics 2012 Edition

9

10 Καπνός τσιγάρου:  4000 χημικές ουσίες,  250 ουσίες τοξικές ή καρκινογόνες Χημική Ουσία στον Καπνό του Τσιγάρου Βρίσκεται επίσης σε… Ακετόνη Αποχρωστικά υλικά Βουτάνιο Υγρό αναπτήρων ΑρσενικόΕντομοκτόνα Κάδμιο Μπαταρίες αυτοκινήτων Μονοξείδιο του άνθρακα Καυσαέρια αυτοκινήτων Τολουένιο Βιομηχανικά διαλυτικά μέσα 1. National Toxicology Program. 11th Report on Carcinogens; Διατίθεται στην ηλεκτρονική διεύθυνση: server.niehs.nih.gov. 2. Mackay J, Eriksen M. The Tobacco Atlas. World Health Organization; Harvard Health Letter. May Surgeon General’s Report. The Health Consequences of Smoking; 2004.

11 Multiplicative Effect on Risk of Death From Top Risk Factors of Cardiovascular Disease x1.5 x2.7 x5.9 x3.5 x2.3 x3.9 x1.7 Hypertension defined as systolic blood pressure = 150 mm Hg; Dyslipidemia defined as total cholesterol=260 mg/ dL; Smoking defined as current smoking. Kannel WB, 1977.

12 The mechanisms of the effects of smoking The mechanisms of the effects of smoking are not fully elucidated but are believed to include: The mechanisms of the effects of smoking are not fully elucidated but are believed to include: 1. Hemodynamic stress 2. Endothelial injury and dysfunction 3. Development of an atherogenic lipid profile 4. Enhanced coagulability 5. Arrhythmogenesis 6. Relative hypoxemia because of the effects of carbon monoxide 7. Cigarette smoking also induces a chronic inflammatory state 8. Genetic predisposition

13 JACC 2004

14 A key factor in AMI and Sudden Death is thrombosis caused by platelet activation. caused by platelet activation. Tobacco smoke activates platelets through several mechanisms. Including: Tobacco smoke activates platelets through several mechanisms. Including: Endothelial dysfunction, Endothelial dysfunction, Oxidative stress, Oxidative stress, Decreased platelet derived nitric oxide (NO) production, Decreased platelet derived nitric oxide (NO) production, Increased fibrinogen and thromboxane Increased fibrinogen and thromboxane. Platelet activation: Platelet activation:

15 Platelet activation occurs soon after exposure Platelet activation occurs soon after exposure Platelet activation has been observed after smoking for 5 minutes, and 20 minutes of breathing second hand smoking 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 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 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 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

16 Endothelial Dysfunction & CAD Risk Factors Endothelial dysfunction is strongly and independently associated with cardiovascular events 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 results in atherosclerosis, plaque rupture, and decreases blood flow owing to thrombosis and vasospasm Tobacco smoke exposure leads to endothelial dysfunction, which is manifest clinically in 15 to 30 min Tobacco smoke exposure leads to endothelial dysfunction, which is manifest clinically in 15 to 30 min NO, secreted by the endothelium and responsible for vasodilatation, is decreased in active and passive smokers NO, secreted by the endothelium and responsible for vasodilatation, is decreased in active and passive smokers

17 Lipid profile in smokers Lipid levels are altered in smokers and passive smokers Tobacco smoke ↑LDL and ↓HDL In addition to altering lipid levels, cigarette smoking renders LDL more prone to oxidation Active and passive smoking have higher levels of products of lipid peroxidation and oxidation LDL

18 Oxidation LDL is rapidly ingested by macrophages which, in turn, forms foam cells in atherosclerotic lesions Active & 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) Active & 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. This Inflammatory state is reduced after smoking cessation.

19 Increased oxidative stress Increased oxidative stress Smokers and passive smokers have been found to have lower levels of anti-oxidants 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 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

20 Genetic Predisposition Genetic Predisposition The atherosclerotic process in smokers may be partially mediated by genetic variants CYP1A1 MSP polymorphism or certain endothelial NO synthase intron 4 polymorphisms increased the susceptibility to cigarette smoke exposure-related atherosclerotic diseases including multi-vessel CAD & MI CYP1A1 MSP polymorphism or certain endothelial NO synthase intron 4 polymorphisms increased the susceptibility to cigarette smoke exposure-related atherosclerotic diseases including multi-vessel CAD & MI The importance of these genetic variants is unknown as their prevalence in the entire population of cigarette smokers has not been determined The importance of these genetic variants is unknown as their prevalence in the entire population of cigarette smokers has not been determined

21 Other Effects: Other Effects: Smoking leads to higher levels of epinephrine and norepinephrine Smoking leads to higher levels of epinephrine and norepinephrine These changes increase myocardial oxygen demand These changes increase myocardial oxygen demand In addition tobacco smoke has also been found to have arrythmogenic potential In addition tobacco smoke has also been found to have arrythmogenic potential Arterial stiffness is also increased in smokers and passive smokers Arterial stiffness is also increased in smokers and passive smokers

22 Cigarette smoking predisposes the individual to several different clinical atherosclerotic syndromes:  Stable angina  Acute coronary syndromes  Sudden death  Stroke  Aortic & peripheral atherosclerosis  Aortic aneurysm  Sexual impotence

23 Smoking: Effect on Coronary Artery Disease Waters et al. Circulation. 1996;94: Progression of Existing Lesions Patients (%) Current Smokers Nonsmokers Formation of New Lesions Patients (%) Current Smokers Nonsmokers P=.002P=

24 Smoking: Increased Risk of Angina a The 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 Relative Risk (95% CI) a /DayNonsmokers15-24/Day  25/Day Cigarettes/Day Current Smokers

25 Smoking: Increased Risk of Acute Nonfatal Myocardial Infarction Current smoking was associated with a 3-fold increase in odds of a nonfatal acute MI compared with nonsmokers a The ratio of the odds of development of disease in exposed persons to the odds of development of disease in nonexposed persons. Teo. Lancet Odds Ratio (95% CI) a Age <40 y Age y Age y Age y Age >70 y  20 NonsmokersEx-smokers1-19

26 Smoking: Increased CAD Mortality a The 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 Relative Risk (95% CI) Relative Risk (95% CI) a Fatal CAD 1-14/DayNonsmokers15-24/Day  25/Day Cigarettes/Day Current Smokers

27 Smoking: Increased Risk of Sudden Cardiac Death a The 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 Relative Risk (95% CI) a

28 Smoking: Increased Risk of Q-Wave MI After Percutaneous Coronary Revascularization a The 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 Q-wave Myocardial Infarction (MI) Relative Risk (95% CI) a

29 Κάπνισμα και ΑΕΕ Στο κάπνισμα οφείλεται το 12% to 14% όλων των θανάτων από ΑΕΕ Το κάπνισμα αυξάνει τον κίνδυνο για ΑΕΕ  oξέως: ευνοεί το σχηματισμό θρόμβων  χρονίως: ευνοεί την αθηρωματική νόσο

30 Smoking: Increased Progression of Carotid Atherosclerosis a Adjusted for demographic characteristics, cardiovascular risk factors, and lifestyle variables (risk factor model and Keys score, education, leisure activity, body mass index, and alcohol use). b To environmental tobacco smoke. Howard et al. JAMA Ex-smokers with Exposure b Current Smokers Nonsmokers without Exposure b Progression of Intima-Medial Thickness, µm/3 y (95% CI) a Ex-smokers without Exposure b Nonsmokers with Exposure b

31 Smoking: Increased Risk of Fatal & Nonfatal Stroke in Women Nonsmokers Relative Risk (95% CI) a a The 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): ≥25 Cigarettes/Day Current Smokers

32 Smoking: Increased risk of hemorrhagic stroke a The 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: Total Hemorrhagic Stroke Relative Risk (95% CI) a Intracerebral Hemorrhage Subarachnoid Hemorrhage Nonsmokers (n=20,339) <15 Cigarettes/day (n=1914)  15 Cigarettes/day (n=3265)

33 Smoking: Increased Stroke Mortality a Twenty-year age-adjusted mortality per 10,000 person-years for men. P<.014 for trend. Hart et al. Stroke. 1999;30: Mortality Rate a ≥25 Cigarettes/Day Current Smokers

34 Περιφερική αποφρακτική αγγειοπάθεια & κάπνισμα Η ΠΑΑ προσβάλει το 20% των καπνιστών > 55 ετών 50% των ασθενών με ΠΑΑ είναι ασυμπτωματικοί 5% to 10% των ασυμπτωματικών θα αναπτύξουν συμπτωματική ΠΑΑ εντός 5 ετών Οι ασθενείς με συμπτωματική ΠΑΑ είναι σε υψηλό κίνδυνο για άλλα καρδιαγγειακά επεισόδια και θάνατο Η 5ετής θνησιμότητα για τους ασθενείς με διαλείπουσα χωλότητα που συνεχίζουν να καπνίζουν είναι 40%-50% JAMA lAm J Epidemiol Gen Pract. 1999; Scand J Prim Health Care Accessed October 8, Build-up of atherosclerotic plaque in arterial wall

35 Asymptomatic Peripheral Vascular Disease: Increased Risk a The 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: Odds Ratio (95% CI) a Ex-smokersCurrent SmokersNonsmokers

36 Περιφερική αποφρακτική αγγειοπάθεια και κάπνισμα 4 φορές πιο συχνή η διαλείπουσα χωλότητα Οι καπνιστές κινδυνεύουν περισσότερο να αναπτύξουν ΠΑΑ παρά ΣΝ Ο κίνδυνος αυξάνει με την ένταση του καπνίσματος Αυξημένος κίνδυνος μετά από αγγειακά χειρουργεία

37 Risk of Peripheral Vascular Disease vs Coronary Artery Disease a The 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): Relative Risk (95% CI) a Moderate SmokersHeavy Smokers

38 Κάπνισμα και ανεύρυσμα κοιλιακής αορτής Vardulaki et al. Br J Surg. 2000;87(2): Odds Ratio (95% CI) a Nonsmokers1 to 910 to 19  to 24 Cigarettes/Day Current Smokers

39 Smoking: Increased Progression of Aortic Atherosclerosis a The 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): Relative Risk (95% CI) a Never Smokers1 to 910 to 19  20 Cigarettes/Day Current Smokers

40 Tobacco is responsible for 17% of all female deaths in the US Tobacco is responsible for 17% of all female deaths in the US Smoking is the most preventable risk factor for heart attack Women who smoke 1-4 cigarettes/day are at almost twice as likely to develop heart disease than nonsmokers A woman who smokes is at risk for heart attack 19 years earlier than one who does not smoke Women of all ages who quit smoking greatly reduce their risk of dying prematurely Smoking-women

41 Kawachi I et al. Circulation 1997;95: “The Nurses' Health Study Cohort”

42 Kawachi I et al. Circulation 1997;95: “The Nurses' Health Study Cohort”

43   20%–30% κίνδυνος εμφάνισης Ca πνεύμονα   25%–30% κίνδυνος εμφάνισης καρδιοπάθειας  Προκαλεί / επιδεινώνει νοσήματα όπως το άσθμα, η ΧΑΠ και το εμφύσημα Secondhand smoke:

44 Παθητικό κάπνισμα και καρδιαγγειακό Years of Follow up Proportion With Major CAD Light active a Heavy passive b Light passive c

45 Office of Environmental Health Hazard Assessment of the California Environmental Protection Agency, Health Effects of Exposure to Environmental Tobacco Smoke, Το ανθρώπινο κόστος του παθητικού καπνίσματος  147 ως 251 θάνατοι μη καπνιστών ανά εργαζόμενους  ως θάνατοι το χρόνο στην Ευρωπαϊκή Ένωση

46 Environmental Tobacco Smoke: Risk of Acute Myocardial Infarction (MI) a The 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: Nonsmokers Odds Ratio (95% CI) a Environmental Tobacco Smoke Exposure (Hours per Week) Never  Exposure to environmental tobacco smoke increased the risk of non-fatal acute MI in a graded manner Exposure to environmental tobacco smoke increased the risk of non-fatal acute MI in a graded manner

47 Συνέπειες παθητικού καπνίσματος σε νεογνά & παιδιά 60% των παιδιών στις ΗΠΑ εκτίθενται σε παθητικό κάπνισμα 60% των παιδιών στις ΗΠΑ εκτίθενται σε παθητικό κάπνισμα Σε κάποιες χώρες  80% των νέων ζουν σε σπίτια όπου οι άλλοι καπνίζουν όταν αυτοί είναι παρόντες Σε κάποιες χώρες  80% των νέων ζουν σε σπίτια όπου οι άλλοι καπνίζουν όταν αυτοί είναι παρόντες Η δευτερογενής έκθεση στον καπνό αυξάνει το φορτίο της νόσου και τη νοσηλεία για τα νεογνά και τα παιδιά. Η δευτερογενής έκθεση στον καπνό αυξάνει το φορτίο της νόσου και τη νοσηλεία για τα νεογνά και τα παιδιά. Μεγάλη Βρετανία  παιδιά <5 ετών νοσηλεύονται ετησίως Μεγάλη Βρετανία  παιδιά <5 ετών νοσηλεύονται ετησίως Αυστραλία  56% μεγαλύτερος κίνδυνος για νοσηλεία εάν η μητέρα κάπνιζε στο ίδιο δωμάτιο με το νεογνό, Αυστραλία  56% μεγαλύτερος κίνδυνος για νοσηλεία εάν η μητέρα κάπνιζε στο ίδιο δωμάτιο με το νεογνό, 73% εάν κάπνιζε ενώ κρατούσε το βρέφος στην αγκαλιά της 73% εάν κάπνιζε ενώ κρατούσε το βρέφος στην αγκαλιά της 95% εάν κάπνιζε ενώ τάιζε το βρέφος 95% εάν κάπνιζε ενώ τάιζε το βρέφος 1 Secondhand smoke; Fact sheet, June Mackay J, Eriksen M. The Tobacco Atlas. WHO; Fagerstrom K. Drugs. 2002; 4. Blizzard L, et al. Arch Pediatr Adolesc Med

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Κατέβασμα ppt "Η σημασία του καπνίσματος στην παθογένεση των καρδιαγγειακών παθήσεων Βασιλική Ν. Γιαννακοπούλου MD, Phds, FESC, FEAS Διευθ. ΕΣΥ Θριάσιο Νοσοκομείο Συνεργάτης."

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