• Like
Dr. Bianco: Humo de segunda mano y riesgos cardiovasculares
Upcoming SlideShare
Loading in...5
×

Dr. Bianco: Humo de segunda mano y riesgos cardiovasculares

  • 2,550 views
Uploaded on

Los profesionales de la salud, incluso aquellos relacionados con la salud cardiovascular, son conscientes …

Los profesionales de la salud, incluso aquellos relacionados con la salud cardiovascular, son conscientes
que el tabaco es uno de los principales factores de riesgo para muchas enfermedades, pero la
mayoría de ellos no han sido entrenados para reconocer al consumo de tabaco como una adicción,
no son conscientes de los mecanismos por los cuales el consumo de tabaco y la exposición al humo
del tabaco causan daños cardiovasculares. La mayoría de ellos tampoco han sido entrenados sobre
cómo abordar al paciente fumador en su práctica clínica diaria y como usar los medicamentos para el
tratamiento de la dependencia al tabaco. Esta conferencia tiene la intención de informar a los asistentes
sobre todos estos temas y estimularlos a obtener más información sobre ellos.

  • Full Name Full Name Comment goes here.
    Are you sure you want to
    Your message goes here
    Be the first to comment
    Be the first to like this
No Downloads

Views

Total Views
2,550
On Slideshare
0
From Embeds
0
Number of Embeds
0

Actions

Shares
Downloads
9
Comments
0
Likes
0

Embeds 0

No embeds

Report content

Flagged as inappropriate Flag as inappropriate
Flag as inappropriate

Select your reason for flagging this presentation as inappropriate.

Cancel
    No notes for slide
  • This training program is designed to equip cardiology providers with evidence-based approaches for assisting patients with tobacco cessation. The program was developed by Judith Prochaska, PhD, MPH, and William Grossman, MD, with expert guidance provided by scientific advisors Neal Benowitz, MD, Stanton Glantz, MD, and Karen Hudmon, DrPH. Funding for the program comes from the Flight Attendant Medical Research Institute, the Charles Schwab Family Foundation, the National Institute on Drug Abuse, and the California Tobacco-Related Disease Research Program.
  • Cardiologists plead ignorance, lack of time, in helping smokers butt out April 22, 2013 Shelley Wood Shelley Wood Managing Editor | shelley@theheart.org Rome, Italy - Smoking rates in Spain are among the highest in Europe, yet cardiologists surveyed admit they do not always ask their patients about smoking. And when they do, they don't often investigate the level of nicotine dependence or offer pharmaceutical aids for quitting.   Those are some of the insights from a survey conducted by Dr Regina Dalmau (Hospital La Paz, Madrid, Spain) and colleagues, presented here at EuroPrevent 2013. "If you have an infarction and you are a smoker, and you quit smoking, your mortality [risk] would be reduced by 36%," Dalmau told heartwire. "If you use statins after an AMI, your mortality [risk] is reduced by 30%. So smoking cessation is actually more effective, but it is something we [cardiologists] don't always do. So many patients keep on smoking because no one, or very few, have told them to stop." Dalmau and colleagues emailed their survey, which permitted anonymous answers and had no financial component, to 3000 cardiologist members of the Spanish Society of Cardiology . Only 328 (11%) responded, which means the results likely represent the "best-case" scenario, Dalmau conceded. The average age of the respondents was 44, 63% were male, 76% were clinical cardiologists, 18% were interventional cardiologists, 29% were past smokers, and 4% were current smokers. As for how cardiologists managed smoking cessation among their patients, only three out of four cardiologists said they would ask their patients about their smoking at every visit, and just 73% said they charted the information. The bulk of respondents estimated that 20% to 30% of their patients were current smokers and that the same percentage relapsed after an AMI. And while 76% of cardiologists said they always recommended smoking cessation, only 40% would set up follow-up visits to assess any progress with quitting. In other key details: Only 22% said they'd have quitting brochures available at their practices. Only 14% have a CO-oximeter. 22% had never heard of the Fagerström test used to gauge level of nicotine dependence. 60% considered their training in smoking cessation to be insufficient. 71% said they wished they could improve their skills in helping patients quit. Cardiologists don't like to communicate, they prefer to prescribe pills and order tests. Dalmau and colleagues also asked physicians about their use of prescription drugs. The vast majority of cardiologists said they had not prescribed any smoking-cessation drugs or nicotine replacement in the last month. By far, the most commonly stated reason for not prescribing medications was lack of familiarity with the drugs (73%), followed by safety concerns (11%). To heart wire , Dalmau stressed that physicians were clear that they wanted to do more for patients but admitted to being uninformed about the treatment options. "I think the real reason is that they are not trained," she said. "You need to be able to talk to the patient, to communicate, and cardiologists don't like to communicate, they prefer to prescribe pills and order tests," she said. "It's true that cardiologists are more attracted by techniques and devices, yet there is really a need for [better smoking-cessation interventions] in improving the prognosis of the patients." Lack of time, cited by 5% of cardiologists, is also a big problem. "The more time you dedicate to this, the more likely you are to get success." And while more people are smoking in Spain than in other parts of the world, Dalmau believes that the reticence among cardiologists is likely more universal and extends to general practitioners as well. For all physicians, she said, "better education is key."
  • Key Point Current smokers have elevated levels of tissue factor (TF), which may be one of the mechanisms by which smoking is associated with increased atherothrombotic complications . TF is highly expressed in atherosclerotic plaques and its presence has been related to plaque thrombogenicity. TF may be present in the blood as well, and plays a role in the propagation of thrombosis. Acute coronary syndromes are associated with atherosclerotic lesion disruption and thrombus formation. Smoking has been implicated in both atherosclerotic progression and atherothrombotic complications. The objective of this study was to evaluate whether the increased rate of atherothrombotic complications observed in current smokers, is mediated through increased circulating levels of TF. Levels of TF were assessed by adding factor X, factor VIIa, and calcium to plasma, and then quantifying the concentration of factor Xa (FXa). Circulating TF was reported as changes in factor FXa per unit time (pmol/L/min). Subjects who smoke  10 cigarettes per day with a smoking history of  10 years were evaluated before and 2 hours after smoking 2 cigarettes. Baseline levels of circulating TF were significantly increased 2 hours after smoking 2 cigarettes (217  72 pmol/L [before] and 283  106 pmol/L/min FXa [after]; P =.003). The authors concluded that smoking has significant modulatory effects on plasma levels of circulating TF. Reference Sambola A, Osende J, Hathcock J, et al. Role of risk factors in the modulation of tissue factor activity and blood thrombogenicity. Circulation. 2003;107:973-977.
  • Key Point Current smokers, without evidence of significant coronary artery disease (CAD), are more likely to have epicardial endothelial dysfunction than nonsmokers . In an attempt to establish whether or not smoking is associated with coronary endothelial dysfunction and inflammation, Lavi et al evaluated 881 patients referred for evaluation of chest pain, who did not have evidence of significant CAD on diagnostic coronary angiography. Patients consisted of 115 current smokers (smoking within the last month) and 766 ex-smokers and nonsmokers. Nonsmokers included both previous and never smokers. All patients underwent diagnostic coronary angiography. Microvascular coronary flow reserve was assessed after infusion with incremental doses of adenosine. Coronary vasoreactivity was assessed after infusion of incremental doses of acetylcholine. Endothelium-independent epicardial coronary artery function was assessed by the change in coronary artery diameter in response to an intracoronary bolus of nitroglycerine. All patients had baseline bloodwork prior to angiography to evaluate white blood cell (WBC) count and other systemic markers of inflammation. Significantly more current smokers were found to have epicardial endothelial dysfunction, 46%, than ex-smokers, and nonsmokers, 34% and 35%, respectively. Reference Lavi S, Prasad A, Yang EH, et al. Smoking is associated with epicardial coronary endothelial dysfunction and elevated white blood cell count in patients with chest pain and early coronary artery disease. Circulation. 2007; 115:2621-2627.
  • Key Point Current smokers without evidence of significant coronary artery disease have significantly increased WBC counts compared with nonsmokers. Elevated WBC counts have been associated with a greater long-term cardiovascular risk. In an attempt to establish whether or not smoking is associated with coronary endothelial dysfunction and inflammation, Lavi et al evaluated 881 patients referred for evaluation of chest pain, who did not have evidence of significant coronary artery disease on diagnostic coronary angiography. Patients consisted of 115 current smokers (smoking within the last month) and 766 ex-smokers and nonsmokers. Nonsmokers included both previous and never smokers. All patients underwent diagnostic coronary angiography. Microvascular coronary flow reserve was assessed after infusion with incremental doses of adenosine. Coronary vasoreactivity was assessed after infusion of incremental doses of acetylcholine. Endothelium-independent epicardial coronary artery function was assessed by the change in coronary artery diameter in response to an intracoronary bolus of nitroglycerine. All patients had baseline bloodwork prior to angiography to evaluate WBC count and other systemic markers of inflammation. Both total WBC count and leukocyte subtypes were higher in current smokers than in nonsmokers. References Stewart R, White H, Kirby A; et al; The Long-term Intervention With Pravastatin in Ischemic Disease (LIPID) Study Investigators. White blood cell count predicts reduction in coronary heart disease mortality with pravastatin. Circulation. 2005;111:1756-1762. Lavi S, Prasad A, Yang E, et al. Smoking is associated with epicardial coronary endothelial dysfunction and elevated white blood cell count in patients with chest pain and early coronary artery disease. Circulation. 2007; 115:2621-2627.
  • Key Point Current smokers have higher levels of oxidative modification in vivo than do nonsmokers. F 2 -isoprostane level is an accurate method of detecting lipid peroxidation, and thereby oxidant injury, in vivo. In this study Morrow et al determined whether smoking induces oxidative modification by evaluating whether production of F 2 -isoprostanes are increased in smokers. Twenty subjects (10 smokers, 10 nonsmokers) had fasting bloodwork drawn on 2 separate occasions. Participants were not allowed to smoke prior to venipuncture. The average of the 2 measurements of F 2 -isoprostanes are demonstrated above. Levels of free F 2 -isoprostanes in plasma from current smokers were significantly higher than those measured in age- and sex-matched nonsmokers (242  147 and 103  19 pmol/L, respectively) ( P =.02) . The levels of F 2 -isoprostanes esterified to lipids in plasma from smokers were also significantly higher than those measured in nonsmokers (574  217 and 345  65 pmol/L, respectively; P =.03). The authors concluded that elevated levels of F 2 -isoprostanes in current smokers indicate that smoking induces oxidative modification of biologic components in humans. Reference Morrow JD, Frei B, Longmire AW, et al. Increase in circulating products of lipid peroxidation (F 2 -isoprostanes) in smokers: smoking as a cause of oxidative damage. N Engl J Med. 1995;332(18):1198-1203.
  • Key Point Smoking is associated with reduced nitric oxide (NO) biosynthesis. NO is the primary vasodilatory substance produced by endothelial cells. Smokers have been noted to have impaired endothelium-dependent vasodilation (EDV). Barua et al hypothesized that reduction in NO biosynthesis contributes to the impaired EDV noted in current smokers. Twenty-three male patients (15 curr e nt smokers, 8 nonsmokers) had fasting bloodwork drawn, while abstaining from smoking for a 6 to 8 hour period. Human umbilical vein endothelial cells (HUVECs) were incubated with serum from participants, and after 12 hours basal NO production in the supernatant was determined. NO production in the cell culture supernatant was evaluated by chemiluminscence. HUVECs incubated with current smoker’s serum showed significantly lower basal NO production compared with HUVECs incubated with nonsmoker’s serum ( P <.0001). The authors concluded that smoking is associated with reduced basal NO production. Reference Barua R, Ambrose JA, Eales-Reynolds LJ, DeVoe MC, Zervas JG, Saha DC. Dysfunctional endothelial nitric oxide biosynthesis in healthy smokers with impaired endothelium-dependent vasodilatation. Circulation. 2001;104: 1905-1010.
  • This slide details the substantial and widespread negative effects of smoking and SHS exposure on the cardiovascular system. The mechanisms by which tobacco use and SHS increase the risk of heart disease are multiple and interact with one another. The physiological systems that play a role in regulating cardiovascular function, developing heart disease, and triggering an acute event (myocardial infarction) are sensitive to tobacco and SHS (Barnoya & Glantz, 2005). Within 5-30 minutes of SHS exposure at levels commonly experienced in the real world, there are effects on vascular function (depressed endothelial function) and platelets (increased activity), among other effects. Both of these changes can trigger an acute event and contribute to the long-term development of heart disease. Smoking and SHS activate blood platelets, increasing the risk of thrombus formation and damaging the lining of arteries, which promotes the development of atherosclerosis. Both active smokers and passive smokers (i.e., those exposed to SHS) have higher levels of inflammatory markers. Smoking and SHS exposure increase arterial stiffness, which may relate to the changes in endothelial function. Treating tobacco dependence and eliminating SHS exposure, in particular, produce dramatic and rapid improvements (within days) in cardiovascular health even in patients with serious CVD. The Centers for Disease Control and Prevention has recommended that people with heart disease avoid SHS exposure. Patients with heart disease and their families should be educated about the effects of SHS. If people cannot or will not stop smoking, they should be urged to smoke outside. In addition to protecting family members from SHS, smoking outside significantly increases the likelihood that smokers will decide to quit and increases their success with quitting. Baronya J, Glantz, SA. (2005). Cardiovascular effects of secondhand smoke. Nearly as large as smoking. Circulation 111:2684-9268.
  • Key Point The risk of fatal CAD may be directly related to the amount smoked. Willett et al prospectively evaluated the incidence of CAD in a cohort of 119,404 female nurses enrolled in the Nurses’ Health Study. Participants completed questionnaires at baseline (1976) and were followed up over a 6-year period. Smoking status was identified. Deaths among nonrespondents were identified through searches of state records and the National Death Index or were reported by family members. More than 98% of the deaths were identified. Fatal CAD was defined as fatal myocardial infarction (MI) confirmed by hospital records or at autopsy, or as CAD recorded on the death certificate, if this was the only cause given and there was previous evidence of CAD. Compared with nonsmokers, the age-adjusted relative risk (RR) of fatal CAD, increased with increasing daily cigarette use: 1.7, 3.7, and 5.4, for 1-14/day, 15-24/day, and  25/day, respectively. Reference Willett WC, Green A, Stampfer MJ, et al. Relative and absolute excess risks of coronary heart disease among women who smoke cigarettes. N Engl J Med . 1987;317(21):1303-1309.
  • Key Point When evaluated by serial quantitative coronary arteriography, it is seen that smoking accelerates progression of existing coronary artery disease (CAD) and new lesion formation. Waters et al evaluated 331 participants (90 current smokers, 241 nonsmokers) with angiographically documented coronary atherosclerosis and fasting cholesterol levels between 220 and 300 mg/dL, enrolled in the randomized, double-blind, placebo-controlled Canadian Coronary Atherosclerosis Intervention Trial (CCAIT). Patients were randomized to receive either placebo or lovastatin 20 mg once daily. In an attempt to achieve a target low-density lipoprotein (LDL) cholesterol level  130 mg/dL, d rug doses were increased over the initial 16 weeks of the trial to a maximum dose of 40 mg twice daily. Participants were evaluated over a 2-year period. Repeat angiography was performed at the conclusion of the study period (except in 21 patients in whom it was performed earlier). Baseline and follow-up coronary angiograms were compared, and a change in minimal lumen diameter  0.4 mm was considered a true change (either progression or regression). A new lesion was defined as a stenosis that was not apparent on the initial angiogram or was <25% in diameter stenosis but that narrowed by ≥0.4 mm in minimal lumen diameter at the second angiogram. Significantly more curr e nt smokers showed evidence of progression. Progression occurred in 41 of 72 (57%) current smokers and 83 of 227 (37%) nonsmokers, P =.002. Significantly more curr e nt smokers developed new atherosclerotic lesions, 36% vs 20%, P =.007. The authors therefore concluded that coronary atherosclerosis progresses more rapidly in curr e nt smokers than in nonsmokers. Reference Waters D, Lesperance J, Gladstone P, et al; the CCAIT Study Group. Effects of cigarette smoking on the angiographic evolution of coronary atherosclerosis: a Canadian Coronary Atherosclerosis Intervention Trial (CCAIT) substudy. Circulation. 1996;94:614-621.
  • Key Point Overall, current smoking was associated with a 3-fold increase in the odds of having a nonfatal acute myocardial infarction (MI) compared with nonsmokers. Teo et al evaluated 12,133 cases of first acute MI and 14,435 age-matched and sex-matched controls in the international, multicenter INTERHEART study. Trained staff administered a questionnaire to both cases and controls in which participants were asked detailed questions about their smoking status. Overall, current smoking was associated with a 3-fold increase in the odds of having a non-fatal acute MI, compared with nonsmokers (odds ratio [OR] 2.95; 95% CI 2.77-3.14; P <.0001). Risk increased with the number of cigarettes smoked. The effect of current smoking was significantly greater in younger (OR, 3.53; 95% CI, 3.23-3.86) than in older participants (OR, 2.55; 95% CI, 2.35-2.76); P <.0001 for interaction. The effect of current smoking was markedly greater in younger subjects, particularly among the heaviest smokers (  20 cigarettes per day) in whom ORs were 5.6 (95% CI, 5.1-6.2) for younger smokers and 3.6 (95% CI, 3.25-3.98) for older smokers ( P <.0001 for interaction). Reference Teo KK, Ounpuu S, Hawken S, et al; on behalf of the INTERHEART Study Investigators. Tobacco use and risk of myocardial infarction in 52 countries in the INTERHEART study: a case-control study. Lancet. 2006;368:647-658.
  • Key Point Current smoking is associated with an increased risk of sudden cardiac death. Wannamethee et al prospectively evaluated 7735 British men, aged 40 to 59 years from the British Regional Heart Study (BRHS). All participants completed questionnaires regarding their smoking habits, alcohol intake, and medical history. Subjects had complete physical exams that included fasting bloodwork, pulmonary function tests (PFTs), and ECG. Participants were followed up for 8 years. Fatal events were defined as death from ischemic heart disease. Sudden cardiac death was defined as an event in which death occurred within 1 hour after the onset of symptoms. Only those men for whom clear information was available about their death within 1 hour were included in the category of sudden death. A Cox proportional hazards model was used to evaluate contribution of risk factors to the risk of sudden cardiac death and to derive the age-adjusted RRs. When adjusted for age, current smokers had an increased risk of sudden cardiac death (RR, 2.3, 95% CI, 1.2-4.0). Reference Wannamethee G, Shaper AG, Macfarlane PW, Walker M. Risk factors for sudden cardiac death in middle-aged British men. Circulation. 1995;91:1749-1756.
  • Key Point Smoking is associated with a significantly increased risk of asymptomatic peripheral vascular disease (PVD). Hooi et al evaluated 3650 residents of the province of Limburg, The Netherlands, in the Limburg Peripheral Arterial Occlusive Disease (PAOD) study. Participants answered a self-administered questionnaire at their doctor’s office, and ankle-brachial pressure index (ABPI) was assessed by means of a pocket Doppler device and a sphygmomanometer. ABPI was calculated as a ratio of the ankle systolic blood pressure to the highest arm systolic blood pressure. Subjects were considered as having evidence of PVD when a minimum of 1 leg’s resting ABPI was <0.95 on 2 evaluations within a 1-week interval. Asymptomatic PVD was defined as the combination of an ABPI <0.95 without symptoms of intermittent claudication. Among study participants, 458 subjects had PVD. One hundred thirty-eight were symptomatic, 314 were asymptomatic, and 6 had unspecified PVD. Current and ex-smoking were significantly associated with asymptomatic PVD, OR 2.8 (1.9-4.0) and 1.6 (1.1-2.4), respectively. Reference Hooi J, Stoffers HEJH, Kester A, et al. Risk factors and cardiovascular diseases associated with asymptomatic peripheral arterial occlusive disease: the Limburg PAOD study. Scand J Prim Health Care. 1998;16:177-182.
  • Key Point Smoking is the most important modifiable risk factor for development of abdominal aortic aneurysm (AAA). Vardulakai et al performed a randomized, controlled trial on 5356 men and women in Chichester, UK, between 1988 and 1995. Anteroposterior measurements of the aorta were obtained with an ultrasound, and aneurysm was defined as an aortic diameter of 30 mm or more. Personal and social history were obtained prior to the baseline physical via a self-administered questionnaire. Men were 5.6 times more likely to have an AAA than women. The chart above depicts that the level of risk for AAA increases with the number of cigarettes smoked daily. Risk of AAA ranges from 0.7, 3.0, 2.9, 5.5 for current smokers who smoked 1-9, 10-19, 20-24, and  25 cigarettes daily, respectively. Reference Vardulaki KA, Walker NM, Day NE, Duffy SW, Ashton AH, Scott RAP. Quantifying the risks of hypertension, age, sex and smoking in patients with abdominal aortic aneurysm. Br J Surg. 2000;87(2):195-200.
  • Key Point The association between smoking and aortic aneurysm is substantially stronger than the association between smoking and coronary or cerebrovascular disease. Lederle et al performed a meta-analysis of all medical articles and reviews (1966-2002) relating to smoking and abdominal aortic aneurysm (AAA). Ten studies that included more than 3 million subjects were included in this analysis. In each study, the association with smoking was substantially greater for AAA than for coronary artery disease (CAD) or cerebrovascular disease. The graph depicts the pooled estimates of curr e nt smokers’ RR for death from aortic aneurysm divided by current smokers’ RR for death from each of the other smoking-related diseases. For men, the association of current smoking with AAA was 3 times greater than the association of current smoking with CAD (95% CI, 2.5-3.4), and 4.7 times greater than the association of current smoking with cerebrovascular disease (95% CI, 3.1-7.2), P <.00001. Reference Lederle RFA, Nelson DB, Joseph AM. Smokers’ relative risk for aortic aneurysm compared with other smoking-related diseases: a systematic review. J Vasc Surg. 2003;38(2):329-334.
  • Key Point Risk of aortic atherosclerotic progression increases with number of cigarettes smoked. Witteman et al evaluated the association between smoking and progression of abdominal aortic atherosclerosis in a population-based cohort of 758 women aged 45 to 64. Women were clinically evaluated at baseline and followed up for a mean of 8.9  0.8 years. Women underwent a second physical evaluation at follow-up. Aortic atherosclerosis was diagnosed by radiographic detection of calcific deposits in the abdominal aorta. Atherosclerotic change was defined as the occurrence (disappearance) of calcifications or enlargement (reduction) of the calcified area present at baseline. All women completed self-administered questionnaires regarding their smoking status at baseline and follow-up. At follow-up, atherosclerotic changes were noted in 284 women. The risk of aortic atherosclerotic progression increased with number of cigarettes smoked per day. Reference Witteman JCM, Grobbee DE, Valkenburg HA, van Herwert AM, Stijnen T, Hofman A. Cigarette smoking and the development and progression of aortic atherosclerosis: a 9-year population-based follow-up study in women. Circulation. 1993;88(part 1):2156-2162.
  • Key Point B oth active smoking and environmental tobacco smoke exposure are associated with increased progression of carotid atherosclerosis. Howard et al evaluated 10,914 participants enrolled in the Atherosclerosis Risk in Communities (ARIC) study, a prospective study that assessed atherosclerotic disease and its clinical consequences in a cohort of approximately 16,000 US adults. Subjects underwent carotid ultrasound to evaluate carotid intima-medial thickness, a surrogate of atherosclerotic progression. Assessments were made at baseline and at a follow-up visit 3 years later. All participants completed self-administered questionnaires based upon which they were classified as current smokers, ex-smokers, nonsmokers, and exposed to environmental tobacco smoke. Current smokers demonstrated the highest rate of atherosclerotic progression (41 µm per 3 years) . Rates of progression followed, in descending order, ex-smokers with environmental tobacco smoke exposure, nonsmokers with environmental tobacco smoke exposure, ex-smokers without environmental tobacco smoke exposure, followed by nonsmokers without environmental tobacco smoke exposure, 39.6 µm, 33.2 µm, 32.5 µm; and 27.0 µm, respectively. The authors therefore concluded that both active smoking and environmental tobacco smoke exposure are associated with increased progression of carotid atherosclerosis. Reference Howard G, Wagenknecht LE, Burke GL, et al; the ARIC Investigators.. Cigarette smoking and progression of atherosclerosis: the Atherosclerosis Risk in Communities (ARIC) Study. JAMA. 1998;279(2):119-124.
  • Cigarette smoking has been identified as a significant risk factor for ischemic stroke, hemorrhagic stroke, as well as subarachnoid hemorrhage. The annual number of stroke deaths attributed to smoking in the United States has been estimated to be between 17,800 and 21,400, or 12% to 14%. Smoking may also potentiate the effects of other stroke risk factors, such as oral contraceptive use. Smoking is thought to increase stroke risk both acutely, through its effect on thrombus formation, and chronically, by increasing the risk of atherosclerosis. Reference Goldstein LB, Adams R, Alberts MJ., et al. Primary Prevention of Ischemic Stroke: A Guideline From the American Heart Association/American Stroke Association Council: Cosponsored by the Atherosclerotic Peripheral Vascular Disease Interdisciplinary Working Group; Cardiovascular Nursing Council; Clinical Cardiology Council; Nutrition, Physical Activity, and Metabolism Council; and the Quality of Care and Outcomes Research Interdisciplinary Working Group: The American Academy of Neurology affirms the value of this guideline. Stroke. 2006;37:1583-1633.
  • Key Point Female smokers have an increased risk of total hemorrhagic stroke as well as intracerebral hemorrhage and subarachnoid hemorrhage. In an attempt to evaluate the impact of smoking on the risk of hemorrhagic stroke, Kurth et al evaluated data obtained from the Women’s Health Study. The Women’s Health Study is a randomized, double-blind, placebo-controlled trial (1993-2003) in which 39,876 healthy women were followed up to determine the benefits of low-dose aspirin and vitamin E for the prevention of cardiovascular disease (CVD). Kurth et al determined subjects’ smoking habits from responses to baseline self-administered questionnaires. Stroke was defined as a focal neurologic deficit of sudden onset and vascular mechanism that lasted more than 24 hours. Hemorrhagic stroke was further classified into intracerebral hemorrhage, subarachnoid hemorrhage, or intraventricular hemorrhage. During a mean of 9 years of follow-up, a total of 70 hemorrhagic strokes occurred. Analysis was adjusted for age, exercise (<4 times per week vs  4 times per week), alcohol consumption (<1 drink per week, 1-6 drinks per week, and  1 drink per day), body mass index (continuous), history of hypertension (self-reported systolic pressure  140 mm Hg, or diastolic blood pressure  90 mm Hg, or current treatment of hypertension, regardless of blood pressure), and history of diabetes. Risk of total hemorrhagic stroke, intracerebral hemorrhage, and subarachnoid hemorrhage increased with quantity of cigarettes smoked. Reference Kurth T, Kase CS, Berger K, Gaziano JM, Cook NR, Buring JE. Smoking and risk of hemorrhagic stroke in women. Stroke. 2003;34:2792-2795.
  • Although some patients may know that smoking is harmful to their health, many patients will not have adequate knowledge of the specific cardiovascular health effects of smoking. Data from the International Tobacco Control Project and the Global Adult Tobacco Survey demonstrate that across multiple countries smokers and non-smokers lack awareness of the cardiovascular health harms of smoking and secondhand smoke (ITC, WHO, WHF, 2012). ☼ Note to international adaptations: Data is available on knowledge of the cardiovascular harms of smoking and SHS across multiple countries in the report below. Check for information on your country. If there is no data in the report, check: http://www.who.int/tobacco/surveillance/gats/en/index.html to see if new data has been released. ITC Project, World Health Organization, and World Heart Federation (April 2012). Cardiovascular harms from tobacco use and secondhand smoke: Global gaps in awareness and implications for action. Waterloo, Ontario, Canada and Geneva, Switzerland. The above report is available in English and Chinese English: http://www.world-heart-federation.org/fileadmin/user_upload/documents/Tobacco/ITCWHFBroApr18v2web.pdf Chinese: http://www.world-heart-federation.org/fileadmin/user_upload/documents/Tobacco/ITCWHFReportChinese.pdf
  • Second-hand smoke (SHS) is the air pollution created by smoking cigarettes (and cigars and pipes) during the 90% of the time that the cigarette is not being smoked. Because the cigarette is burning at a lower temperature when it is not being smoked, the combustion is less complete and the smoke is richer in toxic chemicals than the mainstream smoke that the smoker inhales. Even though nonsmokers receive a much lower total dose of these chemicals (because the smoke is diluted in the air before nonsmokers inhale it), the effects on blood vessels, blood, and the heart are surprisingly large. Marriage to a smoker or working where smoking is permitted is associated with about a 30% increase in the risk of heart disease incidence or death (about one-third the effect of active smoking). Despite the tobacco industry ’s efforts to cast doubt on the link between SHS and health risks (USDHHS, 2006), few scientists and clinicians would deny that SHS is harmful. Major conclusions of the 2006 Surgeon General ’s report The Health Consequences of Involuntary Exposure to Tobacco Smoke (USDHHS, 2006) are listed below. The negative health consequences of most relevance to cardiology providers are presented on the slide. 1. SHS causes premature death and disease in children and in adults who do not smoke. 2. Children exposed to SHS are at an increased risk for sudden infant death syndrome, acute respiratory infections, ear problems, and more severe asthma. Smoking by parents causes respiratory symptoms and slows lung growth in their children. 3. Exposure of adults to SHS has immediate adverse effects on the cardiovascular system and causes coronary heart disease and lung cancer. 4. The scientific evidence indicates that there is no risk-free level of exposure to SHS. 5. Many millions of Americans, both children and adults, are still exposed to SHS in their homes and workplaces despite substantial progress in tobacco control. 6. Eliminating smoking in indoor spaces fully protects nonsmokers from exposure to SHS. Separating smokers from nonsmokers, cleaning the air, and ventilating buildings cannot eliminate exposures of nonsmokers to SHS. A comprehensive literature reviewed conducted by Barnoya and Glantz (2005) concluded that the cardiovascular effects of SHS are substantial and rapid. The effects of even brief exposure (minutes to hours) are often nearly as large (averaging 80 – 90%) as those of chronic active smoking. Barnoya J, Glantz SA. (2005). Cardiovascular effects of secondhand smoke: nearly as large as smoking. Circulation 11:2684 – 2698. U.S. Department of Health and Human Services (USDHHS). (2006). The Health Consequences of Involuntary Exposure to Tobacco Smoke: A Report of the Surgeon General. U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, Coordinating Center for Health Promotion, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health.
  • A review of the literature concluded that the cardiovascular effects of SHS are nearly as large as those of smoking. The relative risk of coronary heart disease (CHD) among active smokers was estimated at 1.78. The relative risk of CHD among passive nonsmokers was 1.31, indicating that long-term SHS exposure in the work or at home is associated with a 30% increased risk for CHD in adult nonsmokers. This is the consensus effect ( RR = 1.31), but most of the studies reviewed were based on questionnaires with the methodology containing a lot of error, which likely underestimates the effect of SHS exposure. Earlier epidemiologic studies that used marriage to a smoker as a surrogate for exposure did not capture exposure to SHS outside of the home (e.g., from workplaces and public places such as restaurants and bars). As a result, the earlier studies underestimated SHS exposure and simply compared more exposed people (nonsmokers married to a smoker but exposed to SHS elsewhere) to less exposed people (nonsmokers married to nonsmokers but exposed to SHS elsewhere). This comparison biases the risk estimate of the effect of SHS downward (Barnoya & Glantz, 2005). One study in the review (Whincup et al., 2004) used biomarker cotinine in a 20-year prospective study. Using a biomarker instead of self-report survey allowed for cleaner demarcation of the “exposed” group vs. a truly unexposed group. This study obtained higher estimates of passive smoke exposure ( RRs = 1.45 and 1.57) depending on the level of SHS exposure (see next slide). Those exposed to high levels of passive smoke did not look much different from light smokers. Baronya J, Glantz, SA. (2005). Cardiovascular effects of secondhand smoke. Nearly as large as smoking. Circulation 111:2684-2698. Whincup PH, Gilg JA, Emberson JR, Jarvis MJ, Geyerabend C, Bryant A, Walker M, Cook DG. (2004) Passive smoking and risk of coronary heart disease and stroke: Prospective study with cotinine measurement. BMJ 329:200-205.
  • Whincup et al. (2004) conducted a 20-year prospective analysis of passive smoking and CHD. The study used cotinine, a stable metabolite of nicotine, as the measure of exposure, which allowed for a more precise assessment of total SHS exposure. Earlier epidemiologic studies that used marriage to a smoker as a surrogate for exposure did not capture exposure to SHS outside of the home (e.g., from workplaces and public places such as restaurants and bars). As a result, the earlier studies underestimated SHS exposure and simply compared more exposed people (nonsmokers married to a smoker but exposed to SHS elsewhere) to less exposed people (nonsmokers married to nonsmokers but exposed to SHS elsewhere). This comparison biases the risk estimate of the effect of SHS downward (Barnoya & Glantz, 2005). Whincup ’s estimate of the risk of major CHD associated with passive smoking was between 1.45 (95% CI = 1.10–2.08) and 1.57 (95% CI = 1.08–2.28), depending on the level of SHS exposure. These estimates are about twice as high as earlier estimates and nearly as high as those observed in light (1–9 cigarettes/day) active smokers (1.66; 95% CI = 1.04–2.68), shown in the figure here. The reference group consisted of the lowest quartile of cotinine levels (0–0.7 ng/ml), which means that even people in the control reference group had some SHS exposure. These results suggest that passive smoking leads to 68–86% of the risk of light smoking, depending on the level of SHS exposure. Baronya J, Glantz SA. (2005). Cardiovascular effects of secondhand smoke. Nearly as large as smoking. Circulation 111:2684-2698. Whincup PH, Gilg JA, Emberson JR, Jarvis MJ, Geyerabend C, Bryant A, Walker M, Cook DG. (2004) Passive smoking and risk of coronary heart disease and stroke: Prospective study with cotinine measurement. BMJ 329:200-205.
  • Key Point Exposure to environmental tobacco smoke increased the risk of nonfatal acute (MI) in a graded manner. Teo et al evaluated 12,133 cases of first acute MI and 14,435 age-matched and sex-matched controls in the international, multicenter INTERHEART study. Trained staff administered a questionnaire to both cases and controls in which participants were asked detailed questions about their smoking status. After adjusting for age, sex, region, physical activity, and consumption of fruits, vegetables, and alcohol, nonsmokers who had no previous environmental tobacco smoke exposure showed increasing risk of nonfatal acute MI with increasing levels of exposure to environmental tobacco smoke. Although the etiology is unclear, this increase in risk was slightly attenuated in subjects with  22 hours per week of environmental tobacco smoke exposure. Reference Teo KK, Ounpuu S, Hawken S, et al, on behalf of the INTERHEART Study Investigators. Tobacco use and risk of myocardial infarction in 52 countries in the INTERHEART study: a case-control study. Lancet. 2006;368:647-658.
  • The harmful effects of smoking do not end with the smoker. Even brief exposure can be dangerous because nonsmokers inhale many of the same carcinogens and toxins in cigarette smoke as smokers. SHS exposure causes serious disease and death, including heart disease and lung cancer in nonsmoking adults and sudden infant death syndrome, acute respiratory infections, ear problems, and more frequent and severe asthma attacks in children. Second-hand smoke causes approx. 603 000 premature deaths worldwide each year. These deaths include 167100 deaths among children (166 000 lower respiratory infections deaths and 1100 from asthma), and 435,800 adult deaths (35 800 deaths from asthma 21 000 deaths from lung cancer, 379 000 deaths from ischaemic heart disease). 87% of adult SHS smoke deaths are CVD deaths. Oberg M, et al., Worldwide burden of disease from exposure to second-hand smoke: a retrospective analysis of data from 192 countries. Lancet. 2011 Jan 8;377(9760):139–46. Also see: http://www.who.int/tobacco/publications/second_hand/global_estimate_burden_disease/en/index.html U.S. Department of Health and Human Services (USDHHS). (2006). The Health Consequences of Involuntary Exposure to Tobacco Smoke: A Report of the Surgeon General. U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, Coordinating Center for Health Promotion, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health.
  • The implementation of comprehensive smoke-free laws in public places has been shown to reduce admission rates for myocardial infarctions. Smoke-free laws are an important policy for reducing heart attacks and promoting cardiovascular health (Tan CE, 2012). 2004 - Helena, Montana (Sargent et al., 2004) – 40% fall of AMI admissions 6 months after smoke-free ordinances; the repeal of the ordinances caused return of admissions rate to the pre-restriction rate 2006 - Piedmont, Italy - the AMI post-ban admissions fell by 11% among men and women under age 60 (Barone-Adesi et al., 2006) 2008 - Scotland - large prospective study of ACS admissions (Pell et al., 2008) as part of a national evaluation of Scotland ’ s smoke-free legislation (Haw et al., 2006) - ACS admission rate fell by 17% Lightwood JM, Glantz SA. Declines in acute myocardial infarction after smoke-free laws and individual risk attributable to secondhand smoke. Circulation. 2009 Oct 6;120(14):1373–9. Mackay DF, Irfan MO, Haw S, Pell JP. Meta-analysis of the effect of comprehensive smoke-free legislation on acute coronary events. Heart. 2010 Oct;96(19):1525–30. Tan CE, Glantz SA. Smoke-Free Air: An Important Strategy to Reduce Heart Attacks. Global Heart. World Heart Federation (Geneva); 2012 Jul;7(2):189–91.
  • The 1990 Surgeon General ’s report on the health benefits of smoking cessation outlines the numerous and substantial health benefits incurred when patients quit smoking (USDHHS, 1990): Health benefits realized 2 weeks to 3 months after quitting include the following: circulation improves and walking becomes easier. One to nine months later, coughing, sinus congestion, fatigue, and shortness of breath decrease. One year later, excess risk of CHD is decreased to half that of a smoker. 3 years later , the risk of myocardial infarction (MI) is similar to that of never-smokers. After 5 to 15 years, stroke risk is reduced to a rate similar to that of never-smokers. Finally, 15 years after quitting, an individual ’s risk of CHD is reduced to a rate similar to that of never-smokers. According to the 2004 Surgeon General ’s report The Health Consequences of Smoking (p. 363), the statement "The excess risk of CHS caused by smoking is reduced by about half after 1 year of smoking abstinence and then declines gradually. After 15 years of abstinence, the risk of CHD is similar to that of persons who have never smoked" is based on the body of evidence reviewed and reported in the 1990 Surgeon General’s report titled The Health Benefits of Smoking Cessation .  The studies assessed for this report included the two Rosenberg studies (on female subjects; see pp. 200-204 in the 1990 report). The two Surgeon General reports are available on the TIPS Web site (www.cdc.gov/tobacco/sgr/index.htm). Thus the benefits of quitting are significant. It is never too late to quit to incur many of the benefits of quitting.   U.S. Department of Health and Human Services (USDHHS). ( 1990). The Health Benefits of Smoking Cessation. A Report of the Surgeon General (DHHS Publication No. CDC 90-8416). U.S. Department of Health and Human Services, Public Health Service, Centers for Disease Control and Prevention and Health Promotion, Office on Smoking and Health. U.S. Department of Health and Human Services (USDHHS). (2004). The Health Consequences of Smoking: A Report of the Surgeon General. U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health.
  • Smoking cessation is a powerful treatment for established heart disease. Effects on mortality are comparable to those of many widely used pharmacologic therapies. Standard treatments reduce the risk of death in patients with CVD by 15-35%: Aspirin = 15% Beta blockers = 23% ACE inhibitors = 23% Statins = 29-35% Smoking cessation reduces risk of death by 36% and reduces the risk of future cardiac events by 50%. With each puff of a cigarette, blood pressure increases on average by 20 mmHg. Smokers are at increased risk of CVD and progressive kidney failure. Blood-pressure-lowering effects of medications is modest for most single agents: 11-15 mmHg systolic blood pressure ; 6-10 mmHg diastolic blood pressure. Smoking increases blood pressure in a dose-dependent response. Smoking cessation can lower blood pressure by 40 mmHg. No other medication compares. Patients who stop smoking also have fewer complications following surgery and respond better to drugs used to treat many conditions. Collins R, Peto R, MacMahon S, et al. (1990). Blood pressure, stroke, and coronary heart disease. Part 2. Short-term reductions in blood pressure: Overview of randomised drug trials in their epidemiological context. Lancet 335(8693):827-838. Critchley J, Capewell S. (2003). Smoking cessation for the secondary prevention of coronary heart disease. Cochrane Database Syst Rev 4:CD003041. Critchley JA, Capewell S. (2003). Mortality risk reduction associated with smoking cessation in patients with coronary heart disease: A systematic review. JAMA 290(1):86-97. Gerber Y, Rosen LJ, Goldbourt U, Benyamini Y, Drory Y; Israel Study Group on First Acute Myocardial Infarction. (2009). Smoking status and long-term survival after first acute myocardial infarction a population-based cohort study. J Am Coll Cardiol. 54(25):2382-7. Reid RD, Quinlan B, Riley DL, Pipe AL. (2007). Smoking cessation: Lessons learned from clinical trial evidence. Curr Opin Cardiol 22(4):280-285. Scandinavian Simvastatin Survival Study Group. (1994). Randomised trial of cholesterol lowering in 4444 patients with coronary heart disease: The Scandinavian Simvastatin Survival Study (4S). Lancet 344(8934):1383-1389. Wen CP, Tsai MK, Chan HT, Tsai SP, Cheng TY, Chiang PH. (2008). Making hypertensive smokers motivated in quitting: Developing 'blood pressure equivalence of smoking'. J Hypertens 26(4):672-677.
  • No other preventive activity produces such significant results from such a small investment in time
  • ☼ Note to international adaptations: Region and country specific data may be added Data by region, country, sex, and age is available at: http://whqlibdoc.who.int/publications/2012/9789241564434_eng.pdf World Health Organization. WHO Global Report: Mortality Attributable to Tobacco. World Health. Geneva; 2012.
  • This section addresses the various medications for quitting smoking. ☼ Note to international adaptations: Consult national guidelines on pharmacological methods for treating tobacco use and dependence and edit this section accordingly. ☼ Note to international adaptations: National treatment guidelines for some countries, including the 2008 guidelines for the United States that are often discussed in this presentation, are available at: http://www.treatobacco.net/en/page_224.php ☼ Note to international adaptations: A brief overview on treatment of tobacco use by country is available at: http://www.who.int/tobacco/surveillance/policy/country_profile/en/index.html Select country to view country profile, and scroll down to the section on ‘Offer help to quit tobacco use.’
  • ☼ Note to international adaptations: *Consult national guidelines on pharmacological methods for treating tobacco use and dependence and edit accordingly. FDA stands for the United States Food and Drug Administration. There are three general classes of FDA-approved drugs for cessation: Nicotine replacement therapy (NRT), which includes the nicotine gum, patch, lozenge, nasal spray, and inhaler. A nicotine sublingual tablet currently is available in Europe. Psychotropics such as bupropion SR. Varenicline , an  4  2 nicotinic acetylcholine receptor partial agonist. According to the U.S. Public Health Service Clinical Practice Guideline for treating tobacco use and dependence, these agents are considered first-line pharmacotherapies for cessation (Fiore et al., 2008). Second-line pharmacotherapies for smoking cessation are nortriptyline and clonidine, both shown in repeated trials to be efficacious for supporting cessation. They are inexpensive, generic drugs, however; and pharmaceutical companies lack the financial incentives to pursue an FDA indication for smoking cessation for the drugs. Fiore MC, Jaen CR, Baker TB, et al. (2008). Treating Tobacco Use and Dependence: 2008 Update. Clinical Practice Guideline. Rockville, MD: U.S. Department of Health and Human Services, Public Health Service.
  • Study abstract: Objectives. Determine the effects of nicotine patch therapy, when used to promote smoking cessation, on myocardial ischemia in patients with coronary artery disease. Background. Nicotine patches substantially increase quit rates among cigarette smokers, but their safety in patients with myocardial ischemia who are attempting to quit smoking is unknown. Methods. This is a prospective study using exercise thallium-201 single-photon emission computed tomography (SPECT) to assess serial changes in the total and ischemic myocardial perfusion defect size at baseline while patients were smoking and during treatment with 14- and 21-mg nicotine patches. Entry criteria required that patients 1) smoked ≥1 pack of cigarettes per day; 2) had known coronary artery disease; and 3) had myocardial ischemia (i.e., ≥5% reversible perfusion defect) on SPECT. All patients performed symptom-limited treadmill exercise, and the baseline SPECT study served as its own control. We interpreted and computer quantified the SPECT images with no knowledge of the testing sequence. Results. Thirty-six of the 40 enrolled patients had exercise SPECT at baseline and during treatment with at least 14-mg nicotine patches. These patients had an initial perfusion defect size of 17.5 ± 10.6% while smoking an average of 31 ± 11 cigarettes per day for 40 ± 12 years. A significant reduction in the total perfusion defect size (p < 0.001) was observed from baseline (17.5 ± 10.6%) to treatment with 14-mg (12.6 ± 10.1%) and 21-mg (11.8 ± 9.9%) nicotine patches. This reduction occurred despite an increase in treadmill exercise duration (p < 0.05) and higher serum nicotine levels (p < 0.001). There was a significant correlation between the reduction in defect size and exhaled carbon monoxide levels (p < 0.001) because patients reduced their smoking by ∼74% during the trial. Conclusions. Nicotine patches, when used to promote smoking cessation, significantly reduce the extent of exercise-induced myocardial ischemia as assessed by exercise thallium-201 SPECT. (J Am Coll Cardiol 1997;30:125–30)
  • A large multisite, randomized, double-blind, controlled trial funded by Pfizer, Inc. examined efficacy and safety of varenicline for smoking cessation in patients with cardiovascular disease. A total of 714 patients with stable, documented CVD (other than hypertension alone) diagnosed for greater than 2 months were enrolled. Participants were randomized to 12 weeks of varenicline or placebo and monitored over 52 weeks. Rigotti NA, Pipe AL, Benowitz NL, Arteaga, C, Garza, D, & Tonstad, S. (2010) Efficacy and safety of varenicline for smoking cessation in patients with cardiovascular disease: a randomized trial. Circulation; 121:221-9.
  • A large multisite, randomized, double-blind, controlled trial funded by Pfizer, Inc. examined efficacy and safety of varenicline for smoking cessation in patients with cardiovascular disease. A total of 714 patients with stable, documented CVD (other than hypertension alone) diagnosed for greater than 2 months were enrolled. Participants were randomized to 12 weeks of varenicline or placebo and monitored over 52 weeks. Rigotti NA, Pipe AL, Benowitz NL, Arteaga, C, Garza, D, & Tonstad, S. (2010) Efficacy and safety of varenicline for smoking cessation in patients with cardiovascular disease: a randomized trial. Circulation; 121:221-9.
  • Varenicline was well tolerated, demonstrated a favorable safety profile, and was associated with no difference from placebo in rates of cardiovascular events or deaths. The most frequent adverse events in the varenicline group were nausea (30%), headache (13%), insomnia (12%), vomiting (8%), and abnormal dreams (8%). Serious adverse events occurred in 6.5% of participants in the varenicline group and 6% in the placebo group. There were no serious adverse event reports of depression, suicidality, or abnormal behavior. The study was presented at the American College of Cardiology meeting in Orlando, Florida, on March 31, 2009. The manuscript reporting study findings is under review for publication. Nancy Rigotti, MD, was the study PI.
  • RCTs, and Quasi-randomized trials (50 trials total). Follow-up for at least six months. Rigotti NA, Clair C, Munafò MR, Stead LF. Interventions for smoking cessation in hospitalised patients. Cochrane Database Syst Rev. 2012 Jan;5(5):CD001837. Meta-analysis: 50 trials included Counselling in hospital plus supportive follow-up one month after discharge: RR=1.37
  • Aziz et al. (in press) conducted a meta-analysis of the literature to examine smoking cessation outcomes following behavioral smoking cessation interventions versus usual care in hospitalized cardiovascular patients. The authors identified 11 randomized trials containing 2,751 hospitalized cardiovascular patients. The trials were published between 1990 and 2007. The analyses examined the point-prevalence abstinence rates for behavioral interventions ( n  = 1,419) versus usual care ( n  = 1,332). Overall quit rates were 42% for the behavioral interventions compared to 34% in usual care. Higher quit rates were found in studies of interventions that had greater than six interactions ( OR = 1.67), that were of greater duration and intensity ( OR = 3.17), and that provided concurrent use of nicotine replacement or bupropion ( OR = 2.13). The authors concluded that behavioral smoking cessation interventions initiated during hospitalization result in a significantly higher quit rate compared to usual smoking cessation advice. Aziz O, et al. (2009). Behavioural interventions for smoking cessation in patients hospitalised for a major cardiovascular event. International Journal of Cardiology, 137, 171-4
  • The World Heart Federation has a goal to reduce global CVD deaths by 25% by 2025; Cardiologists have an important role to play in this goal by helping reduce the toll of tobacco use and secondhand smoke on cardiovascular disease; cardiologists are an important point of front-line contact with their patients, and are a respected and trusted source of health advice. Quit smoking and serve as non-tobacco using role model Approach tobacco use as a chronic disease and document smoking status of all patients Advise tobacco users to quit, and nonsmokers to avoid secondhand smoke Ensure that smoking cessation support is widely accessible and that health and educational facilities where you work are smoke-free Educate medical students and trainees on impact of tobacco use and exposure and equip them with the skills to address these issues Support implementation of the FCTC Call on professional networks and associations to comply with the Code of Practice on Tobacco Control for Health Professionals Organizations Refuse to collaborate with the tobacco industry in research, reviews, promotion or other activities and never accept industry funding Note: See the Code of Practice on Tobacco Control for Health Professionals Organizations, the code is available in all WHO languages at: http://www.who.int/tobacco/communications/events/codeofpractice/en/

Transcript

  • 1. www.globalbridges.org
  • 2. CONSUMO Y EXPOSICIÓN AL HUMO DEL TABACO Y SALUD CARDIOVASCULAR Dr. Eduardo Bianco Director para Latinoamérica de FCA Presidente , CIET Uruguay
  • 3. Rx for Change Internacional Cardiologia Curso de Entrenamiento en Cesación de Tabaquismo para cardiólogos clínicos Cardiology Rx for Change fue desarrollado con el financiamiento de l Flight Attendant Medical Research Institute y la Fundación de la Familia Charles Schwab . La World Heart Federation ha adoptado este recurso como parte de un proyecto financiado por una beca de educación médica irrestricta de Pfizer, Inc.
  • 4. RECONOCIMIENTOS  Project PI: Alice Granger-Gasser  Curriculum desarrollado por: Judith Prochaska, PhD, MPH  Colaboradores en el estudio:  Neal Benowitz, MD Eduardo Bianco, MD  Ding Rong Jing, MD Georges Saade, MD  Staff de apoyo: Sara Hitchman, PhD & Nicholas Orozco, MD  Apoyo en beca: Steven Schroeder, MD & Margaret Meriwether, PhD  Expertos revisores:  Mira Aghi, PhD Stanton Glantz, PhD Tom Glynn, PhD, MS, MA  Richard Hurt, MD Harry Lando, PhD Lisa Kroon, PharmD  William Oetgen, MD Andrew Pipe, MD Martin Raw, PhD  Nancy Rigotti, MD Robert West, PhD Adaptación Internacional del curriculum fue liderada por:
  • 5. Temas a abordar  ¿Qué grado de conocimiento tiene el público y de compromiso los cardiólogos, con respecto a tabaco y salud CV?  Repasaremos el daño CV causado por el tabaco y sus mecanismos.  Exposición al humo del tabaco y daño CV  Medicamentos para dejar de fumar y sistema CV  Abordaje del paciente CV hospitalizado.
  • 6. Conciencia de Riesgo CV por fumar- Estudio ITC
  • 7.  Una encuesta anónima a cardiologos en España  11% (328) respondieron ( el mejor escenario)  3 de cada 4 dijo que siempre preguntaba a sus pacientes acerca de su tabaquismo y recomendaba a los fumadores el abandono  1 de cada 5 tenía material impreso sobre cesación en el consultorio  2 de cada 5 hacía seguimiento para evaluar progresos  La mayoría no estaba familiarizado con las medicaciones para cesación (73%) y querian mejorar sus habilidades en tratamiento (71%) CARDIOLOGOS CLÍNICOS de España
  • 8. REPASANDO EL DAÑO CARDIOVASCULAR CAUSADO POR EL TABACO Y SUS MECANISMOS
  • 9. Tabaco : Aumenta Trombogenicidad  El factor tisular (TF) está altamente presente en placas ateroscleroticas y puede jugar un rol en la trombosis  TF fue evaluado por factor Xa (FXa)  Los fumadores tienen significativos mayores niveles de actividad de TF circulante que los no fumadores Sambola et al. Circulation. 2003;107:973-977. 217 283 0 100 200 300 400 Current Smokers Prior to Smoking 2 Cigarettes Current Smokers After Smoking 2 Cigarettes FactorXa(FXa)pmol/L/min P=.003
  • 10. Tabaco : Disfunción endotelial Lavi et al. Circulation. 2007;115:2621-2627.  Los fumadores tienen más frecuentemente disfunción endotelialLos fumadores tienen más frecuentemente disfunción endotelial epicardica que los no fumadoresepicardica que los no fumadores EndothelialDysfunction(%) P=.03 60 45 30 15 0 Nonsmokers Ex-smokers Current Smokers 46% 34%35%
  • 11. Tabaco: Aumenta Número Leucocitos  Elevación de Leucocitos se ha asociado a mayor riesgo CV.  Fumadores tienen leucocitosis más elevada que no fumadore Lavi et al. Circulation. 2007;115:2621-2627; Stewart et al. Circulation. 2005;111:1756-1762 8 6 4 2 0 P<.0001 P=.03 P<.0001 P<.0001 CellCounts(109 /L) Fumadores Ex-fumadores GB Neutrofilos Linfocitos Monocitos No fumadores
  • 12. Tabaquismo: Aumenta estrés oxidativo a F2-isoprostane 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. 640 560 480 400 320 240 160 80 Current Smokers Nonsmokers FreeF2-Isoprostanesa (pmol/L) 1000 900 800 700 600 500 400 300 Current Smokers Nonsmokers EsterifiedF2-Isoprostanesa (pmol/L)
  • 13. Tabaquismo: Reduce la biosíntesis de Oxido Nitrico (NO) Barua et al. Circulation. 2001;104:1905-1910. 5000 0 No fumadores Fumadores 4000 3000 2000 1000 NOConcentration(nmol/L) P<.0001 1266 3613
  • 14. EFECTOS del Fumar y SHS sobre el Sistema CARDIOVASCULAR  Activación Plaquetaria  Disfunción Endotelial  Inflamacion e infeccion  Aterosclerosis  Bajos niveles HDL  Inestabilidad Plaquetas  Aumento oxidación LDL  Estres Oxidativo  Metabolismo Energético disminuido  Aumento de la Resistencia a la Insulina  Resultando en:  Aumento tamaño IAM  Disminución de variabilidad de FC  Aumento de rigidez parietal  Aumento de riesgo de eventos coronarios agudos Barnoya & Glantz. (2005). Circulation111:2684-
  • 15. MECANISMOS FISIOPATOLÓGICOS de la Enf CV relacionados al TABAQUISMO OXIDANT CHEMICALS OTHER COMBUSTION PRODUCTS Inflammation Reduced Oxygen Availability Platelet Activation/ Thrombosis Coronary Vasoconstriction Increased Myocardial Oxygen Demand Reduced Myocardial Oxygen Supply Myocardial Ischemia Myocardial Infarction Sudden Death CARBON MONOXIDE NICOTINE Increased heart rate Increased blood pressure Increased myocardial contractility PARTICULATES Sympathetic nervous system activation Endothelial dysfunction
  • 16. Tabaquismo: Aumenta mortalidad coronaria 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. 1987;317(21):1303-1309. 1.0 5.4 3.7 1.7 0 2 4 6 8 10 12 RelativeRisk(95%CI)RelativeRisk(95%CI)a Fatal CADFatal CAD 1-14/Day1-14/DayNonsmokersNonsmokers 15-24/Day15-24/Day ≥≥25/Day25/Day
  • 17. Tabaquismo: Efecto sobre Coronariopatía Waters et al. Circulation. 1996;94:614-621. 0 10 20 30 40 50 60 Progresion Lesiones Patients(%) FumadoresNo fumadores 0 10 20 30 40 50 60 Formacion de nuevas Lesiones Patients(%) FumadoresNo Fumadores P=.002 P=.007 5757 3737 3636 2020
  • 18. Tabaquismo: Aumento de riesgo de IAM no fatal  Tabaquismo triplica el riesgo de IAM no fatal comparado con no fumadores. 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. 2006;368:647-658. OddsRatio(95%CI)OddsRatio(95%CI)aa 1010 99 88 77 66 55 44 33 22 11 00 Age <40 yAge <40 y Age 40-49 yAge 40-49 y Age 50-59 yAge 50-59 y Age 60-69 yAge 60-69 y Age >70 yAge >70 y ≥≥2020NonsmokersNonsmokers Ex-smokersEx-smokers 1-191-19
  • 19. Tabaquismo: Aumenta riesgo de muerte súbita cardíaca 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. 1995;91:1749-1756. 1.0 2.3 0.0 1.0 2.0 3.0 4.0 Nonsmokers Current Smokers RelativeRisk(95%CI)RelativeRisk(95%CI)aa
  • 20. Enfermedad Vascular Periférica asintomática: Aumenta riesgo 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;16:177-182. 1.0 2.8 1.6 0.0 1.0 2.0 3.0 4.0 OddsRatio(95%CI)OddsRatio(95%CI)aa Ex-fumadores FumadoresNo fumadores
  • 21. Tabaquismo y AAA: Aumenta Riesgo AAA= Abdominal Aortic Aneurysm 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 and sex. Vardulaki et al. Br J Surg. 2000;87(2):195-200. 1.0 5.5 0.7 3.0 2.9 0.0 3.0 6.0 9.0 12.0 OddsRatio(95%CI)a No fumadores 1 to 9 10 to 19 ≥2520 to 24 Cigarettes/Day Current Smokers
  • 22. 1.0 4.7 3.0 0 1 2 3 4 5 6 7 8 AAA: Fumadores tienen mayor riesgo que de Coronariopatía o Stroke.  La asociación entre tabaquismo y aneurisma aórtico es sustancialmente más fuerte que la asociación con enfermedad coronaria o cerebro vascular AAA= Abdominal Aortic Aneurysm; CAD=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. Lederle et al. J Vasc Surg. 2003(2);38:329-334. Aortic Aneurysm to CAD Aortic Aneurysm to Cerebrovascular Disease Never Smokers PooledEstimatesofRatioof CurrentSmokers’RRa P<.00001
  • 23. 1.00 2.30 2.00 1.40 0 1 2 3 Tabaquismo: Acelera la progresión de la Ateromatosis Aortica 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):2156-2162. RelativeRisk(95%CI)a Never Smokers 1 to 9 10 to 19 ≥20 Cigarettes/Day Current Smokers
  • 24. 20 30 40 50 progresion de Aterosclerosis Carotídea  Tanto fumar como exponerse al humo del tabaco estan asociados con acelerar la progresion de la aterosclerosis carotídea. 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. 1998;279(2):119-124. Ex-fumadores con Exposiciónb FumadoresNo fumadores no Expuestosb ProgressionofIntima-Medial Thickness,µm/3y(95%CI)a Ex-fumadores sin Exposiciónb No fumadores Expuestosb 43.043.0 38.838.8 31.631.6 32.832.8 25.925.9
  • 25. Tabaquismo y Stroke  El tabaquismo sería responsible del 12% al 14% de las muertes por stroke .  Fumar puede potenciar los efectos de otros factores de riesgo  Fumar aumenta riesgo de stroke  Agudo: efectos sobre formación de trombos  Cronico: aumenta la carga de enfermedad aterosclerótica MRI Cerebral con Stroke Isquémico AgudoGoldstein et al. Stroke. 2006;37:1583-1633;. Accessed October 19, 2007.
  • 26. 0 2 4 6 8 10 12 Tabaquismo: Aumenta riesgo de Stroke Hemorrágico 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;34:2792-2795. Total Stroke Hemorrágico RelativeRisk(95%CI)a Hemorragia Intracerebral Hemorragia Subaracnoidea Nonsmokers (n=20,339) <15 Cigarettes/day (n=1914) ≥15 Cigarettes/day (n=3265) 2.062.06 3.433.43 2.392.39 2.892.89 1.741.74 4.044.04
  • 27. EXPOSICIÓN AL HUMO DEL TABACO Y ENFERMEDAD CARDIOVASCULAR
  • 28. FALTA DE CONCIENCIA DE QUE EL SHS CAUSA ENFERMEDAD CV  Aunque los fumadores generalmente son conscientes de los efectos del tabaquismo sobre la salud respiratoria , pocos tienen conciencia de los efectos CV: Encuesta Mundial de Tabaquismo en Adultos (GATS): En Viet Nam (85.9%) y China (57.5%) la mayoría de los fumadores no tienen conocimiento de que el SHS causa enfermedad cardícaca. Estudio Internacional sobre Control del Tabaco (ITC): En Mexico (24.3%), Australia (48.6%), y Corea del Sur (43.4%) muchos fumadores no son conscientes de que el SHS daña la salud CV.
  • 29. USDHHS. (2006). The Health Consequences of Involuntary Exposure to Tobacco Smoke: Report of the Surgeon General. Institute of Medicine. Secondhand Smoke Exposure and Cardiovascular Effects : Making Sense of  the Evidence. Exposure. Washington, D.C.: The National Academies Press; 2010.  La exposición al humo del tabaco (EHT) causa muerte y enfermedad prematura en no fumadores :  Efectos adversos inmediatos sobre el sistema CV – los mismos efectos que el consumo de tabaco  Aumenta el riesgo de cardiopatía y cáncer de pulmón.  La prohibición de fumar en espacios públicos reduce la exposición al humo y los eventos cardíacos agudos. EXPOSICIÓN AL HUMO DEL TABACO Y ENF CV No existe nivel mínimo seguro de exposición al humo del tabaco .
  • 30. Activación plaquetaria y HSM La exposición durante 60 minutos al HSM aumenta la activación plaquetaria; exposiciones repetidas durante varios días llevan a los no fumadores a niveles comparables a los fumadores. *P>0.05. Circulation 2005;111:2684-98
  • 31. META-ANALISIS de RIESGO CV DEBIDO a EXPOSICIÓN CRÓNICA al Humo del Tabaco entre NUNCA FUMADORES  Overall RR = 1.78 para fumadores  Overall RR = 1.31 para expuestos al humo del tabaco. 1 1.2 1.4 1.6 1.8 2 Never Smoker SHS Never Smoker Active Smoker Barnoya & Glantz. (2005). Circulation111:2684–2698. La exposición crónica al Humo del Tabaco en el trabajo u hogar está asociada a un 30% de incremento de riesgo de CHD en adultos no fumadores. Relativerisk N = 29 studies
  • 32. Copyright ©2004 BMJ Publishing Group Ltd. Whincup et al. (2004). BMJ 329:200-205. "Light passive" refers to the lowest quarter of cotinine concentration among nonsmokers (0-0.7 ng/ml), "heavy passive" to the upper three-quarters of cotinine concentration combined (0.8-14.0 ng/ml), "light active" to men smoking 1-9 cigarettes a day. ESTAR FUERTEMENTE EXPUESTO AL HUMO DEL TABACO ES COMO SER UN FUMADOR LIVIANO
  • 33. Exposición al Humo del Tabaco: Riesgo de Infarto Agudo de Miocardio (IAM) . Adapted from Teo et al. Lancet. 2006;368:647-658. No fumadoresNo fumadores OddsRatio(95%CI)OddsRatio(95%CI)aa Exposición al humo de tabaco ambiental (Horas por semana)Exposición al humo de tabaco ambiental (Horas por semana) NeverNever 1-71-7 8-148-14 15-2115-21 ≥≥2222 44 22 11 0.750.75  La exposición al humo de tabaco ambiental aumenta el riesgo deLa exposición al humo de tabaco ambiental aumenta el riesgo de IAM no fatal de manera gradualIAM no fatal de manera gradual
  • 34. , Oberg M, et al., Lancet. 2011. • Humo de Segunda Mano causa un estimado de 603,000 muertes prematuras cada año en el mundo • 87% de las muertes por SHS en adultos son debidas a cardiopatía isquémica Muertes a nivel Mundial por EXPOSICIÓN AL HUMO DEL TABACO Ischaemic heart disease 63% 379,000 deaths Lung cancer 4% 21,000 deaths Asthma 6% 37,000 deaths O s 0% >100 deaths Lower Respiratory Infec ons 27% 165,000 deaths El Humo de Segunda Mano (SHS) es el humo exhalado por fumadores o por combustión de tabaco
  • 35. Helena, Montana, EE.UU. Admisiones por IAM Año  En junio de 2002 se prohibió fumar en espacios cerrados  El 03/12/02 la medida fue impugnada a nivel estatal y se levantó
  • 36. REDUCIENDO EXPOSICIÓN A SHS DISMINUYEN INGRESOS POR IAM EN HOSPITALES Estudios reportando reduccion en ingresos por IAM/eventos coronarios agudos siguiendo la legislaciones sobre ambientes libres de humo One study has been published that did not detect evidence of a reduction in hospital admissions for acute heart disease (Edwards et al., 2008)
  • 37. Impacto de la prohibición de fumar sobre ingresos hospitalarios por IAM (Uruguay, 2004-2008) Hospital admissions for acute myocardial infarction before and after implementation of a comprehensive smoke-free policy in Uruguay. E. Sebrie´, E.Sandoya, A. Hyland, E. Bianco, S. A Glantz, K M Cummings, Tobacco Control ,2011. 22%
  • 38. Olmsted County AMI & SCD per 100,000 Population/Year Pre-Ordinance Post-Ordinance Hurt R.D. et al Arch TNT Med
  • 39. Asociación dosis- respuesta entre exposición al humo del tabaco y enfermedad isquémica cardíaca. NO ES UNA RESPUESTA LINEAL . Pechacek, T. F et al. BMJ 2004;328:980-983 (Adapted from Law and Wald) . Agregación plaquetaria y trombosis Otros factores
  • 40. Al dejar de fumar … < 30 min 8 hr 24 hr 48 hr 72 hr 2-12 sem 1 año 3 años 5-15 años Presión arterial y pulso retornan a normalidad Niveles de CO en sangre retornan a normales Mejora Endotelio, disminuye chance Evento CV Terminaciones nerviosas comienzan a regenerar Respirar es más fácil; aumenta capac pulmonar Func Pulmonar aumenta30%; circulación mejora Riesgo CV mitad del fumador Riesgo de AMI es similar a nunca fumadores Riesgo Stroke reducido al de nunca fumadores
  • 41.  Los tratamientos habituales reducen el riesgo de muerte en pacientes con enfermedad CV en 15–35%  Aspirina = 15%  Beta bloqueantes = 23%  ACE inhibidores = 23%  Estatinas = 29–35%  El abandono del tabaquismo en pacientes con enfermedad CV reduce el riesgo muerte en 36% y el riesgo de futuros eventos cardíacos en 50% LA CESACIÓN DE TABAQUISMO es un TRATAMIENTO para la Enf CV
  • 42. El TRATAMIENTO del TABAQUISMO es el GOLD STANDARD Intervencion Resultado NNT Estatinas Previene 1 muerte cada 5 años 107 Aspirina Previene 1 IAM cada 5 años 118 Tratamieno Antihipertensivo Previene 1 stroke, IAM,muerte cada año 700 Screening de cáncer cervical Previene 1 muerte cada 10 años 1140 5 min consejo médico cesación Previene 1 muerte prematura 80 + medicación para cesación Previene 1 muerte prematura 38-56 + apoyo conductual Previene 1 muerte prematura 16-40 Anthorison, 2006, Ann Intern Med; McQuay & Moore, 2006, Bandolier; Gates 2001, Am Fam Phys; Cochrane Reviews by Stead, Bergeson, et al., 2008; Stead, Perera, et al. 2012; Stead & Lancaster, 2012; Cahill et al., 2010; and USPSTF, 2009 NNT = Número necesario de tratar
  • 43. MORTALIDAD CV Y TABAQUISMO WHO Global Report: Mortality Attributable to Tobacco. World Health. Geneva; 2012.  Mundial: 10% de todas las muertes CV en adultos + 30 años son atribuibles al tabaco  Varía según region: Africa: 4%, Americas: 15%, Sudeste Asiático: 9%, Europa: 15%, Mediterraneo Oriental: 8%, Pacifico Occidental: 6% ¿Qué proporción de su práctica dedica UD al problema del tabaco?
  • 44. MOTIVAR PARA EL CAMBIO... A. Pipe (2013). Ottawa Model for Smoking Cessation “Los fumadores no necesitan más información…o discursos. Quieren ayuda”.
  • 45. MEDICACIONES PARA DEJAR DE FUMAR Y SISTEMA CV
  • 46. Nicotina en TRN vs. Fumada  Absorción más lenta (efectos menos agudos)  Absorción venosa  No CO! No oxidantes!  Respuesta simpáticomimética atenuada  Curva dosis-respuesta de nicotina y efectos CV aplanada  Más de 7000 químicos
  • 47. Mahmarian et al. (1997) JACC 30:125-130. PARCHE DE TRN REDUCE ISQUEMIA MIOCÁRDICA INDUCIDA POR EJERCICIO en FUMADORES con CAD Total and reversible perfusion defect size both  when on the patches. Only baseline PDS and final CO significantly predicted the final defect size Fumadores con CAD usando parches de nicotina : Compared to baseline smoking, use of the 14mg & 21mg patch led to  Plasma nicotine & cotinine &  Expired CO & cigarettes/day
  • 48. La TRN NO tiene riesgo Cardiovascular La seguridad de TRN en pacientes CV es apoyada por evidencia : RCTs, estudios de eficacia, datos observacionales , y estudios fisiológicos. Joseph et al., Prog in CVD, 2003 Altas dosis de nicotina, aú fumando, no causaron efectos cardiovasculares en el corto plazo Zevin, Peyton, Benowitz, Clin Pharmacol Ther, 1998 El uso de TRN no está asociada con ningún incremento del riesgo de IAM, ACV, o muerte. N=33,247 Hubbard et al., Tob Control, 2005
  • 49. con CVD: EFICACIA Y SEGURIDAD  Estudio de 629 pacientes con cardiopatía estable documentada (diferente de HTA aislada) con diagnóstico > 3 meses  49% AMI, 42% procedimientos cardiacos, 35% angina estable, 33% AOC, 6% falla cardíaca  Randomizados 7 weeks bupropion o placebo  Monitorizados por 52 semanas  Estudio multicéntrico financiado por GSK Tonstad et al. (2003). Euro Heart J; 24:946-55.
  • 50. BUPROPION: EVENTOS ADVERSOS  Los eventos adversos más frecuentes fueron :  Insomnio (24%), boca seca (18%), nauseas (13%), cefalea (11%), mareos (8%), constipacion (5%), sudoración (5%)  Discontinuación debido a efectos adversos: 5% para bupropion vs. 6% en placebo  No impacto sobre signos vitales como Presión Arterial  Serios Eventos Adversos ocurrieron in 2.6% con bupropion vs. 1.3% en placebo  No reportes de depression, intentos de suicidios , o comportamiento anormal  Eventos CV 1.2% bupropion vs. 0.6% placebo  Muertes 0.6% bupropion o placebo  Abandono comparable entre placebo (6%) y bupropion (5%) Tonstad et al. (2003). Euro Heart J; 24:946-55.
  • 51. VARENICLINA: RIESGO CV  3 meta-analisis sobre vareniclina y riesgo CV  Diferentes conclusiones  Si hay , es pequeño  “Estos eventos fueron poco frecuentes tanto el grupo de Varenicle como en el de placebo, y el incremento de riesgo no fue estadísticamente significativo” – FDA Singh et al (2011) CMAJ Prochaska & Hilton (2012) BMJ Chantix product label
  • 52. VARENICLINE en PACIENTES con CVD: EFICACIA Y SEGURIDAD  Estudio de 714 pacientes con cardiopatía estable documentada ( diferente de hipertensión arterial sola) diagnosticada por > 2 meses  51% angina, 49% AMI, 49% Revascularización coronaria  Randomizado: 12 semanas vareniclina o placebo  Seguimiento: 52 semanas  Multicéntrico financiado por Pfizer, Inc. Rigotti et al. (2010). Circulation; 121:221-9.
  • 53. VARENICLINA: EFECTOS ADVERSOS  Los efectos adverso más frecuentes fueron :  Nauseas (30%), cefalea (13%), insomnio (12%), vomitos (8%), y sueños anormales (8%)  Discontinuación por Efectos Adversos : 10% varenicline vs. 4% placebo  Efectos Adversos Serios ocurren en 6.5% con varenicline vs. 6% con placebo  No reportes de depresion, suicidio , o comportamiento anormal  Eventos CV 7% varenicline vs. 6% placebo  Muertes CV 0.3% varenicline vs. 0.6% placebo  Mayor abandono con placebo (20%) vs. varenicline (15%)
  • 54. TRABAJOS DE CESACIÓN en PACIENTES HOSPITALIZADOS  Mayores tasas de cesación entre pacientes hospitalizados  Ingresados por Enf CV, RR=1.42  Proporcionado por unidad de consejo con seguimiento de apoyo por >1 mes luego del alta , RR=1.37  Recibieron TRN, RR=1.54  No efectos con intervenciones menos intensas  Insuficiente evidencia para agregar bupropion (3 estudios) or vareniclina (2 estudios) Rigotti, NA, Cochrane Database Syst Rev., 2012 Meta-analysis, 25 trials
  • 55. TRATAMIENTO DEL TABAQUISMO en PACIENTES HOSPITALIZADOS por ENF CV • Tasas de cesación: intervencion (42%) vs. cuidado usual (34%) • Pacientes abandonarán más frecuentemente si se proporciona tratamiento: • 6+ interacciones: OR = 1.67 • Mayor duración e intensidad: OR = 3.17 • Agregado de TRN o bupropion: OR = 2.13 Intervenciones conductuales de cesación iniciadas durante hospitalización resultan en una significativa mayor tasa de abstinencia comparado con el consejo de abandono habitual . Aziz et al. (2009). Int J Cardiology. Meta-analysis of 11 RCTs (N=2751), 1990-2007
  • 56. PRINCIPIO FUNDAMENTAL Tratar el Tabaquismo de exactamente la misma manera en UD maneja cualquier otro factor de riesgo cardiovascular A. Pipe (2013) The Ottawa Model of Smoking Cessation
  • 57. Ser un modelo no fumador Aborde el tabaquismo como una enfermedad crónica; registre el estado de fumador Aconsejar el abandono a todos los fumadors y a todos los pacientes que eviten exponerse al humo Apoye Centros de Salud y Educativos Libres de Humo Ofrezca a los estudiantes capacitación y motivación para tratar el tabaquismo Apoye el CMCT Cumpla con el Código de Práctica de los Profesionales de la Salud sobre el Control del tabaco Rechace colaborar y recibir financiación de la Industria del tabaco Asegure que el apoyo para cesación es accesible Ayudar a reducir la mortalidad CV prematura en un 25% para el 2025 Los cardiólogos tenemos una gran responsabilidad
  • 58. MUCHAS GRACIAS! biancoeduardo1@gmail.com