Managing Tobacco Use
Managing Tobacco Use
Tobacco use is a well-established risk factor for CVD incidence and mortality. Smoking increases an individual's risk of death from all vascular diseases two- to three-fold (Figure 1). Worldwide, 10–30% of all CVD deaths are attributable to tobacco. Among men aged 30–44 years, however, 48% of cardiovascular deaths are attributable to tobacco use. Smokers' excess risk of CVD increases with number of cigarettes smoked daily, but exists even for smokers of one to five cigarettes per day. Few data exist about occasional (non-daily) smoking, but in one study men but not women who smoked cigarettes occasionally had an increased risk of total and cardiovascular mortality.
(Enlarge Image)
Figure 1.
Cardiovascular mortality for current smokers compared to never smokers (hazard ratios were adjusted for age, educational level, alcohol consumption, and body-mass index. Adapted from Jha et al.). HR, hazard ratios; CI, confidence intervals.
Cigarette smoking has been specifically identified as a cause of coronary heart disease (CHD) [including myocardial infarction (MI) and sudden death], cerebrovascular disease (stroke), peripheral artery disease (PAD), and abdominal aortic aneurysm. Smokers risk of heart failure is twice the risk of non-smokers, and smokers with heart failure have a worse prognosis than non-smokers with heart failure. Smoking can also induce and worsen serious cardiac arrythmias by many mechanisms.
Among individuals with established CVD, smoking reduces the success of treatments. Smokers who undergo percutaneous coronary interventions (PCIs) or coronary artery bypass graft surgery are at increased risk of myocardial re-infarctions and death compared with non-smokers. Current smoking is an independent predictor of long-term stent thrombosis after PCIs. Cigarette smoking also influences the efficacy of antiplatelet therapies. It is correlated with aspirin resistance, probably due to its stimulating effect on platelet aggregation. Cigarette smoking (but not nicotine alone) induces the cytochrome P450 1A2 (CYP1A2), which is involved in the metabolism of clopidogrel. This results in greater inhibition of platelet aggregation in smokers compared with non-smokers. This finding is corroborated by a study suggesting that clopidogrel is effective in smokers with CVD to preventing all-cause and cardiovascular mortality but not in non-smokers or former smokers. Newer antiplatelet therapies (prasugrel, ticagrelor, and ticlopidine) do not seem to be influenced by smoking.
The cardiovascular risk of tobacco use is not limited to smokers. Non-smokers who are regularly exposed to other people's tobacco smoke also have an increased risk of CVD. Exposure to secondhand smoke (SHS) increases the risk of CHD morbidity and mortality by 25–30% among non-smokers. Globally, CVD is responsible for >87% of the estimated 430 000 adult deaths caused by SHS. The risk is rapidly reversible, as shown in multiple studies documenting a rapid decline in hospital admissions for MI after the adoption of smoking bans. In a meta-analysis of 11 studies assessing the cardiovascular benefits of bans on smoking in public places, there was an overall 17% decreased risk of acute MI after implementation of smoking bans in public places. A Cochrane review has also shown a consistent reduction in hospital admissions for cardiac events after smoking bans have been implemented.
Cardiovascular Risks of Cigarette Smoking and Exposure to Secondhand Smoke
Tobacco use is a well-established risk factor for CVD incidence and mortality. Smoking increases an individual's risk of death from all vascular diseases two- to three-fold (Figure 1). Worldwide, 10–30% of all CVD deaths are attributable to tobacco. Among men aged 30–44 years, however, 48% of cardiovascular deaths are attributable to tobacco use. Smokers' excess risk of CVD increases with number of cigarettes smoked daily, but exists even for smokers of one to five cigarettes per day. Few data exist about occasional (non-daily) smoking, but in one study men but not women who smoked cigarettes occasionally had an increased risk of total and cardiovascular mortality.
(Enlarge Image)
Figure 1.
Cardiovascular mortality for current smokers compared to never smokers (hazard ratios were adjusted for age, educational level, alcohol consumption, and body-mass index. Adapted from Jha et al.). HR, hazard ratios; CI, confidence intervals.
Cigarette smoking has been specifically identified as a cause of coronary heart disease (CHD) [including myocardial infarction (MI) and sudden death], cerebrovascular disease (stroke), peripheral artery disease (PAD), and abdominal aortic aneurysm. Smokers risk of heart failure is twice the risk of non-smokers, and smokers with heart failure have a worse prognosis than non-smokers with heart failure. Smoking can also induce and worsen serious cardiac arrythmias by many mechanisms.
Among individuals with established CVD, smoking reduces the success of treatments. Smokers who undergo percutaneous coronary interventions (PCIs) or coronary artery bypass graft surgery are at increased risk of myocardial re-infarctions and death compared with non-smokers. Current smoking is an independent predictor of long-term stent thrombosis after PCIs. Cigarette smoking also influences the efficacy of antiplatelet therapies. It is correlated with aspirin resistance, probably due to its stimulating effect on platelet aggregation. Cigarette smoking (but not nicotine alone) induces the cytochrome P450 1A2 (CYP1A2), which is involved in the metabolism of clopidogrel. This results in greater inhibition of platelet aggregation in smokers compared with non-smokers. This finding is corroborated by a study suggesting that clopidogrel is effective in smokers with CVD to preventing all-cause and cardiovascular mortality but not in non-smokers or former smokers. Newer antiplatelet therapies (prasugrel, ticagrelor, and ticlopidine) do not seem to be influenced by smoking.
The cardiovascular risk of tobacco use is not limited to smokers. Non-smokers who are regularly exposed to other people's tobacco smoke also have an increased risk of CVD. Exposure to secondhand smoke (SHS) increases the risk of CHD morbidity and mortality by 25–30% among non-smokers. Globally, CVD is responsible for >87% of the estimated 430 000 adult deaths caused by SHS. The risk is rapidly reversible, as shown in multiple studies documenting a rapid decline in hospital admissions for MI after the adoption of smoking bans. In a meta-analysis of 11 studies assessing the cardiovascular benefits of bans on smoking in public places, there was an overall 17% decreased risk of acute MI after implementation of smoking bans in public places. A Cochrane review has also shown a consistent reduction in hospital admissions for cardiac events after smoking bans have been implemented.
