Tobacco smoke is also an important cause of stroke. The Framingham study followed a cohort of over 4,000 people for 26 years and reported a significant increase in stroke risk in smokers compared to nonsmokers (Wolf et al. 1988). Additionally, a dose–response curve was evident, with heavy smokers at much greater risk compared to light smokers. Excess stroke risk reduced to nonsmoker levels 5 years after quitting smoking. A meta-analysis of 32 studies investigating the risk of stroke associated with cigarette smoke reported a relative risk of 1.5 (Shinton and Beevers 1989). Stroke risk in smokers is greater during middle age, with a risk of 2.9 under 55 years compared to 1.1 for smokers over 75, when stroke incidence is much higher in the general population. A recent review of studies conducted around the world put the excess risk of stroke in smokers at two to four times that of nonsmokers or those who had quit 10 years previously (Shah and Cole 2010).

The Framingham Heart Study reported an increase in sudden cardiac death for smokers compared to nonsmokers with a relative risk of 2.5 over 26 years of follow-up (Kannel et al. 1975). Other studies reported similar associations, for example, an odds ratio of 1.8 for sudden cardiac death in current smokers in the National Mortality Followback Survey (Escobedo and Caspersen 1997). Sudden cardiac death may or may not be preceded by diagnosis of CHD, and it may be the first sign of underlying heart disease. Two-thirds of sudden cardiac deaths due to acute coronary thrombosis occur in cigarette smokers.

It is generally accepted that a dose–response relationship exists between tobacco smoke and adverse cardiovascular outcomes (Fig. 8.2). Indeed, this is one of the features that allowed demonstration of a causal relationship. However, some studies do not support a linear relationship, and there is some evidence of a large effect from a small exposure. A meta-analysis of epidemiological studies found the risk of ischemic heart disease for smoking one cigarette per day to be approximately half that associated with a 20-a-day habit, but still 30 % more than unexposed nonsmokers (Law et al. 1997). Environmental exposure of individuals living with a smoker was similarly associated with a 30 % increased risk of heart disease, although the amount of smoke ingested is around 100 times less than that of an active smoker. This scale of effect from secondhand exposure was calculated as increasing the risk of CHD death in British nonsmoking men aged 60–69 from 5 to 6 % (Law et al. 1997). A prospective study conducted in Norway assessed the risks associated with smoking one to four cigarettes per day and reported that compared to never smokers, light smokers had a surprisingly high relative risk of 2.74 of ischemic heart disease mortality (Bjartveit and Tverdal 2005).

In recent years, and due to the indisputable evidence concerning the adverse health effects of cigarettes, low tar or “light” brands have been increasingly marketed as less harmful than ordinary cigarettes. There is some debate however as to the true nature of this harm reduction strategy. A large prospective study found modest reductions in coronary heart disease mortality associated with a 15 mg reduction in tar (Tang et al. 1995). However, a review of research undertaken in this area concluded that only a minority of studies examining cardiovascular endpoints had evidence to support reduced risk associated with low tar cigarettes and that the reduction was at best modest, cited as approximately 10 % (Kabat 2003). Furthermore, in a case–control study of MI patients, no reduction in MI risk was seen in smokers of low-yield cigarettes (Negri et al. 1993). While reductions in cancer risk may be greater due to reduced tar content, cigarette components other than tar, such as nicotine and carbon monoxide, are largely responsible for the increased CV risk seen in smokers. It has additionally been proposed that laboratory smoking machines which test tar yields do not accurately portray the way that cigarettes are smoked and that smokers may compensate when smoking “light” cigarettes by smoking more intensively.

Secondhand exposure to tobacco smoke, or passive smoking, is known to have severe adverse health outcomes, via the same mechanisms as active smoking. A study of the burden of disease resulting from secondhand smoke in 192 countries estimated that 40 % of children and 34 % of adult nonsmokers are exposed to tobacco smoke worldwide, causing an estimated 379,000 annual deaths from ischemic heart disease (Oberg et al. 2011). Furthermore, almost three million disability-adjusted life years were attributed to CHD caused by passive smoking. Passive smoking is estimated to increase the risk of CHD by approximately 25–30 % (Barnoya and Glantz 2005; He et al. 1999), while the increased risk of an acute cardiovascular event associated with regular exposure to secondhand smoke (SHS) has been reported to be as high as 90 % (Panagiotakos et al. 2002). Even occasional exposure was associated with a 26 % increased risk in the same study. Indeed, acute effects of SHS have been demonstrated within hours of exposure including endothelial dysfunction, reduced heart rate variability, and increased arrhythmia (Kato et al. 2006; Chen et al. 2008). Further studies have shown impaired endothelial function and oxidative stress resulting from exposure to as little as 30 min of SHS (Kato et al. 2006; Raupach et al. 2006; Otsuka et al. 2001; Heiss et al. 2008). It has been estimated that passive smoking causes between 21,000 and 75,000 CHD deaths and up to 128,000 MIs per year in the USA alone, entailing a yearly health bill of $2–6 billion (Lightwood et al. 2009).

A systematic review of the literature reported that the adverse effects of passive smoking can already be seen in children, with exposed children – measured by serum cotinine – showing unfavorable blood lipid profiles and decreased vascular function, predisposing them to develop CVD (Metsios et al. 2010). Randomized controlled trials specifically found impaired endothelial function and aortic elasticity in children exposed to secondhand smoke (Kallio et al. 2007). Inflammatory markers have also been shown to be increased in passive smokers. A British study found that healthy adults with high levels of cotinine from secondhand exposure had higher risk of all-cause and cardiovascular deaths, with around half of the elevated risk explained by higher levels of C-reactive protein (Hamer et al. 2010); while a parallel study found elevated fibrinogen and homocysteine levels associated with passive exposure (Venn and Britton 2007).

Many studies assessing the risks of passive exposure to tobacco smoke involve nonsmokers who live with smokers and are therefore exposed on a daily basis. Research has shown significant increases in both total and cardiovascular death rates in this population (Svendsen et al. 1987; Helsing et al. 1988; Sandler et al. 1989; Garland et al. 1985). Indeed, a review by Wells suggested that “ischemic heart disease appears to be by far the major mortality risk from passive smoking” (Wells 1994). A review of the literature reported the effects of SHS to be almost as large as that of active smoking (Barnoya and Glantz 2005), somewhat contradicting the dose–response theory. While smokers receive about 100 times more smoke than do those affected by secondhand smoke, the risks do not increase in a comparative fashion, for example, relative risks of developing CHD according to a meta-analysis were 1.8 for smokers compared to 1.3 for nonsmokers who live with smokers (Law et al. 1997). A large-scale study of nonsmokers living with smokers followed up for 12 years found a death rate of 1.2 compared to non-exposed individuals, a rate comparative to that of ex-smokers and light smokers and about half the rate of heavy smokers (Sandler et al. 1989). The risk of cardiovascular death was even higher, reported as 1.3 in exposed men and 1.2 in exposed women (Helsing et al. 1988). Multiple investigations have shown a greater risk of SHS exposure at a younger age (Helsing et al. 1988; Sandler et al. 1989).

There are several limitations inherent to research on SHS. Exposed individuals (i.e., living with a smoker) are frequently compared to unexposed individuals (i.e., those not living with a smoker); however, this dichotomy is rather crude, since people may be exposed to SHS in other places such as their place of work. Later studies used biomarkers such as cotinine (metabolized nicotine in the blood) to assess exposure to smoke, with levels in a multicity study indicating that even the “non-exposed” control group had some level of SHS exposure (Whincup et al. 2004). Exposure to passive smoking was reported to be associated with between 68 and 86 % of the risk of light smoking, defined as smoking less than ten cigarettes per day.

Recent evidence has accumulated concerning the dangers of thirdhand or environmental tobacco smoke, residual toxic compounds which remain on surfaces and in dust after a cigarette has been smoked. These are then reemitted into the air and react with other compounds, yielding secondary pollutants (Matt et al. 2011). An early study of this issue found household dust to contain modest amounts of nicotine (Hein et al. 1991). Thirdhand smoke is thought to particularly affect children living with smokers, where high levels of smoke pollution can be found on household materials. In a study of households with infants, levels of environmental smoke were five to seven times higher in smoking compared to nonsmoking households even when smokers actively tried to protect their children by smoking outdoors (Matt et al. 2004). Levels in households where smoking was permitted indoors were substantially higher. The health impact of thirdhand smoke remains controversial and requires further investigation.

Around the world, tobacco habits vary, and in some countries, smokeless tobacco – which includes wet and dry snuff and chewing tobacco – is very common. Since the adverse effects of smoking have come to light and received so much negative press, tobacco companies are seeking new products to sell, including smokeless tobacco, which is marketed as a healthier option. The worldwide Interheart study examined the risk of MI in different types of tobacco users and found that tobacco chewers had more than double the odds of suffering an MI compared to non-tobacco users (Teo et al. 2006). The Atherosclerosis Risk in Communities study also found increased cardiovascular risk in users of smokeless tobacco (Yatsuya and Folsom 2010). The AHA released a statement in 2010 affirming that while smokeless tobacco is less harmful than cigarettes, long-term use is associated with increased risk of fatal MI and stroke, as well as reducing post-MI survival odds (Piano et al. 2010).

Tobacco smoke has both acute and chronic effects, being associated with vascular inflammation and autonomic dysfunction (Wells 1994). The components of tobacco smoke which increase the risk of developing CVD are oxidizing chemicals, nicotine, carbon monoxide, and particulate matter which together produce a chronic inflammatory state (USDHHS 2010). Short-term effects include decreased platelet sensitivity leading to increased platelet aggregation and decreased oxygen supply to the heart (Wells 1994). Platelet aggregation and blood viscosity affect the blood lipid profile in the long term, increasing triglycerides and lowering high-density lipoprotein cholesterol (Blache et al. 1992), all factors which contribute to the development of CHD. Of the many toxic components of tobacco smoke, nicotine seems to be largely responsible for the change in platelets and increased heart rate and blood pressure (Davis et al. 1985), while the reduction in the blood’s ability to supply oxygen is due to a buildup of carbon monoxide (Wells 1994). Indeed, men who lived with smokers were found to have raised levels of expired carbon monoxide compared to controls (Svendsen et al. 1987). Longer-term effects of smoking begin from damage to the arterial endothelium and involve a buildup of plaque leading to atherosclerosis, increasing the risk of thrombosis, often detected via carotid artery wall thickness, and an imbalance of blood lipids.

The key pathways through which tobacco smoke causes and exacerbates CVD are atherosclerosis and endothelial injury (USDHHS 2004). Atheroma, the underlying pathological process preceding most coronary and cerebrovascular events, develops over years or decades. Atherosclerosis underlies CHD and involves a hardening of the arteries due to fat deposition and thickening of arterial walls, which cause a narrowing of the lumen and consequently reduced blood flow. A thrombus or clot can then form and break off, causing an infarct or stroke. The toxic components of tobacco smoke affect these processes. The 2004 Surgeon General’s report found sufficient evidence to infer a causal relationship between smoking and subclinical atherosclerosis, the early development of atherosclerosis before clinical symptoms manifest (USDHHS 2004). The effects of smoking can be seen in the carotid and popliteal arteries, with greater presence of atherosclerosis. While earlier studies examined the correlation between smoking and cardiac endpoints such as MI or cardiac death, more recent research has investigated earlier effects which begin the cascade of events and go further in explaining the pathogenic pathways. Carotid intima medial thickness is often used as a marker of atherosclerosis since it is a subclinical sign yet is related to both CHD and stroke. Coronary calcium can also be measured to assess the presence of atherosclerosis. The Atherosclerosis Risk in Communities study followed up healthy participants for 3 years and found that smoking was strongly related to carotid atherosclerosis after controlling for age, with smokers showing greater intima medial thickness and incidence of CHD events (Sharrett et al. 1999). Studies have shown that atherosclerosis is already present at a young age, for example, an autopsy study of young people aged 15–34 showed atherosclerotic lesions in the carotid artery of the majority, increasing with age (Strong et al. 1999). Lesions have been shown to progress more rapidly in smokers compared to nonsmokers.