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1.1 Tobacco smoke exposure and cardiovascular disease More than 1 in every 10 cardiovascular deaths in the world during the year 2000 were attributable to smoking, demonstrating that it is an important preventable cause of cardiovascular mortality (Ezzati et al., 2005). It has been clearly established that exposure to environmental tobacco smoke increases the risk of cardiovascular disease among persons who have never smoked (Steenland, 1992). The cardiovascular effects of secondhand smoke are nearly as large as those confronting the principal smoker (Barnoya & Glantz, 2005). Non-smokers living with smokers have about a 25% increase in risk of death from heart disease and are more likely to suffer a stroke. Exposure to secondhand smoke may increase the risk of heart disease by non-smokers as much as 60% (Whincup et al., 2004). In 2004, Ong & Glantz estimated that only about 69% of U.S. indoor workers were covered by a smoke-free workplace policy. Making all workplaces smoke free as been accomplished for the commercial aircraft industry (Repace, 2004) would in one year prevent about 1500 myocardial infarctions and 350 strokes, and result in nearly 49 million dollars in savings in direct medical costs. These estimates are supported by reports of reduced incidence of admissions for myocardial infarction associated with smoking bans (Sargent et al., 2004). The cardiovascular effects of tobacco smoke exposure have been summarized in several excellent reviews (for example, see Barnoya and Glantz, 2005). Among the strongest pathophysiological correlates of tobacco smoking are accelerated endothelial dysfunction (Puranik & Celermajer, 2003) and acute clinical events, the latter being largely thrombotic (Ambrose & Barus, 2004). Recent studies indicate that increased oxidative stress is a potential mechanism for initiating cardiovascular dysfunction (Yang et al., 2004; Talukder et al, 2011). Tobacco smoke has also been demonstrated to increase inflammatory markers in patients exposed to secondhand smoke, including homocysteine, C-reactive protein, fibrinogen, and oxidized LDL cholesterol, (Panagiotakos et al., 2004) suggesting that an increased inflammatory response may contribute to accelerated atherosclerosis. Clearly, the incidence of ischemic coronary and peripheral vascular disease is increased in patients exposed to tobacco smoke, either as smokers or through exposure to secondhand tobacco smoke (Ambrose & Barus, 2004; Benowitz, 2003; Law & Wald, 2003; Burns, 2003; Leone et al., 2004). The cardiovascular effects of tobacco smoke exposure are summarized in Table l.

Exacerbation of Viral Myocarditis by Tobacco Smoke: The Catecholamine Hypothesis