one constituent of tobacco smoke—nicotine—is currently used as short-term therapy for smoking cessation, and as discussed elsewhere in this volume, nicotine is being considered for extended use as an aid to smoking reduction. This necessitates a detailed consideration of the cardiovascular pharmacology of nicotine. The results of the Lung Health Study (Anthonisen et al., 1994) is notable in the consideration of the cardiovascular effects of long-term nicotine replacement therapy (NRT) since it was found that long-term use of nicotine gum for the purpose of smoking cessation did not result in an increased incidence of cardiovascular complications. Furthermore, it is pertinent to strategies being deployed by tobacco product manufacturers to eliminate selectively discrete constituents of tobacco and cigarettes and then market them as “safer.” This implies a knowledge of the relative contributions of a myriad of tobacco constituents to CVD, which simply does not exist. This chapter summarizes the current scientific basis of our understanding of smoking and CVD, suggests modern methodologies that might usefully be applied to enhance understanding in this area, and highlights areas for further research.

CORONARY HEART DISEASE

The incidence of coronary artery disease (CAD), including sudden cardiac death, is more than doubled in cigarette smokers as a group and is increased fourfold in heavy smokers. There is a dose-response relationship between cigarette smoking and CAD, such that the risk increases with the number of cigarettes smoked daily, the extent of inhalation, and the number of years of smoking. Cigarettes that nominally deliver less tar or nicotine have not been shown to confer any protection from ischemic heart disease.

The clearest understanding of smoking-induced ischemic heart disease emerges from integration of data from epidemiological and pathophysiologic investigations. In considering the participation of smoking in the etiology of CHD, it is useful to separate the effects of smoking on the development of atherosclerotic stenosis of the coronary arteries from its effects on the process that converts coronary atherosclerosis to acute coronary events.

Acute coronary events represent an abrupt transition from stable chronic CAD to one of the major consequences of ischemia: unstable angina, myocardial infarction, and sudden cardiac death. Abundant evidence supports the concept that the rupture of a lipid-rich atherosclerotic plaque with attendant thrombus formation is the initiating event in the development of the vast majority of these ischemic syndromes (Davies and Thomas, 1984; Oates, 1989).



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