Impact of Tobacco Smoking and Smoking Cessation on Cardiovascular Risk and Disease

Christopher Bullen

Disclosures

Expert Rev Cardiovasc Ther. 2008;6(6):883-895. 

In This Article

The Role of Genes

As Benowitz has observed, if 50% of lifelong smokers die prematurely from smoking-related diseases then 50% of such smokers do not.[8] Some develop severe cardiovascular disease at an early age whereas others who have smoked for many years appear to be resistant. This variation may be explained not only by the presence and force of other risk factors for cardiovascular disease besides smoking but also to genetics. The review of the genetic influences of cigarette smoking-induced cardiovascular diseases by Wang et al. showed that genetic variants can indeed modify the development of atherosclerosis in smokers.[82] Polymorphisms (such as endothelial NO synthase polymorphisms) may increase susceptibility to coronary heart disease and AMI. However, it is difficult to assess their clinical importance since the prevalence of these variants in populations of smokers is as yet unknown.[82]

Recently, researchers have begun to explore the genetic basis of nicotine dependence. Thorgeirsson et al. identified a common variant in the nicotinic acetylcholine receptor gene cluster on chromosome 15q24 with an effect on the number of cigarettes smoked per day, nicotine dependence and the risk of PVD in populations of European descent.[83] Lou et al. have found an association between GABAA receptor-associated protein and DLG4 with nicotine dependence in chromosome 17p13 of European–Americans.[84] In a large study targeting 348 candidate genes, Saccone et al. identified cholinergic nicotinic receptor genes that have an association with nicotine dependence.[85] Such studies are important but need replicating and their relevance to therapeutic interventions is as yet unclear.

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