Article

Influence of smoking on incidence and prevalence of peripheral arterial disease

Maastricht University, Maestricht, Limburg, Netherlands
Journal of Vascular Surgery (Impact Factor: 2.98). 01/2005; 40(6):1158-65. DOI: 10.1016/j.jvs.2004.08.049
Source: PubMed

ABSTRACT Many studies have been published regarding the influence of smoking on the incidence and prevalence of peripheral arterial disease (PAD). A systematic review was performed to establish the magnitude of the effect of smoking on the development of PAD, and a possible dose-response relationship.
English-language articles were reviewed by 2 observers using a standardized form, and were summarized in tabular form. Data were extracted by 2 independent observers. Where possible, outcome data, expressed in terms of prevalence or incidence, were recalculated as odds ratio or relative risk, with never-smokers as the reference group, or if this was not available the nonsmoker group. Most studies did not provide primary data. Therefore the weighted means were reported as a summary estimate, provided that a funnel plot between sample size and observed effect size made publication bias unlikely.
Sixteen articles describing 17 studies were included in the analysis. Four of the studies were prospective, and 13 were cross-sectional. The prevalence of symptomatic PAD was increased 2.3-fold in current smokers. Even in former smokers the prevalence was substantially increased by a factor of 2.6. A clear dose-response relationship, with a strong increase in risk for PAD in heavy smokers was observed. In countries where approximately 30% of the population are smokers, 50% of PAD can be attributed to smoking.
Smoking is a potent risk factor for symptomatic PAD, with an important and consistent dose-response relationship. With the persistence of high risk for PAD in former smokers, tobacco control programs should continue to advocate smoking cessation, but focus even more on preventing future generations from ever starting to smoke.

Download full-text

Full-text

Available from: Edith M Willigendael, Aug 04, 2015
0 Followers
 · 
121 Views
  • Source
    • "Cigarette smoking leads to heart attacks, strokes, chronic obstructive pulmonary disease, and cancer. It also causes peripheral vascular disease, hypertension, and gastrointestinal disorders (Willigendael et al., 2004; Wright et al., 2005; Hogg and Timens, 2009; Hymowitz, 2011; Leone, 2011; Chu et al., 2013). In the United States, smoking is the leading cause of morbidity and mortality, accounting for 30% of all cancer deaths and 80% of deaths from chronic obstructive pulmonary disease (Centers for Disease Control and Prevention, 2008). "
    [Show abstract] [Hide abstract]
    ABSTRACT: Abstract Cholinergic signaling mediated by nicotinic receptors has been associated to a large number of physiological and behavioral processes such as learning, memory, attention, food-intake and mood disorders. Although it is well established that many nicotinic actions are mediated through an increase in serotonin (5-HT) release, the physiological mechanisms by which nicotine produces these effects are still unclear. The dorsal raphe nucleus (DRN) contains the major amount of 5-HT neurons projecting to different parts of the brain. DRN also contains nicotinic acetylcholine receptors (nAChRs) located at somatic and presynaptic elements. Nicotine produces both inhibitory and excitatory effects on different subpopulations of 5-HT DRN neurons. In this review, we describe the presynaptic and postsynaptic mechanisms by which nicotine increases the excitability of DRN neurons as well as the subtypes of nAChRs involved. We also describe the inhibitory effects of nicotine and the role of 5-HT1A receptors in this effect. These nicotinic actions modulate the activity of different neuronal subpopulations in the DRN, changing the 5-HT tone in the brain areas where these groups of neurons project. Some of the physiological implications of nicotine-induced 5-HT release are discussed.
    Reviews in the neurosciences 09/2013; 24(5):1-15. DOI:10.1515/revneuro-2013-0012 · 3.31 Impact Factor
  • Source
    • "Furthermore, the association is dosedependent ; increasing exposure to cigarette smoke is associated with earlier onset of symptoms and more severe PAD (Fowler et al 2002; Willgendael et al 2004). Finally, smoking cessation in patients with PAD is associated with a reduction in severity of IC and risk of developing rest pain (Girolami et al 1999), albeit to a lesser degree than the reduction in risk of coronary heart disease and stroke (Willgendael et al 2004). This may drive some of the increasing incidence seen in the elderly. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Symptomatic and asymptomatic peripheral arterial disease (PAD) is a common problem in the elderly. The management of PAD includes the prevention of cardiovascular events and relief of symptoms--most commonly intermittent claudication (IC). Both require treatment of the causes and consequences of atherothrombosis, but some strategies are more effective for prevention of cardiovascular events and others are more effective for the relief of symptoms. Priorities for the prevention of cardiovascular events include smoking cessation, exercise, antiplatelet therapy, and the treatment of dyslipidemia, hypertension, and diabetes. Walking time and ability are improved by exercise. The benefit of numerous drugs in the treatment of IC has been assessed. The results have generally been disappointing, but there is some evidence that statins and cilostazol (an inhibitor of phosphodiesterase 3) are of benefit. Meta-analyses suggest that cilostazol increases maximum walking distance by 40%-50% and improves other objective measures of walking. The safety profile of cilostazol in patients with PAD appears to be acceptable although the mechanism for its effect on IC is unclear. In addition to risk factor management, treatment with cilostazol should be considered in patients with disabling IC.
    Clinical Interventions in Aging 02/2008; 3(1):17-23. · 1.82 Impact Factor
  • Source
    • "Exposure to tobacco smoke is associated with changes in cellular function, leading to increased oxidative DNA damage and faster cell aging. Toxic chemicals present in cigarette smoke induce biochemical changes in many organs and tissues, likely responsible for the early occurrence of vascular degeneration and cancer in various organs and sites [1] [2]. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Healthy volunteers (n=50) were enrolled for studying the variation of gene expression induced by smoking in peripheral lymphocytes. RNAs from smokers (>3 cigarettes/day, n=20) and passive smokers (exposed to tobacco smoke >3 h/day, n=10) were hybridized versus a reference pool obtained by mixing equal amounts of RNA from 20 nonsmokers, and gene expression was analyzed using DNA microarrays containing 13,971 oligos. Principal component analysis showed that 99.7% of gene expression variability was related to plasma cotinine, age, and DNA oxidation damage. SAM and GenMAPP/MAPPFinder analyses showed that smokers, compared to nonsmokers, had 129 down-regulated and 87 up-regulated genes, whereas passive smokers, compared to nonsmokers, had 44 down-regulated and 159 up-regulated genes, mainly involved in pathways associated with the activation of defensive responses. Hierarchical cluster analysis identified two distinct clusters of smokers, characterized by different oxidative DNA damage: smokers with high DNA oxidation damage, compared to smokers with low DNA oxidation damage, had a large number (150) of down-regulated genes, mainly associated with xenobiotic metabolism, DNA damage and repair, inflammatory responses, lymphocyte activation, and cytokine activity, suggesting a reduced cellular response to toxic agents in this subset of smokers that could lead to an increased DNA oxidation damage.
    Free Radical Biology and Medicine 08/2007; 43(3):415-22. DOI:10.1016/j.freeradbiomed.2007.04.018 · 5.71 Impact Factor
Show more