Tobacco smoking is one of the most common forms of recreational drug use and the leading cause of a myriad of diseases, including (lung) cancer, Chronic Obstructive Pulmonary Disease (COPD), erectile dysfunction, cardiovascular diseases and many other. It is also the single largest and most preventable risk factor for development of peripheral artery disease (PAD).
Smoking rates are declining or have levelled off in the developed world, while developing world is experiencing an ongoing rise in the number of active smokers. This is largely due to aggressive anti-smoking campaigns and legislation limiting the marketing and sale of tobacco products and greater public awareness (in developed countries) about the detrimental health effects of smoking.
Important contributors are likewise smoking cessation programs since timely abstinence eliminates or at least greatly decreases the risk of developing a myriad of diseases [1, 2, 3, 4, 5]. However these beneficial effects are not as dramatic when it comes to PAD, as although the risk factor is substantially reduced, former smokers are still at an increased risk of this insidious disease in comparison with those who have never smoked .
There are several well-recognised risk factors for PAD, including diabetes, hyperlipidaemia, hypertension and obesity, but none are as prominent as (tobacco) smoking [7, 8, 9, 10].
Why is this? Looking at the bigger picture of cardiovascular health there are several mechanisms at work, the most important being the reduction of Flow-mediated Dilation (FMD) through damage to the endothelial cells due to the chemicals in tobacco smoke . This is of course conductive to atherogenesis which can be accelerated by other factors . Namely, many smokers have other medical issues (diabetes, hyperlipidaemia, hypertension etc.) or are subject to risk factors (male gender, advanced age or family history) that increase the probability and severity of atherosclerosis. On the whole, when regarding CVDs in general, smoking is responsible for 10 % of all cardiovascular issues .
If we focus solely on PAD the picture is far grimmer. In general, the prevalence of symptomatic PAD is 2.3 times greater in current smokers (in comparison with non-smokers) and 2.6 times greater in former smokers .
Studies have shown that smoking dramatically increases the incidence of PAD in men and this association is 2 to 3 times stronger in comparison to Coronary Artery Disease (CAD) .
In other words, smoking has a two to threefold worse effect on PAD than CAD, which is the leading cause of mortality amongst the CVDs . It should be noted that smoking has different effects on sub groups of PAD patients, specifically with regards to gender and ethnicity. Studies have shown that people of colour have higher risk rates for PAD than white people and that this was even more pronounced in smokers [17, 18].
Furthermore, female smokers are 20 times more at risk than females who never smoked . No exact statistics exist about the number of smokers who have PAD, but some have estimated that in countries where 30 % of population are smokers, 50 % of PAD can be attributed to tobacco smoking .
The best indicator of PAD and its severity is the Ankle-Brachial (pressure) Index (ABI) and both current and former smokers, regardless of the absence of other CVDs or risk factors and common PAD symptoms, should have their ABI measured.