Discussion
In the present study, we set out to investigate CVD risk factors among men and women aged 46 years based on their smoking history.
Smoking history and cardiovascular risk factors
Smoking, lipid abnormalities and high blood pressure are well-established risk factors for CVD. Apart from being an individual risk factor for CVD, smoking has generally been associated with many of the other risk factors such as a poorer lipid profile and elevated blood pressure. According to previous research, smokers have higher serum cholesterol, triglyceride and LDL levels, and lower levels of HDLs than non-smokers, but the effect of smoking cessation on lipid profile seems to be quite modest.12–14 A meta-analysis of 27 prospective studies on the effect of smoking cessation found a small but significant increase in the level of HDL, favouring former smokers over current smokers when the measurement intervals ranged from 30 days to 2 or more years.13 The same study found no significant changes in the level of total cholesterol, LDL or triglycerides. In the present analysis, we observed statistically significant differences in lipid levels, favouring individuals who had never smoked over current smokers. However, these differences were modest and clinically insignificant at the group level. Interestingly, lipid levels were slightly above recommendations in all groups studied.15 The use of antihypertensive or hypolipidemic medication was slightly more common among current smokers when compared with the group of never smokers. Also, type 2 diabetes was more common among smokers than never smokers, contributing to the higher Framingham total score in this group.
In the present study, there were no clinically major differences in blood pressure between the groups, and the mean blood pressure was within recommendations in all groups.15 Smoking causes acute increase in blood pressure, which declines quickly after smoking.16 However, there is no consensus regarding the role of smoking in long-term blood pressure in generally healthy people.17 Though lifelong non-smokers seem to have lower blood pressure than current smokers, the effect of smoking cessation on blood pressure remains unclear with contradictory findings.13 ,17–19 In one study, no significant change in blood pressure was found after two and a half years after smoking cessation in either the group of former smokers or the control group of never smokers.13 We were not able to find such a long-term effect in our population aged 46 years either.
Obesity and diabetes are also known to contribute to the absolute risk of CVD.12 In the present study, the group of former smokers had the highest BMI. Indeed, people who stop smoking often gain weight, which is probably due to nicotine acting as an appetite suppressant.20
While the risk of CVD decreases immediately after smoking cessation, the extent and speed of the risk reduction are not clear.21 Depending on the study, the CVD risk of former smokers reverts to the level of lifelong non-smokers within 3–15 years.21 ,22 In our study, the total increase in CVD risk among current smokers resulted mainly from the smoking itself, rather than from the aggregation of multiple risk factors in these individuals. Therefore, our results support the assumption that smoking is predominantly a major individual risk factor for CVD, instead of increasing other risk factors or being an indicator for harmful lifestyle habits.2 Indeed, contrary to our hypothesis, the differences in individual risk factors for CVD were not clinically significant among smokers, non-smokers, former smokers and recent quitters.
Mechanisms of smoking-induced cardiovascular events
The mechanisms underlying cigarette smoke-induced atherosclerosis, arterial thrombosis and their clinical manifestations as CVD are only partially understood and can be divided into several systemic pathways. First, reactive oxygen species induce cardiac remodelling, seen as left ventricular hypertrophy and atrial fibrosis, which increase the risk of stroke.23 Oxidative stress caused by systemic oxygen free radicals causes systemic and local inflammation, which is seen as elevation in levels of C reactive protein and peripheral leucocytes, in addition to other proinflammatory cytokines, which promote arterial thrombosis.24 Second, nicotine-stimulated release of adrenal medulla hormones modifies cardiac output by increasing heart rate, ventricular contractility and blood pressure, which might lead to cardiac ischaemia.25 Third, compounds in cigarette smoke expose smokers to myocardial ischaemia by causing deficient vasomotor functions, which is seen as thickening of the arterial wall and intima media, reduced ability to expand and contract vessels, as well as increased arterial stenosis.26 ,27 There are currently also many other known mechanisms by which smoking contributes to the increased CVD risk.28 ,29
Strengths and limitations of the study
While the rate of cardiovascular mortality is at a steady decline in the Western world, CVD remains the leading cause of death in our Finnish setting.30 Even though cardiovascular events lead to death all the more seldom, they are extremely costly for the healthcare system. Moreover, especially non-fatal stroke can have devastating consequences for the quality of life of the patient and their family. It is thus of key importance to recognise which measures are impactful in CVD prevention.
Large, prospective, population-based study samples, such as the Northern Finland Birth Cohort used in the present study, are optimal for studying common diseases and their risk factors. In the present sample, the participants’ smoking history and changes to it were thoroughly mapped throughout their lives. Considering the fact that participation in the study takes several days at each point of data collection, the dropout rate has been very small. This may indicate high motivation of the participants, which is likely to increase the reliability of the self-reported data on smoking status and history. On the other hand, it is also possible that individuals with little interest in health issues may be under-represented in the sample. In the present study, we deliberately did not adjust analyses for the participants' socioeconomic status, which was expected to further highlight the differences in CVD risk factors between the groups. This is because smoking and other harmful health behaviour, such as an unhealthy diet, high alcohol consumption or lack of physical exercise, typically occur in lower socioeconomic classes.6 However, we did adjust for a common indicator of these harmful habits—BMI—when comparing individual risk factors and absolute risk scores between people with different smoking histories. Adjusting for family history might have further strengthened our results but could not be done with our data.
Clinical conclusions
Our aim was to characterise gender-specific CVD risk factors in relation to smoking behaviour and history in a large population-based Finnish study sample. Many risk factors were elevated among smokers in comparison with never smokers or to the group of participants who had quit smoking. However, these differences were modest and are not likely to have major clinical implications. The difference in these risk factors was so small between those who had smoked in some point in their lives but later quit and those who had never smoked that a statistically significant difference in absolute CVD risk for these groups could not be detected. Many deleterious changes caused by smoking are relatively quickly reversible, and therefore smoking cessation could have a great significance in reducing cardiovascular morbidity and mortality. In the UK, a 35% decline in smoking prevalence over two decades has resulted in nearly 30 000 (24%) fewer coronary heart disease deaths. This effect was much greater than that achieved by lowering cholesterol, which resulted in some 4700 (4%) fewer deaths.31 Based on the results presented here, only modest aggregation of other CVD risk factors exists in smokers aged 46 years when compared with never smokers or ex-smokers. Therefore, quitting smoking at this age might even decrease CVD risk to approximately the same level with non-smokers.