SIGN 97: Risk estimation and the prevention of cardiovascular disease

Guideline Index Page | SIGN Methodology

6 Smoking

6.1 Tobacco exposure and cardiovascular risk

This section summarises the evidence describing the relationship between tobacco exposure and cardiovascular health and focuses on cessation interventions for two vulnerable population subgroups: those with a history of depression or schizophrenia. No relevant evidence was identified for interventions in ethnic subgroups.

6.1.1 Active smoking

Tobacco smoking is strongly and dose-dependently associated with all cardiovascular events, including CHD, stroke, peripheral arterial disease (PAD) and cardiovascular death.106,107 Smoking cessation reduces these risks substantially, although the decrease is dependent on the duration of cessation. 108,109Men who smoke are three times more likely to die aged 45-64 years, and twice as likely to die aged 65-84 years than non-smokers.106 Studies done among women during the 1950s and 1960s reported relative risks for total mortality ranging from 1.3 to 1.4. Smokers in the Nurses' Health Study were at nearly 1.9 times the risk compared with people who have never smoked.110 Evidence level 2++, 4

The additional risk of cardiovascular disease conferred by smoking is mediated by the number of cigarettes smoked. A large case control study noted the strong relation between risk of myocardial infarction (MI) and number of cigarettes smoked, with individuals who smoked over 40 cigarettes per day having almost ten times the relative risk of MI as non-smokers (odds ratio 9.16, 99% CI 6.18 to 13.58).19 Evidence level 2++

The prevalence of regular (at least weekly) smoking among 13 year olds has decreased since 1998 from 9% to 5% among boys and from 11% to 7% among girls. Among 15 year old boys, the prevalence of regular smoking has decreased from 30% in 1996 to 15% in 2000 and has since remained around that level. The drop among 15 year old girls over the same period (from 30% in 1996 to 24% in 2000) was smaller and not statistically significant; prevalence has remained at 24% since 2000.111 There is evidence that young people can become addicted to tobacco very quickly112 and many want to stop smoking.113 Evidence level 4

[Good practice point] Priority should be given to identifying and supporting young people to help them stop smoking.

The prevalence of smoking is highest amongst those on low incomes. Amongst some groups smoking rates as high as 75% have been reported.114 Evidence level 4

[Good practice point] Priority should be given to developing programmes and targeting smokers on low incomes to stop smoking, recognising the particular difficulties experienced by this group of smokers.

A prospective cohort study of over 120,000 males suggested that smoking cigars increases risk of early death from CHD.115 The association between cigar smoking and death from CHD was stronger among younger men and current rather than former smokers, as is observed with cigarette smoking. No increased risk was observed among current cigar smokers aged 75 years or older, or for former cigar smokers of any age. For men younger than 75 years who were current cigar smokers at baseline, the adjusted rate ratio for CHD mortality was 1.30 (95% CI 1.05 to 1.62). Evidence level 2++

A case control study involving 587 case subjects and 2,685 controls who smoked cigarettes with known tar yields indicated that smoking higher-yield cigarettes is associated with an increased risk of MI. The study revealed a dose-response relationship between total tar consumption per day 2+ and MI.116 The odds ratios for subjects smoking medium- and high compared with low-tar-yield cigarettes were 1.86 (95% CI 1.21 to 2.87) and 2.21 (95% CI 1.47 to 3.34), respectively. Evidence level 2+

BAll people who smoke should be advised to stop and offered support to help facilitate this in order to minimise cardiovascular and general health risks.

6.1.2 Passive smoke exposure

Several systematic reviews and observational studies provide evidence that exposure to environmental tobacco smoke (ETS) is associated with CVD events.

One systematic review calculated that environmental exposure to tobacco smoke causes an increase in relative risk of CHD of around 25%. It is of similar magnitude to the effects of exposure to environmental tobacco smoke on lung cancer, but the number of excess death from heart disease compared with lung cancer will be far greater in non-smokers due to the higher prevalence of CHD.

Individuals who have never smoked have an estimated 30% increased relative risk of CHD if they live with a smoker (p<0.001). The excess risk from smoking one cigarette per day is 39%, similar to the risk in a non-smoker living with a smoker. Reversal of the effect would reduce the risk of CHD by about as much as taking aspirin or by what many people could achieve through dietary change.107 Other systematic reviews highlight the increased risk of CHD events through exposure to ETS in the workplace117 and at home. 118 Evidence level 2++, 2+

Two observational studies indicated that non-smokers exposed to cigarette smoke had an increased risk of acute coronary syndromes of 51% (OR = 1.51, 95% CI 1.21 to 2.99) compared with non-smokers not exposed to smoke.119,120 Evidence level 2++

Another case control study examined the relationship between ETS and MI, in the workplace and at home.121 The odds ratio for MI was 1.58 (95% CI 0.97 to 2.56) for an average daily passive exposure to the smoke from 20 cigarettes per day or more at home. Combined exposure at home and work showed an increasing odds ratio for MI, up to 1.55 (95% CI 1.02 to 2.34) in the highest category of weighted duration, that is, more than 90 "hour-years" of exposure (1 "hour-year" = 365 hours, or one hour per day for one year). In addition, more recent exposure appeared to convey a higher risk. This study confirms an increased risk of MI from exposure to ETS and suggests that intensity of spousal exposure, combined exposure from home and work, and time since last exposure are important.

BExposure to passive smoking increases cardiovascular risk and should be minimised.

 

6.2 Smoking cessation interventions

6.2.1 The general population

There are many guidelines and policy documents covering mainstream NHS smoking cessation services and wider primary prevention.122-124 Evidence level 4

One systematic review and two RCTs comparing smoking cessation interventions were identified.

A systematic review of 20 studies concluded that quitting smoking is associated with a 36% reduction in crude relative risk of mortality for patients with CHD who quit compared with those who continued smoking (RR 0.64; 95% CI 0.58 to 0.71).125 Evidence level 2++

Two RCTs addressed lifestyle advice/training and reported a reduction in smoking in those who went through an educational programme.126,127 Both studies only included male patients and lacked sufficient power to allow a firm conclusion to be derived.

In the Oslo Diet and Antismoking Trial, advice to change diet and smoking habits reduced the relative risk of CHD mortality after 23 years in men with high triacylglycerol concentrations. Men with normal triacylglycerol concentrations did not appear to achieve this long term benefit of lifestyle intervention.126 Evidence level 1+

The Vestfold Heartcare Study Group trial investigated whether a comprehensive programme of lifestyle modification could favourably influence dietary and exercise habits in addition to smoking cessation.127 After following a low-fat diet, regular exercise, smoking cessation and psychological support and education sessions, patients in the lifestyle intervention group reduced the intake of saturated fat, sugar and cholesterol (p<0.001), increased their exercise level (p<0.01) and stopped smoking (p<0.05) when compared with the usual care group. Results indicated a relative risk reduction of 22% in five-year risk of CHD in males (95% CI 9 to 35), however, the study lacked statistical power and should be interpreted with caution. Evidence level 1+

One systematic review which compared different forms of nicotine replacement therapy (NRT) concluded that all forms of NRT can help people to stop smoking, almost doubling long term success rates. The odds ratio (OR) for abstinence with NRT compared to control was 1.77 (95% CI 1.66 to 1.88).128 Evidence level 1++

A systematic review of the effect of antidepressants on smoking cessation showed that buproprion and nortryptiline approximately doubled the odds of a motivated individual stopping smoking.129 Based on 19 trials of bupropion monotherapy with over 4,000 participants the pooled odds ratio for smoking cessation was 2.06 (95% CI 1.77 to 2.40). Serious adverse effects using bupropion at the doses indicated for smoking cessation are rare (less than one per 1,000 treated).130 Evidence level 1++

Nortryptiline is not licensed for use in smoking cessation and is contraindicated in patients with recent myocardial infarction or arrhythmias (particularly heart block).131 Evidence level 4

ANicotine replacement therapies or bupropion should be used as part of a smoking cessation programme to augment professional advice and increase long term abstinence rates.

6.2.2 Special populations

Patients with depression

One meta-analysis132 and three RCTs133-135 were identified which considered smoking cessation in individuals with clinical depression.

The meta-analysis considered whether a history of major depression is associated with failure to quit smoking. No differences in either short term (= three months) or long term abstinence rates (≥ six months) were observed between smokers who were positive versus negative for history of depression. The authors conclude that a lifetime history of major depression does not appear to be an independent risk factor for cessation failure in smoking cessation treatment. Evidence level 2++

The three RCTs considered different smoking cessation strategies for patients with depression. One trial investigated the effect of nortriptyline hydrochloride and cognitive behaviour therapy (CBT) on smoking treatment outcome in smokers with a history of major depressive disorders.133 Nortriptyline produced higher abstinence rates than placebo, independent of depression history and alleviated a negative affect occurring after smoking cessation. Cognitive behaviour therapy was more effective for participants with a history of depression. Evidence level 1+

A smaller trial investigated the effect of sertraline as a cessation aid to patients with clinical depression.Thetrialshowedthatsertralinedidnotaddtotheefficacyofanintensiveindividual counselling. However, given that the end-of-treatment abstinence rate for the placebo group was much higher than expected, it is unclear whether a ceiling effect of the high level of psychological intervention received by all subjects prevented an adequate test of the drug.134 Evidence level 1+

One small trial examined the efficacy of a mood management intervention for smoking cessation in abstinent alcoholics with a history of major depression.135 Patients were randomised to either behavioural counselling (BC) alone or counselling with a CBT component. Significantly more smokers in the CBT group had quit smoking by the end of the intervention period (69.2%; 9 of 13) than in BC (31.3%; 5 of 16) ( p=0.04). The abstinence rates remained unchanged at one month follow up. At three months follow up, differences in smoking abstinence rates were not significant between CBT (46.2%; 6 of 13) and BC (25.0%; 4 of 16) conditions. At 12 months follow up, significantly more participants in CBT were abstinent from smoking (46.2%; 6 of 13) than in BC (12.5%; 2 of 16) (p=0.04). Evidence level 1-

Antidepressants have an effect on smoking cessation rates in this group (but are not licensed specifically for this indication). It is not clear whether this effect is mechanistic or related directly to the treatment of depression. There are no significant trials of other pharmacological interventions (eg NRT, buproprion) in this group of patients.

BSmokers with coronary heart disease and comorbid clinical depression should have their depression treated both for alleviation of depressive symptoms and to increase the likelihood of stopping smoking.

Patients with schizophrenia

Two poor quality RCTs136,137 and a follow up study138 were identified which considered smoking cessation in individuals with schizophrenia.

One trial of the effect of adding sustained-release bupropion to CBT on smoking behaviour and stability of psychiatric symptoms was identified in patients with schizophrenia. The study was flawed by omission of method of randomisation and concealment, and also involved only nine patients in experimental and control arms. Bupropion treatment was associated with an apparently greater reduction in smoking, as measured by self-report and carbon monoxide expiration, which may not have been sufficiently sensitive to detect changes in smoking status. Bupropion was only used at half the dose recommended because of seizure risk.136 Evidence level 1-

A study which followed up the same patients suggested that most individuals who achieved ≥50% reduction in smoking at the end of the trial maintained at least that level of reduction after two years. Smoking reduction during the treatment intervention was correlated with smoking reduction at follow up (r=0.60, p=0.01).138 Evidence level 2-

Another small RCT compared sustained-release bupropion with placebo for smoking cessation in patients with schizophrenic disorders. Results indicated an increase in self-reported smoking abstinence with bupropion compared with placebo at 10 weeks but no significant difference at six months. Patients who consented and were proven to be highly motivated using a Likert scale were not likely to be typical of people with schizophrenia. The method of randomisation was not described.137 Evidence level 1-

Independent studies of bupropion for smoking cessation in people with schizophrenia are needed.

Patients from ethnic minorities

There have been no statistically reliable nationwide surveys of the prevalence of smoking or effectiveness of cessation interventions among ethnic minorities in Scotland. Research from England done in the late 1990s provides some information on tobacco use and cessation rates in ethnic subgroups (see Table 4).139

Table 4: Cigarette smoking by sex and minority ethnic group in England (as a percentage of the population)

General population Black Caribbean Black African Indian Pakistani Bangladeshi Chinese
Men 24 25 21 20 29 40 21
Women 23 24 10 5 5 2 8

In general, smoking rates among ethnic minorities were the same, or lower, than those found in the wider population of England. While smoking rates for men and women in the UK on the whole are converging, amongst minority ethnic groups there are still marked gender differences in smoking behaviour. Rates are low in particular among South Asian women, however research conducted by Action on Smoking and Health (ASH) Scotland has indicated that smoking is escalating among South Asian girls in Scotland, particularly in young Pakistani women.140

ASH Scotland has conducted a mapping exercise to identify smoking cessation projects, services, resources and training courses available to individuals from ethnic subgroups. Although some material was identified which had been specifically targeted to ethnic subgroups (mostly leaflets), generally, mainstream tobacco services were not attracting representative proportions of individuals from ethnic subgroups.141

section 7>

Guideline Index Page | SIGN Methodology

Scottish Intercollegiate Guidelines Network, Healthcare Improvement Scotland, Gyle Square, 1 South Gyle Crescent, Edinburgh EH12 9EB
Tel. 0131 623 4720 Web contact duncan.service@nhs.net
Last modified 13/09/13 © SIGN 2001-2013

Risk estimation and the prevention of CHD <Guidelines <Home