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When will we learn that smoking is bad?
  1. Yaron Arbel
  1. Correspondence to Dr Yaron Arbel, Cardiology Department, Tel Aviv Medical Center, Weizman St 6, Tel Aviv 64239, Israel; yarona{at}tlvmc.gov.il

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In their Heart publication, Lloyd et al1 collected close to 1800 patients with ST-elevation myocardial infarction (STEMI) in England. They found that smokers were more common in this population (48.5% compared with 22.4%). They found that smoking was exceptionally common in young patients with STEMI (75%). Patients under the age of 50 had an eightfold increase in risk for myocardial infarction (MI) compared with non-smokers their age. This study supports previous studies that have shown the importance of smoking as a major risk factor for young patients with STEMI. As previous studies have shown, on average, smokers experience an MI 10 years younger compared with non-smokers. Cigarette smoking leads to heart disease by multiple biological mechanisms (box 1).

Box 1

Potential mechanisms linking heart disease and smokers

  • Endothelial dysfunction

  • Increased blood viscosity

  • Increased inflammation

  • Platelet activation

  • Deoxyribonucleic acid changes

  • Metabolic abnormalities (altered lipids, insulin resistance)

  • Low haemoglobin oxygen-binding capacity (high carbon monoxide)

  • Activation of the sympathetic system

  • Prothrombotic effects (inhibition of tissue plasminogen activator release from endothelium, increase in fibrinogen)

  • Increased homocysteine

  • Oxidative stress

Despite advances in medical therapy over recent years, the short-term and long-term risks for mortality have not diminished in smokers compared with non-smokers.2 This was explained by the lack of conventional risk factors in smokers and the fact that most smokers continue to smoke post-STEMI.3 In addition, smokers are less compliant with evidence-based therapies. In a recent European study, many patients with coronary artery disease do not achieve the guideline standards for secondary prevention with high prevalence of persistent smoking.4

We should focus our efforts in two directions:

  1. Prevention and education: Increase the awareness to the dangers of smoking and in young patients especially. Most smokers know that smoking is bad. However, exact numbers (ie, eightfold increase in MI rates) have a tendency to hit home more often. Therefore, studies like the present one are especially important.

  2. Treatment: Since most patients lack conventional risk factors, they benefit less from common therapies. Our goal should be on providing them with tools to achieve abstinence. Many studies have shown that a combination of drug (nicotine replacement, varenicline and bupropion) and behavioural therapy increase the success rates of patients achieving abstinence.5 However, in difficult cases, even reducing the number of cigarettes smoked daily might make a difference.6 Therefore, reduction of smoking is also a worthy approach in patients failing to achieve abstinence. Changing these habits can lead to drastic short-term improvements on a population base.7 Patients who quit smoking have reduced rates of recurrent events.8 This should be emphasised to the patients.

Our societies should play a more active role in preventing and treating smoking habits in the general population. These should include medical, legislative, commercial and educational efforts. Without all these efforts, we will not reduce the risks associated with smoking.9

References

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    This web only file has been produced by the BMJ Publishing Group from an electronic file supplied by the author(s) and has not been edited for content.

Footnotes

  • Competing interests None.

  • Provenance and peer review Commissioned; internally peer reviewed.

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