Article Text

Download PDFPDF

Smoking verification and the risk of myocardial infarction
  1. G F Cope1,
  2. N Battersby1
  1. 1Institute of Research and Development, University of Birmingham, UK
  1. Correspondence to:
 Dr G F Cope
 University of Birmingham, Birmingham Research Park, Vincent Drive, Edgbaston, Birmingham B15 2SQ, UK;
  1. N S Godtfredsen2,
  2. J Vestbo2,
  3. M Osler2,
  4. I Andersen2,
  5. E Prescott2
  1. 2Institute of Preventive Medicine, Hellerup, Denmark

    Statistics from

    Request Permissions

    If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.

    We read the paper by Godtfredsen et al with interest.1 The paper reported on the effect of smoking reduction on the incidence of myocardial infarction (MI) and found that although patients who stopped smoking had a decreased risk of MI, those who reportedly reduced their smoking did not. The conclusions drawn were that smoking reduction, rather than complete cessation, did not produce any benefit with regard a reduction of risk of MI.

    The major drawback to this study is that the information about smoking was totally reliant on self reported smoking habit. There is abundant evidence that patients who smoke, when questioned about a smoking related illness, frequently under-report their cigarette consumption or deny smoking altogether. The more significant the effect smoking has, the greater the “social desirability bias”, so increasing the likelihood of denial. To overcome this bias biochemical verification of smoking by measurement of nicotine metabolites, specifically cotinine, has become almost obligatory.

    To improve the accuracy of information about smoking and to facilitate easier nicotine metabolite measurements we developed a six minute point of care test called SmokeScreen.2 The easy to use colorimetric urine test can provide qualitative, semi-quantitative, and quantitative measurements of nicotine intake. Using this test we undertook an audit of smoking habits of 154 new patients attending a large inner city hospital cardiology outpatient clinic, comparing the test identification of smoking with self completed questionnaire of current smoking habit. The results identified 112 (72.7%) patients as non-smokers, 30 (19.5%) as confessed smokers, and 12 (7.8%) as “smoking deceivers”.

    We followed this with another study of the same population (n = 85, 33 smokers and 52 never-smokers) to examine the interaction of smoking and risk factors associated with coronary artery disease, as assessed by a biochemical screen and a blood count. Interestingly, none of the parameters measured in the biochemical screen, such as cholesterol, HDL and triglycerides, urea and electrolytes, and liver function tests were associated with smoking habit or quantitative assessment of nicotine intake. Whereas white blood cell count was significantly higher in smokers (p = 0.002), in particular, neutrophils (p = 0.01) and eosinophils (p = 0.02). Lymphocytes, monocytes, and basophiles were higher but failed to reach significance. Quantitative assessment of nicotine intake of the smokers further revealed a positive correlation with white blood cell count (p = 0.0001, neutrophils (p = 0.001), eosinophils (p = 0.004) and lymphocytes(p = 0.02), with monocytes approaching significance (p = 0.7).

    It would seem from this pilot study that smoking or the amount of tobacco consumed does not influence the biochemical risk factors for coronary artery disease, such as cholesterol and HDL. However, smoking does seem to increase many of the immune cells associated with both the formation and destabilisation of the atheromatous plaque. It would seem logical therefore that a reduction in nicotine intake would be accompanied by a reduced risk of MI, as supported by our quantitative findings. One reason for the poor association between smoking reduction and subsequent MI in the Godtfredsen et al study1 may be the inaccuracy of self report. We suggest that identification of smokers with the point of care test is a more valuable method of smoking assessment. Coupling this test with subsequent advice on smoking cessation could have a significant impact on reducing a major risk factor associated with coronary artery disease and decrease cardiovascular events and mortality.


    Authors’ reply

    We appreciate the comments from Cope and Battersby on our paper reporting the association between smoking cessation and smoking reduction and subsequent risk of myocardial infarction. Specifically, they propose that the lack of a beneficial effect of reduced smoking—in contrast with smoking cessation—could be attributable to inaccuracy (underreporting) of the self reported tobacco consumption. In addition, they raise the important question of which measurement method most accurately reflects tobacco exposure in the individual smoker.

    We agree that nowadays almost every study of smoking habits apply one or more measurements of biochemical marker of smoking in addition to self report. It is also correct that in our paper the study participants are divided into the different smoking categories on basis of self reported smoking and changes in smoking. However, as mentioned in the discussion, measurements of expired carbon monoxide (CO) and serum cotinine were undertaken in one of the follow up examinations. We found increasing levels of CO (table 2) and cotinine (not shown) with increasing self reported tobacco consumption, indicating that underreporting of smoking alone cannot explain our results, but clearly misclassification cannot be ruled out in this observational study. Furthermore, a previous review and meta-analysis1 concluded that self reported smoking is an accurate measure of tobacco exposure in population based studies, whereas this is not the case in intervention and clinical studies. Our data were based on a sample of the general population; participants with known coronary heart disease before study entrance were excluded. In addition, information on smoking habits and changes in smoking were part of a large questionnaire initiated in the late 1970s and the 1980s, thus minimising the risk of “social desirability bias” in this study.

    Cope and Battersby describe a pilot study using a urine cotinine test for measuring nicotine intake. There are various methods of validating tobacco intake including biochemical markers, and cotinine is one of the better because of its comparatively long half life and the possible linear relation with number of cigarettes smoked. However, cotinine is not very useful in smoking reduction studies as most of the participants in these trials are supplied with nicotine replacement medications. Interestingly, the intervention studies of smoking reduction all report that despite nicotine replacement the percentage decline in amount of tobacco is followed by a smaller decline in biochemical markers of smoking exposure.

    Evidence of the effects of reduced smoking on risk of coronary heart disease is limited. The few ongoing smoking reduction trials report favourable changes in blood analyses of parameters of arteriosclerosis up to two years after smoking reduction. Unfortunately, these studies have a very high “drop out” percentage, but it will be interesting to see the clinical results of a long term follow up in this type of “risk reduction” study.

    In summary, we believe that the self reported smoking habits in our study are fairly precise. However, biochemical verification of smoking is necessary in intervention and clinical studies although there are no ideal markers of tobacco exposure specifically with respect to assessment of smoking reduction.


    Linked Articles