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Cardiac risk factors and prevention
Original research article
The impact of passive and active smoking on inflammation, lipid profile and the risk of myocardial infarction
  1. Ritienne Attard1,
  2. Philip Dingli1,
  3. Carine J M Doggen2,
  4. Karen Cassar3,
  5. Rosienne Farrugia1 and
  6. Stephanie Bezzina Wettinger1
  1. 1 Department of Applied Biomedical Science, Faculty of Health Sciences, University of Malta, Msida, Malta
  2. 2 Health Technology and Services Research, MIRA, University of Twente, Enschede, The Netherlands
  3. 3 Faculty of Medicine and Surgery, University of Malta, Msida, Malta
  1. Correspondence to Dr Stephanie Bezzina Wettinger; stephanie.bezzina-wettinger{at}um.edu.mt

Abstract

Objective To investigate the effect of passive smoking, active smoking and smoking cessation on inflammation, lipid profile and the risk of myocardial infarction (MI).

Methods A total of 423 cases with a first MI and 465 population controls from the Maltese Acute Myocardial Infarction (MAMI) Study were analysed. Data were collected through an interviewer-led questionnaire, and morning fasting blood samples were obtained. ORs adjusted for the conventional risk factors of MI (aORs) were calculated as an estimate of the relative risk of MI. The influence of smoking on biochemical parameters was determined among controls.

Results Current smokers had a 2.7-fold (95% CI 1.7 to 4.2) and ex-smokers a 1.6-fold (95% CI 1.0 to 2.4) increased risk of MI. Risk increased with increasing pack-years and was accompanied by an increase in high-sensitivity C reactive protein levels and an abnormal lipid profile. Smoking cessation was associated with lower triglyceride levels. Exposure to passive smoking increased the risk of MI (aOR 3.2 (95% CI 1.7 to 6.3)), with the OR being higher for individuals exposed to passive smoking in a home rather than in a public setting (aOR 2.0 (95% CI 0.7 to 5.6) vs aOR 1.2 (95% CI 0.7 to 2.0)). Passive smoke exposure was associated with higher levels of total cholesterol, triglycerides and total cholesterol:high-density lipoprotein cholesterol ratio compared with individuals not exposed to passive smoking.

Conclusions Both active and passive smoking are strong risk factors for MI. This risk increased with increasing pack-years and decreased with smoking cessation. Such effects may be partly mediated through the influence of smoking on inflammation and lipid metabolism.

  • Passive smoking
  • Active smoking
  • Inflammation
  • Lipid profile, Myocardial Infarction

This is an Open Access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/

https://doi.org/10.1136/openhrt-2017-000620

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    Footnotes

    • Contributors All authors reviewed and provided edits and comments on manuscript drafts. In addition, authors had the following responsibilities: SBW designed the MAMI Study and was the principal investigator; RA was involved in research subject recruitment, laboratory testing, sample processing and all data analyses and was responsible for writing this manuscript; PD was involved in research subject recruitment, clinically assessed all cases to verify they fit in the recruitment criteria, and was responsible for waist and hip measurements; CD was responsible for overall study design and for overseeing data analysis; KC was responsible for ethical issues, clinical aspects, and logistics in recruitment; RF was involved in recruitment, selection of testing methodology, running of the project, and scientific advice. SBW had full access to all the data, oversaw all phases of the study and takes responsibility for the integrity of the data, accuracy of the data analysis and contents of this article.

    • Funding This work was carried out as part of the MAMI Study, a collaboration between the University of Malta and the Malta Department of Health. It was supported by national funding through the R&I program 2008 administered by the Malta Council for Science and Technology (MCST). The research work disclosed in this publication was also partially funded by the Malta Government Scholarships Scheme (MGSS). Open access publication fees were funded by Train MALTA, a European Union's Horizon 2020 research and innovation program under grant agreement No. 692041.

    • Competing interests None declared.

    • Ethics approval Research Ethics Committee, University of Malta.

    • Provenance and peer review Not commissioned; externally peer reviewed.