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Epidemiology
Does cigarette smoking exacerbate the effect of total cholesterol and high-density lipoprotein cholesterol on the risk of cardiovascular diseases?
  1. K Nakamura1,2,
  2. F Barzi2,
  3. R Huxley2,
  4. T-H Lam3,
  5. I Suh4,
  6. J Woo5,
  7. H C Kim4,
  8. V L Feigin6,
  9. D Gu7,
  10. M Woodward2,8
  1. 1
    Department of Epidemiology and Public Health, Kanazawa Medical University, Uchinada, Japan
  2. 2
    Nutrition and Lifestyle Division, The George Institute for International Health, Sydney, Australia
  3. 3
    Department of Community Medicine, University of Hong Kong, Hong Kong, People’s Republic of China
  4. 4
    Department of Preventive Medicine, Yonsei University College of Medicine, Seoul, Korea
  5. 5
    Division of Geriatrics, Department of Medicine and Therapeutics, Chinese University of Hong Kong, Hong Kong, People’s Republic of China
  6. 6
    National Research Centre for Stroke, Applied Neurosciences and Neurorehabilitation, Auckland University of Technology, Auckland, New Zealand
  7. 7
    Cardiovascular Institute and Fu Wai Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, People’s Republic of China
  8. 8
    Department of Medicine, Mount Sinai School of Medicine, New York University, New York, USA
  1. Dr K Nakamura, Department of Epidemiology and Public Health, Kanazawa Medical University, 1-1 Daigaku, Uchinada, Ishikawa 920-0293, Japan; knaka{at}kanazawa-med.ac.jp

Abstract

Objective: To explore whether an interaction between smoking and serum total cholesterol (TC) and/or decreased levels of serum high-density lipoprotein cholesterol (HDLC) exists for any major subtype of cardiovascular disease.

Design: An individual participant overview of 34 cohort studies.

Setting: The Asia-Pacific region.

Participants: People aged ⩾20 years without a particular condition or risk factor.

Mean outcome measures: Hazard ratios (HRs) and 95% confidence intervals (CIs) for both TC and HDLC by smoking status were estimated using Cox proportional hazard models adjusted for age and systolic blood pressure and stratified by study and sex.

Results: During follow-up (median 4.0 years), 3298 coronary heart disease (CHD) and 4318 stroke events were recorded. For CHD, the HR (95% CI) for an additional 1.06 mmol/l increment in TC was greater in current smokers than in non-smokers: 1.54 (1.43 to 1.66) versus 1.38 (1.30 to 1.47); p = 0.02. Similarly, the HR (95% CI) for an additional 0.40 mmol/l decrement in HDLC was greater in current smokers than in non-smokers: 1.67 (1.35 to 2.07) versus 1.28 (1.10 to 1.49); p = 0.04. The positive association of TC with ischaemic stroke, and the negative association of TC with haemorrhagic stroke, were broadly similar for current smokers and non-smokers. Similarly, the risks of both the subtypes of stroke remained broadly unchanged as HDLC decreased in both current smokers and non-smokers.

Conclusions: Smoking exacerbated the effects of both TC and HDLC on CHD, although no interaction between smoking and TC or HDLC existed for either of the subtypes of stroke.

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Footnotes

  • Funding: This project has received support from a National Health and Medical Research Council of Australia programme grant (358395) and an unrestricted educational grant from Pfizer Inc. This study has been partially supported by a grant from the Korea Health 21 R&D Project, Ministry of Health and Welfare, Republic of Korea (grant no A040152).

  • Competing interests: MW has received honoraria from Pfizer Inc to speak on material related to this paper at conferences.

  • Ethics approval: Ethics committee approval obtained.

  • The sponsors had no influence on the design, analysis, or interpretation of results and took no part in the writing of this paper.

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