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Asia Pacific region: Smoking reduces cardioprotective effects of HDL cholesterol
New data from the Asia Pacific Cohort Studies Collaboration indicates that smoking mitigates the protective effects of high-density lipoprotein (HDL) cholesterol on coronary risk. The data were reviewed by HDL Forum Editor Professor Philip Barter.
Nakamura K, Barzi F, Huxley R et al, for the
Evidence indicates that smoking decreases HDL cholesterol (1,2). However, there remain questions as to whether smoking also impacts on the cardioprotective properties of HDL cholesterol. The available studies tend to be limited to mainly Western populations and have been hampered by insufficient data to permit meaningful analysis.
Dyslipidemia is also an important cardiovascular risk factor in Asian populations. In particular, recent data indicate an increasing prevalence of low HDL cholesterol levels in Asian countries, associated with increasing urbanization and adoption of Western lifestyles (3). Given trends showing that smoking rates here are also among the highest globally, with nearly two-thirds of men in
The Asia Pacific Cohort Studies Collaboration (APCSC) includes 44 pre-existing cohort studies. This analysis included data from 33 cohorts (18 in Asian subjects), involving 76,974 subjects with information on smoking status (self-reported) and HDL cholesterol levels. Subjects were classified by HDL-C levels: £1.0 mmol/L (38.7 mg/dL), 1.1-1.3 mmol/L, 1.4-1.5 mmol/L and ³1.6 mmol/L. Outcomes evaluated (fatal and non-fatal) were coronary heart disease (CHD) events, haemorrhagic stroke (HS) and ischaemic stroke (IS). Diagnosis of HS or IS was confirmed by CT/MRI or autopsy in about 50% of cases.
The median duration of follow-up was 4 years (4.0 years for smokers and 4.9 years for non-smokers).
Cox proportional hazard analysis showed that the risk for CHD increased log-linearly with decreasing HDL cholesterol levels, in both smokers and non-smokers. The inverse relationship between HDL cholesterol and CHD was stronger in smokers than non-smokers (p=0.04).
Each 0.40 mmol/L (15.4 mg/dL) decrease in HDL cholesterol was associated with about 70% increased risk for CHD in smokers, compared with 30% increased risk in non-smokers (Table 1).
This effect was especially notable in men (increase in coronary risk 74% vs. 23% in non-smokers p=0.03) and subjects aged <65 years (increase in coronary risk 126% vs. 19% in non-smokers, p=0.004) (Table 2). Sensitivity analyses confirmed the robustness of these findings.
There was no evidence of any significant association between HDL cholesterol and risk for either IS or HS in either smokers or non-smokers.
Based on these findings, the authors concluded that cigarette smoking may mitigate the protective effects of HDL cholesterol on coronary risk. These data suggest that the benefits of interventions aimed at raising HDL cholesterol, together with smoking cessation therapy, are likely to be greater than previously expected.
References
1. Criqui MH, Wallace RB, Heiss G, Mishkel M, Schonfeld G, Jones GT. Cigarette smoking and plasma high-density lipoprotein cholesterol. The Lipid Research Clinics Program Prevalence Study. Circulation. 1980 Nov;62(4 Pt 2):IV70-6.
2. Garrison RJ, Kannel WB, Feinleib M et al. Cigarette smoking and HDL cholesterol: the
3. Pan-Asian Consensus Panel on HDL-C. Role of nicotinic acid in raising high-density
lipoprotein cholesterol (HDL-C) to reduce cardiovascular risk: an Asian/Pacific consensus. Br J Diabetes Vasc Dis 2005;5(suppl 2):S1–S16.
4. WHO/Regional Office for the Western Pacific. Fact sheets. Smoking statistics. Available from: http://www.wpro.who.int/media_centre/fact_sheets/fs_20020528.htm
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