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Updated: Jul 16, 2026

Cell-free Biochemical Fluorometric Enzymatic Assay for High-throughput Measurement of Lipid Peroxidation in High Density Lipoprotein
Published on: October 12, 2017
Smoking, lipoproteins and coronary heart disease risk. Data from the Münster Heart Study (PROCAM)
P Cullen1, H Schulte, G Assmann
1Institut für Klinische Chemie und Laboratoriumsmedizin, an der Universität Münster, Germany.
Aims:
The mechanism of the increase in coronary heart disease risk associated with smoking is unclear, but may partly be due to smoking-related changes in intermediate risk factors such as lipid levels, fibrinogen and blood pressure. We therefore examined the distribution of these variables among smokers and non-smokers in the Münster Heart Study.
Methods:
20696 men, aged 41.7+/-2.7 years (mean +/- SD) and 10212 women, aged 37.0+/-2.6 years, were enrolled between 1978 and 1995. Thirty-two percent of women and 36% of men smoked. Compared to non-smokers, mean levels of low density lipoprotein cholesterol, total cholesterol, triglycerides and fibrinogen were increased, respectively, by 1.4%, 0.9%, 15% and 12.1% in male and by 2.0%, 5.5%, 12% and 3.4% in female smokers. Mean high density lipoprotein cholesterol levels, body mass index and blood pressure were reduced, respectively, by 6.4%, 3.8%, and 2% in male, and by 6.7% 1.2% and 2% in female smokers. In the subgroup of 4639 men aged 40 to 65 with 8 years of follow-up, the coronary event rate (definite myocardial infarction, sudden cardiac death) in cigarette smokers was more than twice that of non-smokers with otherwise identical risk factors.
Conclusion:
In the Münster Heart Study, smoking was associated with adverse changes in lipids (of greater magnitude in women), and fibrinogen (of greater magnitude in men). However, these changes explained only a small part of the smoking-related increase in coronary heart disease risk.
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