Smoking, lipoproteins and coronary heart disease risk. Data from the Munster heart study (PROCAM)

Abstract

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 Munster Heart Study. Methods. 20,696 men, aged 41.7 ± 2.7 years (mean ± SD) and 10,212 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 Munster 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 corollary heart disease risk.