Current and ex-smokers faced an increased risk of early carotid atherosclerosis only in the presence of chronic infections (OR 3.3; 95% CI 1.8-6.2; P<0.001).
Cohort
Do chronic infections modify the risk of early and advanced carotid atherosclerosis associated with active and passive smoking?
The proatherogenic effects of cigarette smoking on early carotid atherosclerosis appear to be mediated in part by the presence of chronic infections.
Effect estimate: OR 3.3 (95% CI 1.8 to 6.2)
p-value: p=<0.001
BACKGROUND AND PURPOSE: Susceptibility of the vasculature to the injurious effects of smoking varies substantially, with some smokers developing severe premature atherosclerosis and others remaining free of advanced atheroma until high ages. The present study sought to estimate the contribution of chronic infections to the variability of atherosclerosis severity among smokers. METHODS: In the community-based Bruneck Study, 5-year changes in carotid atherosclerosis were assessed by high-resolution ultrasound. Early atherogenesis was defined by the development of nonstenotic plaques and advanced atherogenesis by the development/progression of vessel stenosis >40%. RESULTS: The risk of early atherogenesis strongly relied on lifetime smoking exposure and remained elevated long-term after cessation of smoking. Remarkably, current and ex-smokers faced an increased atherosclerosis risk only in the presence of chronic infections (odds ratios 95% CIs, 3.3 1.8 to 6.2 and 3.4 1.8 to 6.3; P<0.001 each), whereas current, past, and nonsmokers without infections did not differ substantially in their estimated risk burden (odds ratios 95% CIs, 1.4 0.8 to 2.4, 0.9 0.6 to 1.6, and 1.0 reference group). In analogy to first-hand smoking, subjects exposed to environmental tobacco smoke were found to be vulnerable to the manifestation of chronic infection, and only those infected experienced a high atherosclerosis risk. The risk of advanced atherogenesis showed a dose-response relation with the number of daily cigarettes, returned to normal shortly after cessation of smoking, and emerged as independent of infectious illness. CONCLUSIONS: Our study provides the first epidemiological evidence that the proatherogenic effects of cigarette smoking are mediated in part by the chronic infections found in smokers. A better understanding of the vascular pathogenetic mechanisms of smoking may offer novel clues for disease prevention supplementary to the primary goal of achieving long-term abstinence.
Kiechl et al. (Sun,) conducted a cohort in Carotid Atherosclerosis. Active and passive smoking with chronic infections vs. Nonsmokers without infections was evaluated on Early atherogenesis (development of nonstenotic plaques) (OR 3.3, 95% CI 1.8 to 6.2, p=<0.001). Current and ex-smokers faced an increased risk of early carotid atherosclerosis only in the presence of chronic infections (OR 3.3; 95% CI 1.8-6.2; P<0.001).