Key result
Continuing smoking from adolescence to young adulthood was associated with higher aorto-iliac pulse wave velocity compared with never smokers (+0.157 m/s; 95% CI 0.026-0.288).
Why the study?
Does continuing smoking from adolescence to young adulthood increase arterial stiffness in young adults?
Cohort (n=424)
Does continuing smoking from adolescence to young adulthood increase arterial stiffness in young adults?
Effect estimate: Difference +0.157 m/s (95% CI 0.026-0.288)
Continuing smoking from adolescence to young adulthood is associated with increased aortic stiffness, emphasizing the need for early smoking prevention.
May support youth smoking prevention; leaves open causal effects on stiffness and reversibility.
OBJECTIVES: To investigate the associations between smoking in adolescence and adulthood, and changes in smoking behaviour between these age periods, with arterial stiffness in young adults; and whether any such associations could be explained by concomitant smoking-related levels of inflammation and endothelial dysfunction. METHODS: We studied 424 individuals (216 women) in whom smoking status was assessed in adolescence (age 15 years) and again in young adulthood (mean age of 22.6 ± 1.6 years), along with aorto-iliac, aorto-radial, and aorto-dorsalis pedis pulse wave velocity (PWV), and markers of inflammation (i.e. C-reactive protein and fibrinogen) and endothelial dysfunction (i.e. von Willebrand factor and tissue-plasminogen activator antigen) in young adulthood only. RESULTS: Smoking in adolescence was associated with higher aorto-iliac PWV, as well as with inflammation and endothelial dysfunction levels (expressed as two scores), independently of other adolescent and adult lifestyles. Compared with never smokers, continuing smokers, but not starters nor quitters, showed higher aorto-iliac PWV, independent of changes in other lifestyle variables: +0.157 m/s (95% confidence interval 0.026-0.288). This difference was attenuated to 0.124 m/s (-0.009 to 0.257) after adjustment for changes in traditional biological risk factors, but was not materially affected when adjusted for the inflammation and endothelial dysfunction scores, despite the continuing smoking-related higher levels of inflammation and endothelial dysfunction. Smoking was not associated with aorto-radial and aorto-dorsalis pedis PWV. CONCLUSION: Starting to smoke in adolescence and continuing to do so up to young adulthood is adversely associated with aortic stiffness. The continuing smoking-related aortic stiffness was not explained by concomitant higher inflammation and endothelial dysfunction. Prevention of smoking should target the young to prevent arterial stiffness in young adults.
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Laar et al. (2011) conducted a cohort in Arterial stiffness (n=424). Continuing smoking vs. Never smokers was evaluated on Aorto-iliac pulse wave velocity (PWV) (Difference +0.157 m/s, 95% CI 0.026-0.288). Continuing smoking from adolescence to young adulthood was associated with higher aorto-iliac pulse wave velocity compared with never smokers (+0.157 m/s; 95% CI 0.026-0.288).
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