Smoking status and common carotid artery intima-medial thickness among middle-aged men and women based on ultrasound measurement: a cohort study

BACKGROUND: Cigarette smoking is an established causal factor for atherosclerosis. However, the smoking effect on different echogenic components of carotid arterial wall measured by ultrasound is not well elucidated. METHODS: Middle-aged men and women who had IMT measurement ≥ 0.7 mm at baseline and follow-up were included (N = 413, age 40–60 years at baseline in 1995). Intima-media thickness of common carotid artery (CCA-IMT) and its components (echogenic and echolucent layers) were measured at baseline and in the follow-up examination 3 years later. IMT and its components were compared across current, former and never smokers. Individual growth models were used to examine how smoking status was related to the baseline and progression of overall IMT and IMT components. RESULTS: For both men and women, current smoking was associated with thicker echogenic layer than never smokers; former smokers exhibited thinner echogenic layer than current smokers after adjustment for cigarette pack-years. Among women, current smoking was also associated with a thinned echolucent layer that resulted in a non-significant overall association of current smoking with IMT for women. CONCLUSION: Cigarette smoking is associated with carotid artery morphological changes and the association is sex-dependent. The atherogenic effect of smoking appears to be partly reversible among former smokers. IMT measurement alone may not be adequate to detect carotid atherosclerosis associated with cigarette smoking among middle-age women

Obesity, metabolic syndrome, diabetes and smoking

It is becoming increasingly clear that arterial stiffness may be determined not only by age(ing) and blood pressure, but also by exposure to other cardiovascular risk factors. This chapter reviews the evidence provided by studies adopting an aetiological model of analyses of determinants of arterial stiffness, mainly derived, if available, from prospective designs. Specifically, the following risk factors are examined: the critical axis (central) obesity – metabolic syndrome – (type 2) diabetes, and also smoking. There is convincing evidence, reinforced by recent aetiological prospective studies, that these risk factors, all of which may be preventable, increase arterial stiffness. This may explain, at least in part, the increased cardiovascular disease risk observed in these conditions. However, the molecular basis of greater arterial stiffness associated with these risk factors remains to be fully elucidated. In addition, the prognostic significance of arterial stiffness indices in individuals with these risk factors, and the extent to which intervention on these risk factors improves cardiovascular outcome through beneficial impact on arterial stiffness, is still unclear. Given the high and/or increasing prevalence of these risk factors, these issues constitute an important research agenda