Cigarette smoking, metabolic syndrome, and subclinical atherosclerosis

Cigarette smoking is a major cardiovascular risk factor. Increased arterial atherosclerosis has been evidenced in smokers. However, less is known about the underlying atherogenic mechanisms caused by cigarette smoking.; Some of the metabolic changes and cardiovascular consequences caused by cigarette smoking are similar to the manifestations of the metabolic syndrome. The metabolic syndrome, which is a clustering of cardiovascular risk factors, is an important mediator in the etiology of atherosclerosis. Therefore, this dissertation was proposed to examine the pathophysiological pathways by which (especially by metabolic syndrome) cigarette smoking induces atherosclerosis.; Three sub-studies were performed around this main theme. The objective of study 1 was to investigate the mechanism relating metabolic syndrome to subclinical atherosclerosis. The objective of study 2 was to examine the direct atherogenic effects of cigarette smoking, in particular, the echographic changes of arterial wall components (detected by ultrasound) induced by cigarette smoking and smoking cessation. The objective of study 3 was to investigate mediational pathways (especially metabolic syndrome-associated) between cigarette smoking and subclinical atherosclerosis. Furthermore, the sex differences in these associations were investigated.; The data for this dissertation were obtained from an ongoing epidemiologic study, the Los Angeles Atherosclerosis Study. Health-related behaviors, physiological and metabolic measures, and subclinical atherosclerosis were assessed among middle-aged adults (304 men and 269 women, age 40–60 yr) who reported no history of cardiovascular heart disease or stroke. Common carotid arterial intima-medial thickness (CCA-IMT) measured by B-mode ultrasound was used as an indicator of subclinical atherosclerosis. Smokers have been oversampled to improve their representation. Three examinations were performed with an interval of 1.5 years. Structural equation modeling and Mixed procedure were used for the analysis of longitudinal data.; The findings from this dissertation confirmed that cigarette smoking is an independent atherogenic risk factor involving direct and indirect pathways and gender-dependency. Some of the mediating pathways are metabolic syndrome-associated. The effects of cigarette smoking on atherosclerosis and intermediate risk factors are partially reversible after quitting. This dissertation exploring atherogenic pathways caused by smoking has important implications on etiology and prevention research of subclinical atherosclerosis.