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Atherosclerosis is a slowly progressing degenerative disease of the arterial wall. Several risk factors, including cigarette smoking, precipitate its development. The purpose of the study was to investigate atherosclerotic morphologic changes in clinically healthy smokers, and to evaluate acute and chronic effects of cigarette smoking on arterial haemodynamics. Using ultrasound we determined thickness of the intima and media of the carotid arteries, and the ability of brachial arteries to dilate during hyperemia. The measurements were done before and after smoking. The study involved 40 smokers aged 19 to 50 years, who were assigned to two groups: group A comprised 20 individuals who had been smoking for less than 15 years and group B 20 subjects with a history of smoking for more than 15 years. The control group consisted of 20 healthy individuals with no major risk factors for atherosclerosis. Laboratory tests showed that smokers had significantly higher platelet, leukocyte and fibrinogen levels, and significantly lower HDL-cholesterol, TIBC and erythrocyte concentrations compared to non-smokers. In comparison to the control group, smokers demonstrated considerably reduced dilation of the brachial arteries during hyperemia (7 ± 4% to 11 ± 4%, p = 0,004) and notably diminished blood flow at rest (78,83 ± 31,87 ml/min to 134,85 ± 45,06 ml/min, p < 0,0001). Smokers showed a significantly greater average intimal and media thickness both of the carotid arteries (0,68 ± 0,13 mm to 0,59 ± 0,04 mm, p < 0,001), and of the carotid bifurcation (0,81 ± 0,18 mm to 0,63 ± 0,40 mm, p < 0,001). The intimal and media thickness is associated with years of smoking and number of cigarettes smoked daily. In all three groups there was a relationship between the intimal and media thickness, and risk factors, including age, body mass index, cholesterol, LDL-cholesterol, triglicerydes, fibrinogen and lipoprotein(a). Our results indicate that cigarette smoking is a strong independent risk factor for atherosclerosis, and that it accelerates atherogenesis even in the absence of other precipitating factors.