Abstract
Cigarette smoking has been reported to cause endothelial dysfunction, increased arterial stiffness, modified plasma lipids, and insulin resistance. These conditions precede the apparent structural and clinicopathological manifestations of atherosclerosis. This study had two aims : to examine how smoking affects coronary endothelial vasodilatory function and the arterial stiffness of the peripheral arteries, and to identify which of the foregoing effects appears earlier in smoking-related atherosclerosis. The following parameters were compared between 9 asymptomatic active smokers (mean age 34.2±4.4 years) and 9 non-smokers (mean age 32.8 ± 6.8 years) : coronary flow velocity reserve (CFR) calculated as the ratio of hyperemia (during drip infusion of adenosine triphosphate) to basal coronary flow velocity with transthoracic color Doppler echocardiography, carotid intima-media thickness, and the stiffness parameter (β) determined by carotid ultrasound. There were no differences between the smokers and non-smokers in baseline characteristics, serum levels of glucose, insulin or lipids, or arterial stiffness parameters. The CFR, however, was significantly lower in smokers than in non-smokers (3.13 ± 0.59 vs. 4.01 ±0.22, P < 0.01) despite similar coronary flow velocities at baseline. The results suggest that smoking promotes coronary vasodilator dysfunction before the occurrence of structural or functional changes in the arterial stiffness of the peripheral arteries of young healthy men.
