Continuous Smoking and Progression of Arterial Stiffening: A Prospective Study

Objectives spectively and longitudinally determined the effects of smoking on the progression of arterial stiffening as well as the involvement of inflammation in this process. ound g is an important avoidable risk factor for cardiovascular disease, and arterial stiffness might be involved in the pathophysiology. No prospective study has examined the effect of continuous smoking on the age-associated progression of arterial stiffening. s 54 Japanese subjects (40 ± 8 years of age), brachial-ankle pulse wave velocity (baPWV) and serum C-reactive protein (CRP) levels were measured at the baseline and the end of a 5- to 6-year follow-up period. s nual rate of change of the baPWV during the study period was significantly greater in the continuous heavy smokers (11.0 ± 1.9 cm/s/year, n = 181) than in the never-smokers (5.5 ± 0.6 cm/s/year, n = 1,018). This difference remained significant even after adjustments for covariates, including age (p < 0.05). In continuous smokers (n = 493), the mean number of cigarettes smoked/day during the study period showed a significant relationship with the changes in baPWV. No significant relationship was found between the change in baPWV and serum CRP levels. sions uous smoking might accelerate the age-associated progression of structural stiffening of the large- to middle-size arteries. We also found a dose–response relationship between cigarette consumption and accelerated arterial stiffening. However, we failed to confirm any significant association between the rate of arterial stiffening and the serum CRP levels in the smokers.