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Published on: December 2, 2014
Airflow limitation in smokers is associated with arterial stiffness: the Nagahama Study
Yasuharu Tabara1, Shigeo Muro2, Yoshimitsu Takahashi3
1Center for Genomic Medicine, Kyoto University Graduate School of Medicine, Shogoinkawaramachi, Sakyo-ku, Kyoto 606-8507, Japan.
Background:
Pathophysiological mechanisms of associations between airflow limitation (AL) and arterial stiffness remain unclear. One factor that might affect both AL and arterial stiffness is habitual smoking. The aim of this study is to investigate a possible interaction of smoking on the association between AL and arterial stiffness.
Methods:
Study subjects consisted of 8790 apparently healthy community residents. Airflow limitation was defined as a ratio of forced expiratory volume in 1 s (FEV1) to forced vital capacity of less than 70%. Brachial-to-ankle pulse wave velocity (baPWV) was used as an index of arterial stiffness. Smoking habit was investigated using a structured questionnaire.
Results:
Subjects with AL had significantly higher baPWV (AL 1381 ± 334, control 1261 ± 227 cm/s, p < 0.001). In a separate analysis by smoking habit, advanced arterial stiffness in AL was observed only in smokers (non-smokers: AL 1300 ± 220, control 1260 ± 218; smokers: AL 1436 ± 384, control 1264 ± 243 cm/s). Other clinical features of subjects with AL were older age; increased plasma hsCRP levels; and a high prevalence of male sex, hypertension, and smoking experience. Multiple linear regression analysis adjusted for these covariates identified the smoking × AL interaction as an independent determinant of baPWV (β = 0.066, p < 0.001). Conversely, baPWV was an independent determinant of AL in current and past smokers, but not in never smokers.
Conclusions:
AL arising from cigarette smoking, but not AL in non-smokers, was associated with arterial stiffness in a general population independently of established risk factors. Measurement of subclinical arterial change in smokers may be useful in identifying persons at risk for AL.
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