title: Increased aortic wave reflection and smaller pulse pressure amplification in smokers and passive smokers confirmed by urinary cotinine levels: the Nagahama Study.
abstract: BACKGROUND
  Central blood pressure (cSBP) is suggested to be a better predictor of cardiovascular risk than brachial BP. Although brachial BP levels among smokers have been reported to be the same or somewhat lower than those in nonsmokers, it is suggested that smoking might have a substantial impact on cSBP.
  
  
  METHODS
  We conducted a cross-sectional study to clarify the association of smoking habit with arterial tone and cSBP in a general population of 8557 participants using urinary cotinine levels as an objective marker of smoking intensity. Absolute pressure of the late systolic peak (SBP2) was obtained by calibrating the radial waveform with brachial systolic BP (bSBP) and considered to be the cSBP.
  
  
  RESULTS
  Confounding factor-adjusted mean pulse pressure amplification (PPa = bSBP-cSBP) was significantly smaller in habitual smokers (current, 9.3 ± 0.15; past, 10.2 ± 0.13; never, 10.6 ± 0.10 mmHg; p<0.001). Further, among smokers, PPa was linearly decreased with increasing urinary cotinine quartile (Q1, 10.9 ± 0.38; Q2, 10.9 ± 0.39; Q3, 10.4 ± 0.39; Q4, 9.7 ± 0.41 mmHg; p = 0.020). Multiple linear regression analysis identified both smoking habit (p = 0.003) and urinary cotinine levels (p = 0.008) as independent determinants of PPa. Urinary cotinine was also detected in a small fraction of never smokers (1.8%). These passive smokers showed a smaller PPa (passive smoker, 9.4 ± 0.4; never smoker, 10.4 ± 0.12 mmHg, p = 0.020) but not bSBP (122.7 ± 0.6, 123.1 ± 0.2 mmHg, p = 0.474).
  
  
  CONCLUSIONS
  Not only habitual smoking but also passive smoking had harmful effects on AIx and central BP. Our results strongly emphasize the importance of avoiding passive smoking to the prevention of cardiovascular risks of which the subject is likely unaware.
authors.affiliation: Center for Genomic Medicine, Kyoto University Graduate School of Medicine, Kyoto, Japan. Electronic address: tabara@genome.med.kyoto-u.ac.jp.
authors.forename: Yasuharu
authors.initials: Y
authors.lastname: Tabara
authors.forename: Yoshimitsu
authors.initials: Y
authors.lastname: Takahashi
authors.forename: Kazuya
authors.initials: K
authors.lastname: Setoh
authors.forename: Shigeo
authors.initials: S
authors.lastname: Muro
authors.forename: Takahisa
authors.initials: T
authors.lastname: Kawaguchi
authors.forename: Chikashi
authors.initials: C
authors.lastname: Terao
authors.forename: Shinji
authors.initials: S
authors.lastname: Kosugi
authors.forename: Akihiro
authors.initials: A
authors.lastname: Sekine
authors.forename: Ryo
authors.initials: R
authors.lastname: Yamada
authors.forename: Michiaki
authors.initials: M
authors.lastname: Mishima
authors.forename: Takeo
authors.initials: T
authors.lastname: Nakayama
authors.forename: Fumihiko
authors.initials: F
authors.lastname: Matsuda
mesh_terms: D062186:Arterial Pressure; D003367:Cotinine / Q000652:urine*; D003430:Cross-Sectional Studies; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D012907:Smoking / Q000503:physiopathology* / Q000652:urine*; D014028:Tobacco Smoke Pollution
chemical_list: D014028:Tobacco Smoke Pollution; D003367:Cotinine
keywords: Arterial waveform; Central blood pressure; Passive smoking; Urinary cotinine