title: Does passive smoking impair endothelium-dependent coronary artery dilation in women?
abstract: OBJECTIVE
  This study sought to examine whether passive smoking is associated with endothelial dysfunction in the coronary arteries.
  
  
  BACKGROUND
  Long-term exposure to cigarette smoking has been reported to suppress endothelium-dependent arterial dilation in humans. Endothelial dysfunction is an early feature of atherogenesis, and the impairment of acetylcholine (ACh)-induced coronary artery dilation indicates coronary endothelial dysfunction.
  
  
  METHODS
  We studied 38 women (40 to 60 years old) who had no known risk factors for coronary artery disease other than tobacco smoking: 11 nonsmokers who had never smoked and had never been regularly exposed to environmental tobacco smoke; 19 passive smokers with self-reported histories of exposure to environmental tobacco smoke of > or = 1 h/day for > or = 10 years; and 8 active smokers. We examined the response of the epicardial coronary artery diameters (proximal and distal segments of the left anterior descending [LAD] and left circumflex [LCx] coronary arteries) to the intracoronary injection of ACh into the left coronary artery by means of quantitative coronary angiography.
  
  
  RESULTS
  ACh significantly dilated the distal segment in nonsmokers (percent change from baseline diameter: LAD 13.7+/-3.4%, p < 0.05; LCx 18.8+/-2.9%, p < 0.01) but not the proximal segment (LAD 7.4+/-3.5%; LCx 3.1+/-5.0%). ACh significantly constricted all segments of the left coronary artery in passive smokers (LAD: proximal -20.3+/-3.7%, p < 0.05; distal -22.3+/-4.1%, p < 0.01; LCx: proximal -20.8+/-3.1%, p < 0.05; distal -17.3+/-2.9%, p < 0.01) and active smokers (LAD: proximal -14.8+/-3.4%, p < 0.05; distal -27.2+/-6.0%, p < 0.01; LCx: proximal -14.5+/-6.6%, p < 0.05; distal -22.4+/-4.0%, p < 0.01). Thus, ACh constricted most coronary arteries in both passive and active smokers and dilated the coronary arteries in nonsmokers.
  
  
  CONCLUSIONS
  Impairment of ACh-induced coronary artery dilation, indicating coronary endothelial dysfunction, may occur diffusely in passive smokers as well as in active smokers.
authors.affiliation: Division of Cardiology, Kumamoto Rosai Hospital, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Sumida
authors.forename: H
authors.initials: H
authors.lastname: Watanabe
authors.forename: K
authors.initials: K
authors.lastname: Kugiyama
authors.forename: M
authors.initials: M
authors.lastname: Ohgushi
authors.forename: T
authors.initials: T
authors.lastname: Matsumura
authors.forename: H
authors.initials: H
authors.lastname: Yasue
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D000328:Adult; D002784:Cholesterol / Q000097:blood; D017023:Coronary Angiography; D003324:Coronary Artery Disease / Q000209:etiology; D003331:Coronary Vessels / Q000187:drug effects / Q000503:physiopathology*; D004730:Endothelium, Vascular / Q000503:physiopathology*; D005260:Female; D006801:Humans; D008875:Middle Aged; D012307:Risk Factors; D012907:Smoking / Q000009:adverse effects; D014028:Tobacco Smoke Pollution / Q000009:adverse effects*; D014661:Vasoconstriction; D014664:Vasodilation / Q000187:drug effects
chemical_list: D014028:Tobacco Smoke Pollution; D002784:Cholesterol; D000109:Acetylcholine