title: Smoking promotes subclinical atherosclerosis in apparently healthy men: 2-year ultrasonographic follow-up.
abstract: BACKGROUND
  Smoking is a major risk factor for cardiovascular disease. Also, inflammatory activation and metabolic disorder are the mediators of smoking-induced atherosclerotic progression. The aim of the present study was to investigate whether current smoking and smoking cessation alter inflammatory or metabolic status and affect subclinical atherosclerosis in apparently healthy men.
  
  
  RESULTS
  Classical risk factors and smoking habit were evaluated in 354 men who completed health examinations annually without any current medications. Carotid intima-media thickness (IMT) was followed for 27.1±4.5 months. At baseline, both maximum and mean IMT significantly changed during 2-year follow-up. They tended to increase along with progression of smoking habit, with significantly greater maximum IMT in current smokers compared with never smokers. Both maximum and mean IMT significantly changed during 2-year follow-up, and tended to increase with progression of smoking habit, with maximum IMT being greatest for current smokers. Past smokers tended to have greater IMT increase than never smokers. Among smoking habit and some atherosclerotic risk markers that showed significant correlation with maximum IMT increase, stepwise regression showed that smoking habit and serum low-density lipoprotein-cholesterol (LDL-C) level were the only independent predictors.
  
  
  CONCLUSIONS
  Significant 2-year progression of subclinical atherosclerosis was associated with continuous smoking and LDL-C. This was only partly moderated in past smokers despite complete reversal of inflammatory activation, suggesting another crucial factor for inhibiting accelerated progression of subclinical atherosclerosis in men.
authors.affiliation: Health Care Center, Osaka University, Toyonaka, Japan.
authors.forename: Shoji
authors.initials: S
authors.lastname: Sanada
authors.forename: Makoto
authors.initials: M
authors.lastname: Nishida
authors.forename: Kouki
authors.initials: K
authors.lastname: Ishii
authors.forename: Toshiki
authors.initials: T
authors.lastname: Moriyama
authors.forename: Issei
authors.initials: I
authors.lastname: Komuro
authors.forename: Keiko
authors.initials: K
authors.lastname: Yamauchi-Takihara
mesh_terms: D052242:Adiponectin / Q000097:blood; D000328:Adult; D000704:Analysis of Variance; D058070:Asymptomatic Diseases; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000032:analysis; D002340:Carotid Artery Diseases / Q000097:blood / Q000000981:diagnostic imaging* / Q000209:etiology; D059168:Carotid Intima-Media Thickness; D008078:Cholesterol, LDL / Q000097:blood; D018450:Disease Progression; D005500:Follow-Up Studies; D006801:Humans; D015850:Interleukin-6 / Q000097:blood; D008297:Male; D008875:Middle Aged; D011237:Predictive Value of Tests; D012044:Regression Analysis; D012307:Risk Factors; D012907:Smoking / Q000009:adverse effects*; D016540:Smoking Cessation; D000074606:Smoking Prevention; D011795:Surveys and Questionnaires; D013997:Time Factors
chemical_list: C499918:ADIPOQ protein, human; D052242:Adiponectin; D015415:Biomarkers; D008078:Cholesterol, LDL; C508600:IL6 protein, human; D015850:Interleukin-6; D002097:C-Reactive Protein