title: Tobacco smoke exposure and endothelial dysfunction in patients with advanced coronary artery disease.
abstract: BACKGROUND
  Exposure to tobacco smoke is associated with a higher cardiovascular risk, especially in patients with coronary artery disease (CAD).
  
  
  OBJECTIVE
  The aim of the study was to evaluate the effect of active and passive tobacco smoking on the activity of endothelial markers in advanced atherosclerosis.
  
  
  METHODS
  We studied 181 consecutive patients with advanced CAD (53 women and 128 men) aged 60 ±8 years, including 102 active self‑declared smokers (56.3%). We determined plasma asymmetric dimethylarginine (ADMA), thrombomodulin (TM), and plasminogen activator inhibitor‑1 (PAI‑1) levels, along with serum cotinine concentrations as a marker of tobacco smoking.
  
  
  RESULTS
  Plasma ADMA levels were higher in active smokers compared with nonsmokers (0.60 ±0.09 μmol/l vs. 0.49 ±0.08 μmol/l, P <0.001). There were similar intergroup differences in TM (4.60 ±2.11 ng/ml vs. 3.0 ±1.7 ng/ml, P <0.0001) and PAI‑1 levels (30.3 ±12.4 ng/ml vs. 23.6 ±11.3 ng/ml, P <0.0001). We observed positive correlations between cotinine and ADMA (r = 0.71, P <0.0001), TM (r = 0.53, P <0.0001), and PAI‑1 (r = 0.58, P <0.0001). In 21 patients (26.6%) who declared to be nonsmokers, cotinine levels (mean, 6.30 ±22.5 ng/ml) significantly correlated with ADMA, TM, and PAI‑1 (all P <0.001). A multivariate regression analysis showed that cotinine was an independent predictor of ADMA, TM, and PAI‑1 in the whole patient group.
  
  
  CONCLUSIONS
  Despite long‑lasting endothelial injury in advanced CAD, continued cigarette smoking is able to further enhance endothelial damage by increasing ADMA levels and resultant inhibition of fibrinolysis.
authors.forename: Dorota
authors.initials: D
authors.lastname: Szpak
authors.forename: Andrzej
authors.initials: A
authors.lastname: Grochowalski
authors.forename: Ryszard
authors.initials: R
authors.lastname: Chrząszcz
authors.forename: Ewa
authors.initials: E
authors.lastname: Florek
authors.forename: Wojciech
authors.initials: W
authors.lastname: Jawień
authors.forename: Anetta
authors.initials: A
authors.lastname: Undas
mesh_terms: D001120:Arginine / Q000031:analogs & derivatives* / Q000097:blood; D015415:Biomarkers / Q000097:blood; D015897:Comorbidity; D003324:Coronary Artery Disease / Q000097:blood* / Q000453:epidemiology; D003367:Cotinine / Q000097:blood; D018450:Disease Progression; D004730:Endothelium, Vascular / Q000378:metabolism*; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D009203:Myocardial Infarction / Q000453:epidemiology; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood; D012044:Regression Analysis; D012907:Smoking / Q000097:blood* / Q000453:epidemiology; D018180:Thrombomodulin / Q000097:blood; D014028:Tobacco Smoke Pollution
chemical_list: D015415:Biomarkers; D017395:Plasminogen Activator Inhibitor 1; D018180:Thrombomodulin; D014028:Tobacco Smoke Pollution; C487735:dimethylarginine; D001120:Arginine; D003367:Cotinine