Tobacco smoke exposure and endothelial dysfunction in patients with advanced coronary artery disease

Dorota Szpak, Andrzej Grochowalski, Ryszard Chrząszcz, Ewa Florek, Wojciech Jawień, Anetta Undas
2013 Polish Archives of Internal Medicine  
474 IntroductIon Tobacco smoking is a major risk factor for cardiovascular diseases. 1 The Global Adult Tobacco Survey showed that 48.6% of men and 11.3% of women in the participating countries were tobacco users. In addition, 40.7% of men (ranging from 21.6% in Brazil to 60.2% in Russia) and 5.0% of women (24.4% in Poland) participating in the survey smoked a tobacco product. 2 Smoking cessation is of paramount importance as secondary prevention of myocardial infarction (MI) but approximately
more » ... but approximately 30% to 45% of the patients continue to smoke, while 59% of the patients refrain from smoking only for a year following MI. 3 Several studies have demonstrated that cessation of smoking reduces the incidence of recurrent MI and associated mortality rates. 4,5 Proatherogenic and prothrombotic effects of cigarette smoking are related to toxicity of tobacco smoke. 6-8 It is estimated that over 4300 chemical compounds are present in tobacco smoke. 9 The most toxic vapor phase is carbon monoxide. The particulate phase is a solid aerosol, of which nicotine constitutes about 85% to 90% of total alkaloid weight. 9 Cotinine, the metabolite orIGInAL ArtIcLE AbstrAct IntroductIon Exposure to tobacco smoke is associated with a higher cardiovascular risk, especially in patients with coronary artery disease (CAD). objEctIvEs 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. PAtIEnts And 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. orIGInAL ArtIcLE Tobacco smoke exposure and endothelial dysfunction... 475
doi:10.20452/pamw.1889 fatcat:nogheragrbbo3nttte6zpndowq