Polskie Archiwum Medycyny Wewnetrznej · 2013
Tobacco smoke exposure and endothelial dysfunction in patients with advanced coronary artery disease.
Клиническое исследованиеСтатьяНазвание и аннотация: Перевод в очереди
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Szpak Dorota, Grochowalski Andrzej, Chrząszcz Ryszard, Florek Ewa, Jawień Wojciech, Undas Anetta
Аннотация
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.
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.