<b>Aims:</b> Tobacco use is involved in endothelial dysfunction, a key marker of cardiovascular diseases. The contribution of tobacco use in their development is assessed by endothelial dysfunction-related biomarkers in smokers and non-smokers.<br />
<b>Methods:</b> 138 smokers and 83 non-smokers were recruited. Parameters reflecting the endothelial function, lipid profile and oxidative and inflammatory status, were quantified. Data were used to determine their ability to differentiate smokers and non-smokers.<br />
<b>Results:</b> Elevation of inflammation and oxidative stress as well as alteration of endothelial function and lipids profile in smokers were observed. Two biomarkers combinations, including one implying only routine parameters, were identified and allowed to correctly classify >84% of cases.<br />
<b>Conclusions:</b> Oxidative status, inflammatory status, and lipids profile were shown altered in smokers, leading to endothelial dysfunction. Endothelial dysfunction-related biomarkers were assessed in terms of their ability to discriminate smokers from non-smokers. The possibility of discrimination based only on classic parameters of blood test appeared conceivable.
Background
Tobacco use is known to be involved in the development of cardiovascular diseases, which leads to premature mortality. Endothelial dysfunction, the first step in this process, was shown induced by smoking. It is reported that quitting smoking could reduce the risk of diseases, but the implied mechanisms are still unclear. This study aimed to evaluate the biological markers of endothelial function in smokers when actively smoking and after cessation.
Methods
Quantification of several biomarkers reflecting inflammation, endothelium activation, oxidative stress, and lipids was performed in 65 smokers when actively smoking and after cessation (median abstinence duration of 70 days).
Results
A possible decrease of inflammation was observed through the concentration reduction of a proinflammatory cytokine (interleukine‐6) on quitting. A decrease of endothelium activation was visible by the reduced level of the soluble intercellular adhesion molecule. Two antioxidants, uric acid and vitamin C, were found at higher concentration than before the cessation, potentially reflecting the decrease of oxidative stress on quitting. Lipid profile was improved post‐quit since HDL level was increased and LDL level was decreased. All these effects were visible at short term with abstinence duration less than 70 days. No sex‐specific difference was observed and no additional changes were observed for longer abstinence duration.
Conclusion
These observations suggest that some adverse effects of smoking on endothelial function could be reversible on quitting smoking. It could encourage smokers to enter a cessation program to reduce the risk for cardiovascular diseases development.
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