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Coronary Progenitor Cells and Soluble Biomarkers in Cardiovascular Prognosis after Coronary Angioplasty
Published on: January 28, 2020
Cigarette smoking increases plasma concentrations of vascular cell adhesion molecule-1 in patients with coronary
Yuksel Cavusoglu1, Bilgin Timuralp, Tercan Us
1Department of Cardiology, Faculty of Medicine, Osmangazi University, Eskisehir, Turkey. yukselc@ogu.edu.tr
Insights
Cigarette smoking significantly increases soluble vascular cell adhesion molecule-1 (VCAM-1) levels in coronary artery disease (CAD) patients. This finding suggests smoking accelerates atherosclerosis by promoting inflammatory cell adhesion.
Area of Science:
- Cardiovascular Disease Research
- Inflammation and Immunology
- Atherosclerosis Pathogenesis
Background:
- Cigarette smoking negatively impacts endothelial function and elevates coronary artery disease (CAD) risk.
- Atherosclerosis pathogenesis involves inflammatory cell-endothelial interactions, with adhesion molecules playing a key role.
- The specific impact of smoking on these inflammatory processes in CAD remains under-investigated.
Purpose of the Study:
- To investigate the effect of cigarette smoking on plasma concentrations of soluble vascular cell adhesion molecule-1 (VCAM-1) in patients with CAD.
- To explore potential mechanisms linking smoking to accelerated atherosclerotic processes.
Main Methods:
- Quantification of soluble VCAM-1 plasma levels using enzyme-linked immunosorbent assay (ELISA).
- Comparison of soluble VCAM-1 levels between smoking CAD patients (n=19) and non-smoking CAD patients (n=10).
- Analysis of soluble VCAM-1 levels in relation to patient history of myocardial infarction (MI), hypertension, and disease severity.
Main Results:
- Soluble VCAM-1 levels were significantly higher in smoking CAD patients compared to non-smokers (32.13 vs 9.46 ng/mL, p < 0.01).
- A trend towards higher soluble VCAM-1 was observed in patients with prior MI, though not statistically significant.
- No significant differences in soluble VCAM-1 were found based on hypertension, vessel disease extent, or MI localization.
Conclusions:
- Smoking elevates soluble VCAM-1 levels in CAD patients, indicating increased endothelial adhesion molecule expression.
- Elevated soluble VCAM-1 in smokers may represent a key mechanism by which smoking accelerates atherosclerosis.
- Further research is warranted to elucidate the full impact of smoking-induced inflammation on cardiovascular disease progression.
Abstract:
Cigarette smoking adversely affects endothelial function and increases risk of coronary artery disease (CAD). The pathogenesis of coronary atherosclerosis is currently thought to involve interactions between inflammatory cells and vascular endothelium. Adhesion molecules play a pivotal role in the accumulation of inflammatory cells at the endothelium. Little is known about the role of cigarette smoking in this atherosclerotic inflammatory process. The aim of this study was to evaluate the effects of cigarette smoking on the plasma concentrations of soluble vascular cell adhesion molecule-1 (VCAM-1) in patients with CAD. The soluble VCAM-1 level was quantified in smoking CAD patients (n = 19) in comparison to those from patients with CAD alone (n = 10). Plasma concentrations of soluble VCAM-1 were measured by enzyme-linked immunosorbent assay. The soluble VCAM-1 level was found significantly higher in smokers than in nonsmokers (32.1279 +/- 21.6421 vs 9.4570 +/- 7.8138 ng/mL, p < 0.01), and in patients with previous myocardial infarction (MI) than in those without previous MI, but not significant statistically (27.7279 +/- 22.8813 vs 17.8170 +/- 15.9172 ng/mL, p > 0.05). No significant difference was observed for soluble VCAM-1 levels between hypertensive and nonhypertensive patients, multivessel and one-vessel disease, or anterior and inferior MI localizations. The present study suggests that in patients with CAD, smoking leads to elevated levels of soluble VCAM-1 that may clarify one of the mechanisms of its accelerating effect on the atherosclerotic process.
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