BACKGROUND - Smoking is a major risk factor for cardiovascular events. One of the potential mechanisms may be related to both coronary endothelial dysfunction and increased inflammatory response. The present study was designed to test the hypothesis that smoking is associated with epicardial coronary endothelial dysfunction and inflammation. METHODS AND RESULTS - Coronary endothelial function in response to acetylcholine was assessed in 881 patients (115 current smokers and 766 nonsmokers, including 314 previous smokers). Smokers were significantly younger than nonsmokers (43±1 versus 51±1 years, P<0.0001), had more epicardial vasoconstriction in response to intracoronary acetylcholine (-19±2% versus -14±1% change in coronary artery diameter, P=0.03), and were more likely than nonsmokers to have epicardial endothelial dysfunction (46% versus 35%, P=0.005), but their microvascular endothelial function was intact. Smokers had higher white blood cell counts than nonsmokers (7.7±0.2 versus 6.6±0.1×10/L, P<0.0001), higher myeloperoxidase (156±19 versus 89±8 ng/mL), higher lipoprotein-associated phospholipase A2 (242±12 versus 215±5 ng/mL), and higher levels of intracellular adhesion molecule (283±14 versus 252±5 ng/mL). There were no differences in the levels of C-reactive protein, fibrinogen, or vascular cell adhesion molecule between the groups. CONCLUSION - Young smokers are characterized by epicardial coronary endothelial dysfunction, preserved microvascular endothelial function, and increased levels of inflammatory biomarkers and oxidative stress. The present study provides further information regarding the potential mechanisms by which smoking contributes to cardiovascular events.
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine
- Physiology (medical)