Smoking correlates with flow-mediated brachial artery vasoactivity but not cold pressor vasoactivity in men with coronary artery disease
Impaired endothelial function is observed as altered vasomotion in both the peripheral and coronary circulation in the presence of cardiovascular risk factors and early atherogenesis. An improvement in endothelium-dependent vasoactivity has been reported with both cholesterol reduction and smoking cessation. This study was performed to determine whether smoking status in coronary artery disease (CAD) effects both flow-mediated and cold pressor vasoactivity. We studied 25 men (ages 30–59), 12 smokers and 13 nonsmokers with angiographically documented coronary artery disease and cardiac risk factors who were grouped as smokers and nonsmokers. Using 7.5MHz ultrasound, we measured brachial artery diameter and Doppler flow velocity at baseline, following 5 mins of ipsilateral blood pressure cuff occlusion and release (flow-mediated), during contralateral ice water hand immersion (cold pressor test) and after sublinqual nitroglycerin administration (an endothelium-independent vasodilator). Flow-mediated percent diameter change was significantly less in the smokers than nonsmokers (1.9 ± 5.7% vs 11.4 ± 7.2%, p <0.001). Both smokers and nonsmokers responded similarly to the cold pressor test (–3.9 ± 2.3 vs –1.2 ± 0.2%) and nitroglycerin (15.1 ± 7.6 vs 17.5 ± 8.3%). Cholesterol level did not appear to be an independent determinant of flow-mediated vasoactivity when smoking status whas taken into account. Flow-mediated vasoactivity is associated with smoking status in the presence of coronary artery disease but cold pressor induced vasoactivity is not.