OBJECTIVES: To explore the effect of acute smoking on vascular endothelial function, arterial stiffness and the possible underlying mechanisms. METHODS: We measured the endothelial function and arterial stiffness in 50 healthy chronic smokers before and after acute smoking with EndoPAT2000. The test was carried out on two separate finger tips. The endothelial function was evaluated by PAT ratio of the finger tip and systemic arterial stiffness was evaluated by augmentation index (AI). Plasma soluble intercellular adhesion molecule-1 (sICAM-1) and tissue plasminogen activator (tPA) before and 20 min after acute smoking were measured with enzyme linked immuno sorbent assay. RESULTS: The PAT ratio was decreased (1.87 ± 0.40 vs. 1.73 ± 0.28, P = 0.004) while AI was significantly increased after acute smoking (2.94% ± 21.77% vs. 7.11% ± 20.65%, P = 0.01). There was no significant changes in sICAM [(306.5 ± 76.1) µg/L vs. (315.7 ± 90.9) µg/L, P = 0.402], but tPA [7.87 (5.41 - 10.08) µg/L vs. 5.77 (3.77 - 9.68) µg/L, P < 0.01] was significantly decreased after smoking. CONCLUSIONS: Smoking could acutely affect endothelia function, arterial stiffness and deteriorate the activity of fibrinolytic system which could lead to coronary thrombosis in smokers.
OBJECTIVES: To explore the effect of acute smoking on vascular endothelial function, arterial stiffness and the possible underlying mechanisms. METHODS: We measured the endothelial function and arterial stiffness in 50 healthy chronic smokers before and after acute smoking with EndoPAT2000. The test was carried out on two separate finger tips. The endothelial function was evaluated by PAT ratio of the finger tip and systemic arterial stiffness was evaluated by augmentation index (AI). Plasma soluble intercellular adhesion molecule-1 (sICAM-1) and tissue plasminogen activator (tPA) before and 20 min after acute smoking were measured with enzyme linked immuno sorbent assay. RESULTS: The PAT ratio was decreased (1.87 ± 0.40 vs. 1.73 ± 0.28, P = 0.004) while AI was significantly increased after acute smoking (2.94% ± 21.77% vs. 7.11% ± 20.65%, P = 0.01). There was no significant changes in sICAM [(306.5 ± 76.1) µg/L vs. (315.7 ± 90.9) µg/L, P = 0.402], but tPA [7.87 (5.41 - 10.08) µg/L vs. 5.77 (3.77 - 9.68) µg/L, P < 0.01] was significantly decreased after smoking. CONCLUSIONS: Smoking could acutely affect endothelia function, arterial stiffness and deteriorate the activity of fibrinolytic system which could lead to coronary thrombosis in smokers.
Authors: Sowmya Venkatasubramanian; Radzi Mohd Noh; Shruti Daga; Jeremy P Langrish; Nikhil V Joshi; Nicholas L Mills; Ethan Hoffmann; Eric W Jacobson; George P Vlasuk; Brian R Waterhouse; Ninian N Lang; David E Newby Journal: J Am Heart Assoc Date: 2013-06-14 Impact factor: 5.501