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Original Research: Tobacco Cessation and Prevention |

Airway Vascular Endothelial Function in Healthy Smokers Without Systemic Endothelial DysfunctionAirway Endothelial Function in Smokers

Eliana S. Mendes, MD; Jose Eduardo D. Cancado, MD; Patricia Rebolledo; Joahna Arana; Meela Parker, RDCS, CCI; Alex Gonzalez, BA; Barry E. Hurwitz, PhD; Adam Wanner, MD, FCCP
Author and Funding Information

From the Division of Pulmonary, Critical Care and Sleep Medicine (Drs Mendes, Cancado, and Wanner and Mss Rebolledo and Arana), and Behavioral Medicine Research Center (Dr Hurwitz, Ms Parker, and Mr Gonzalez), University of Miami Miller School of Medicine, Miami, FL.

Correspondence to: Eliana S. Mendes, MD, 1600 NW 10th Ave, Room 7064-A, Miami, FL 33136; e-mail: emendes@med.miami.edu


Funding/Support: This study was supported by an academic grant from GlaxoSmithKline plc [CAD111340].

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details.


Chest. 2013;143(6):1733-1739. doi:10.1378/chest.12-1033
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Background:  Cigarette smoking can lead to systemic endothelial dysfunction. Since the airway circulation is exposed to a high concentration of cigarette smoke constituents, we reasoned that airway vascular endothelial dysfunction could be present in healthy smokers without systemic endothelial dysfunction.

Objectives:  The purpose of this study was to compare airway and systemic endothelial function and measure markers of systemic inflammation in lung-healthy current smokers. Since endothelial dysfunction in smokers has been related to systemic inflammation, we also investigated its response to an inhaled glucocorticosteroid (ICS).

Methods:  Fifteen healthy, current smokers and 17 healthy, lifetime nonsmokers were enrolled. Smokers were randomly assigned to 3-week treatments with inhaled fluticasone propionate or placebo in a crossover design. Vascular endothelial function was assessed in the airway by the airway blood-flow response to inhaled albuterol (ΔQaw) and in the extrapulmonary circulation by brachial arterial flow-mediated vasodilation (FMD). Venous blood was collected for C-reactive protein and IL-6.

Results:  Baseline parameters did not differ between groups except for ΔQaw, which was greater in nonsmokers (45% ± 12%) than smokers (1% ± 12%) (P = .001). In the smokers, ICS treatment increased Qaw to 41% ± 7% (P < .001), but had no effect on FMD or inflammatory markers. There was an inverse relationship between baseline and ICS-induced changes in ΔQaw.

Conclusions:  Healthy smokers with no signs of systemic inflammation or endothelial dysfunction display impaired airway vascular endothelial function, possibly preceding systemic endothelial dysfunction. Airway endothelial function was restored with an ICS, and the response was directly related to the severity of endothelial dysfunction.

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