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Angiology
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Endothelial Dysfunction in Chronic Obstructive Pulmonary Disease

Leo Moro, MD

Area di Geriatria, Università Campus Biomedico, Rome, Italy, l.moro{at}unicampus.it

Claudio Pedone, MD, PhD, MPH

Area di Geriatria, Università Campus Biomedico, Rome, Italy

Simone Scarlata, MD

Area di Geriatria, Università Campus Biomedico, Rome, Italy

Vincenzo Malafarina, MD

Area di Geriatria, Università Campus Biomedico, Rome, Italy

Filippo Fimognari, MD

Respiratory Unit, Division of Internal Medicine, ASL Roma G-Leopoldo Parodi Delfino Hospital, Colleferro, Rome, Italy

Raffaele Antonelli-Incalzi, MD

Area di Geriatria, Università Campus Biomedico, Rome, Italy

Background: Cardiovascular diseases are prevalent in people with chronic obstructive pulmonary disease (COPD). We hypothesized that endothelial dysfunction could be a marker of the proatherogen status in COPD. Methods and results: We measured endothelial dysfunction by flow-mediated dilation (FMD) and after sublingual administration of nitroglycerin (nitrate-mediated dilation: NMD) in 44 COPD patients and 48 controls. Compared with controls COPD patients had worse mean FMD (5.4% vs 8.2%, P < .001) and NMD (12.0% vs 13.9%, P = .007). FMD was inversely related to FEV1/VC ratio (r = –0.327, P = .030). The negative association between COPD and FMD was confirmed after correction for potential confounders in a multiple linear regression model (β = –0.019, P = .002). In the same model NMD (β = 0.396, P < .001) was positively associated with FMD. Conclusions: Endothelial-dependent and, to a lesser extent, endothelial-independent dilations are significantly impaired in COPD, and the impairment is proportional to the severity of bronchial obstruction.

Key Words: endothelial dysfunction • COPD • atherosclerosis

This version was published on July 1, 2008

Angiology, Vol. 59, No. 3, 357-364 (2008)
DOI: 10.1177/0003319707306141


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