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The Role of Smoking in Coagulation and Thromboembolism in Chronic Obstructive Pulmonary Disease

Division of Pulmonary and Critical Care, Duke University Medical Center, Durham, North Carolina

Correspondence and requests for reprints should be addressed to Victor F. Tapson, M.D., Professor of Medicine, Division of Pulmonary & Critical Care Medicine, Duke University Medical Center, Room 351 Bell Building, Durham, NC 27710. E-mail: tapso001{at}mc.duke.edu

Pulmonary embolism and deep vein thrombosis both account for many deaths in stable patients with chronic obstructive pulmonary disease (COPD), and the frequency of these events is higher during COPD exacerbations. The morbidity and mortality from deep vein thrombosis and pulmonary embolism in patients with COPD is not surprising given the reduced mobility associated with this disorder, in addition to the presence of coagulation abnormalities in smokers. The potential influence of inflammation on coagulation offers further potential to contribute to thrombogenesis in all smokers. Plasma fibrinogen levels are elevated in smokers and are further elevated during acute COPD exacerbation. Oral contraceptives cause significant increases in fibrinogen levels in smokers and nonsmokers, but only the latter appear to have a compensatory increase in antithrombin III activity. Factor XIII, which stabilizes fibrin clots, is increased in smokers. Quantitative exposure to passive smoke has been positively correlated with blood coagulation activity. Exposure to nicotine may also increase plasminogen activator inhibitor-1 (a major regulator of fibrinolysis), although the extent to which nicotine enhances coagulation is unresolved. Venous thromboembolism is a frequent and potentially fatal complication of patients with COPD. The interrelationship between smoking, COPD, and coagulation is intriguing and awaits further characterization.

Key Words: coagulation • COPD • smoking • fibrinogen • thromboembolism

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