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Is Systemic Inflammation Responsible for Pulmonary Hypertension in COPD?

Don D. Sin, MD, MPH, FCCP; S. F. Paul Man, MD, FCCP
Author and Funding Information

Affiliations: Vancouver, BC, Canada
 ,  Drs. Sin and Man are affiliated with the James Hogg iCAPTURE Center for Cardiovascular and Pulmonary Research, St. Paul’s Hospital and the Department of Medicine, Division of Respirology, The University of British Columbia.

Correspondence to: Don D. Sin, MD, MPH, FCCP, James Hogg iCAPTURE Center for Cardiovascular and Pulmonary Research, St. Paul’s Hospital, Room 368A, 1081 Burrard St, Vancouver, BC, V6Z 1Y6 Canada; e-mail: dsin@mrl.ubc.ca



Chest. 2006;130(2):310-312. doi:10.1378/chest.130.2.310
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Extract

Mild pulmonary hypertension is a common complication in patients with COPD, even in those without significant arterial hypoxemia, and is independently associated with poor prognosis.12 Pathologically, the pulmonary vessels in such individuals demonstrate arterial remodeling, which fails to reverse with supplemental oxygen therapy. Curiously, the remodeling process in COPD patients involves all layers of the vasculature and not just the medial (muscular) layer, as would be expected in patients with hypoxia-induced conditions,3 which suggests the involvement of other factors. Other putative causes of pulmonary hypertension in COPD patients include loss of the capillary bed secondary to emphysema, vessel compression from dynamic hyperinflation, endothelial dysfunction related to cigarette smoking, and abnormal proliferation and delayed apoptosis of smooth muscle cells secondary to genetic alterations or infectious agents.3

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