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Pulmonary Hypertension*: Cellular and Molecular Mechanisms

Carlyne D. Cool, MD; Steve D. Groshong, MD, PhD; John Oakey, PhD; Norbert F. Voelkel, MD
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*From the Department of Pathology, University of Colorado Health Sciences Center and National Jewish Medical and Research Center, Denver, CO; Chemical Engineering Department, Colorado School of Mines, Golden, CO; and Pulmonary Hypertension Center and Pulmonary and Critical Care Medicine Division, University of Colorado Health Sciences Center, Denver, CO.

Correspondence to: Carlyne D. Cool, MD, Department of Pathology, B216, 4200 E Ninth Ave, University of Colorado Health Sciences Center, Denver, CO 80262; e-mail: carlyne.cool@uchsc.edu



Chest. 2005;128(6_suppl):565S-571S. doi:10.1378/chest.128.6_suppl.565S
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The pathology of pulmonary hypertension can be conveniently divided into endothelial, smooth-muscle, and/or adventitial abnormalities, although not all compartments of the pulmonary artery wall are involved in each case of severe pulmonary hypertension. The classic lesion of severe pulmonary hypertension is the plexiform lesion, an abnormal proliferation of predominantly endothelial cells. Smooth-muscle thickening can be seen in all forms of the disease but is not a constant feature in the idiopathic (primary) form of the disease. The adventitia is often markedly remodeled in patients with certain forms of collagen vascular diseases associated with severe pulmonary hypertension, most notably scleroderma (Fig 1 ).

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