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J Am Coll Cardiol, 2004; 43:25-32
© 2004 by the American College of Cardiology Foundation
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Pathologic assessment of vasculopathies in pulmonary hypertension

Giuseppe G. Pietra, MD*,*, Frederique Capron, MD{dagger}, Susan Stewart, MD{ddagger}, Ornella Leone, MD§, Marc Humbert, MD, Ivan M. Robbins, MD, Lynne M. Reid, MD|| and R. M. Tuder, MD**

* Department of Pathology, University of Pennsylvania, School of Medicine, Philadelphia, Pennsylvania, USA
{dagger} Service d'Anatomie Pathologique 1, Hôpital de la Pitié, 83, bd de l'Hôpital 75651 Paris Cedex, 13, France
{ddagger} Papworth Hospital, Papworth Everard, Cambridge, United Kingdom
§ Department of Pathology, Azienda Ospedaliera S. Orsola-Malpighi of Bologna, Bologna, Italy
Service de Pneumologie et Réanimation Respiratoire, Hôpital Antoine Béclère, Assistance Publique, Hôpitaux de Paris, Université Paris-Sud, Clamart, France
Vanderbilt University Medical Center, Adult Pulmonary Hypertension Center, Vanderbilt University, Nashville, Tennessee, USA
|| Department of Pathology, Harvard Medical School, Boston, MassachusettsBaltimore, Maryland, USA
** Division of Cardiopulmonary Pathology, The Johns Hopkins University, School of Medicine, Baltimore, Maryland, USA



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Figure 1 Main histopathological features of pulmonary arteriopathy (see text for details). (All histological sections were stained with Verhoeff-van Gieson unless specified.) Medial hypertrophy: (A) preacinar pulmonary artery, x80; (B) intra-acinar artery, x600. Concentric laminar intimal thickening: (C) intra-acinar artery, x500; (D) pre-acinar artery. The vessel was decorated with anti-smooth muscle actin antibodies (SMA), revealing the intimal thickening (white arrow) to be composed of SMA-positive cells, x150. Eccentric (E) x100 and concentric nonlaminar (F) x100 intimal thickening of pre-acinar arteries. Plexiform lesions: (G) intra-acinar artery decorated with SMA showing SMA-negative endothelial cells (arrow) surrounded by a rim of SMA-positive cells (rusty color), x380; (H) pre-acinar artery adjacent to a plexiform lesion (arrow) and dilation lesions (shown by asterisk) x60. (I) Dilation lesions (arrows), x40; (J) colander-like lesion, HE x400; (K) lymphomonocytic arteritis, HE, x300.

 


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Figure 2 Pulmonary occlusive venopathy. (A) Septal veins with nearly occluded lumens by fibrous intimal thickening (asterisk), marked lymphatic dilation (arrow), and congested alveolar capillaries. Verhoeff-van Gieson staining, x50. (B) Obstructive fibrous intimal thickening and recanalization channels in a septal vein, x200. Pulmonary microvasculopathy. (C) Focal thickening of alveolar septa by proliferated capillaries, HE,x20. (D) Nodular capillary proliferation, hemosiderin-laden alveolar macrophages and type II pneumocytes (arrows), HE, x300.

 





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