Pathologic assessment of vasculopathies in pulmonary hypertension
Giuseppe G. Pietra, MD*,*,
Frederique Capron, MD
,
Susan Stewart, MD
,
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
Service d'Anatomie Pathologique 1, Hôpital de la Pitié, 83, bd de l'Hôpital 75651 Paris Cedex, 13, France
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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Copyright © 2004 by the American College of Cardiology Foundation.