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Open AccessJournal ArticleDOI

Pathologic assessment of vasculopathies in pulmonary hypertension.

TLDR
A histopathological classification is proposed that includes both the predominant segment of the pulmonary vasculature affected and the possible coexistence of pathological changes in other vascular segments in PAH.
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This article is published in Journal of the American College of Cardiology.The article was published on 2004-06-16 and is currently open access. It has received 676 citations till now. The article focuses on the topics: Pulmonary Veno-Occlusive Disease & Pulmonary hypertension.

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Special article2015 ESC/ERS Guidelines for the Diagnosis and Treatment of Pulmonary Hypertension

TL;DR: This article is being published concurrently in the European Heart Journal and the European Respiratory Journal and is identical except for minor stylistic and spelling differences in keeping with each journal’s style.
References
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Journal ArticleDOI

Pulmonary arterial hypertension.

TL;DR: There is no cure for pulmonary arterial hypertension but several novel therapeutic options are now available that can improve symptoms and increase survival.
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Pulmonary vascular lesions occurring in patients with chronic major vessel thromboembolic pulmonary hypertension.

TL;DR: Primary pulmonary hypertension cannot be differentiated from potentially correctable CTEPH on the basis of histopathologic findings in small pulmonary arteries, and development of these hypertensive changes may explain the deterioration which these patients experience preoperatively over time.
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Mature vascular endothelium can give rise to smooth muscle cells via endothelial-mesenchymal transdifferentiation: in vitro analysis.

TL;DR: In vitro data show that mature bovine systemic and pulmonary endothelium contains cells that can acquire a SM phenotype via a transdifferentiation process that is transforming growth factor-&bgr;1– and cell-cell contact–dependent, but proliferation-independent.
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Monoclonal endothelial cell proliferation is present in primary but not secondary pulmonary hypertension.

TL;DR: The data of a frequent monoclonal endothelial cell proliferation in PPH suggests that a somatic genetic alteration similar to that present in neoplastic processes may be responsible for the pathogenesis of PPH.
Journal ArticleDOI

Treatment of pulmonary hemangiomatosis with recombinant interferon alfa-2a.

TL;DR: In this paper, the authors describe a patient with pulmonary hemangiomatosis who presented with digital clubbing and bilateral interstitial pulmonary disease, and they used interferon alfa-2a for 14 months.
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