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Clinical Investigations: CARDIOLOGY |

Plasma Markers of Endothelial Dysfunction in Pulmonary Hypertension*

Giuseppe Cella, MD; Fabio Bellotto, MD; Francesco Tona, MD; Alessandra Sbarai, MD; Gabriella Mazzaro, MD; Giovanna Motta, MD; Jawed Fareed, PhD
Author and Funding Information

From the Department of Medical and Surgical Sciences (Drs. Cella, Sbarai, Mazzaro, and Motta) and the Department of Cardiology (Drs. Bellotto and Tona), University of Padova, Medical School, Padova, Italy; and the Department of Pathology and Pharmacology (Dr. Fareed), Loyola University of Chicago, Maywood, IL.

Correspondence to: Giuseppe Cella, MD, Dipartimento di Scienze Mediche e Chirurgiche, Università degli Studi di Padova, Via Ospedale Civile 105, 35100 Padova, Italy; e-mail: giuseppe.cella@unipd.it



Chest. 2001;120(4):1226-1230. doi:10.1378/chest.120.4.1226
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Study objectives: To evaluate and to correlate endothelial cell dysfunction, using recently available plasma markers, with the magnitude of pulmonary artery pressure in patients with severe pulmonary hypertension (PH).

Design: Selected plasma markers of endothelial cell dysfunction were studied: nitric oxide (NO), thrombomodulin, tissue factor pathway inhibitor, and soluble endothelium, leukocyte, and platelet selectins (sE-, sL-, sP-selectins, respectively).

Setting: Padova University Hospital and Department of Pathology and Pharmacology, Loyola University of Chicago, Chicago, IL.

Patients: Fifteen patients had severe PH (four men and 11 women; mean age, 49.7 ± 2.9 years: seven patients had primary pulmonary hypertension [PPH] and eight patients had secondary pulmonary hypertension [SPH]), and 20 patients were healthy control subjects.

Measurement and results: In patients with PH, sP- and sE-selectins were elevated, whereas sL-selectin was lower in comparison with the selectin levels in control subjects. However, the differences between patients with PH and control subjects were significant only for sL-selectin (p < 0.0001) and sE-selectin (p < 0.03). The NO level was significantly lower in patients with PH compared with the NO level in control subjects (p < 0.01). No difference in tissue factor pathway inhibitor level was noted between control subjects and patients with PH. Only a weak correlation was found between thrombomodulin plasma levels and magnitude of systolic pulmonary artery pressure (r = −0.528, p < 0.05).

Conclusions: Our data are in keeping with the evidence for significant endothelial cell dysfunction in patients with PH and the need for chronic anticoagulation believed to increase survival in these patients. In addition, these data seem to suggest a need for newer agents that are able to increase the antithrombotic endothelial function.

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