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Original Research |

Hemodynamics and Epoprostenol Use Are Associated With Thrombocytopenia in Pulmonary Arterial Hypertension

Kelly M. Chin, MD*; Richard N. Channick, MD, FCCP; James A. de Lemos, MD; Nick H. Kim, MD; Fernando Torres, MD; Lewis J. Rubin, MD, FCCP
Author and Funding Information

*From the Department of Internal Medicine (Drs. Chin, de Lemos, and Torres), University of Texas Southwestern Medical Center, Dallas, TX; and Department of Internal Medicine (Drs. Channick, Kim, and Rubin), University of California, San Diego, CA.

Correspondence to: Kelly M. Chin, MD, University of Texas Southwestern Pulmonary Hypertension Program, 5909 Harry Hines Blvd, Dallas, TX 75235-9254; e-mail: kelly.chin@utsouthwestern.edu

*No significant difference in platelet counts was seen based on PAH etiology.

*Etiology, use of endothelin receptor antagonists, and use of sildenafil were not associated with thrombocytopenia (data not shown). ORs are for a 1-unit change.

*Data are presented as mean ± SD. Svo2 was higher among epoprostenol-treated patients, while other hemodynamic results were similar between the two groups.

*Based on the multivariable model, platelet count can be estimated as platelet count = 295,000 – (1.22 × epoprostenol dose) – (6 × mean right atrial pressure). Given the R2 of the model, these variables account for a statistically significant but numerically modest portion of the overall variability in platelet counts.

This work was performed at University of Texas Southwestern and University of California, San Diego.

Drs. Chin, Channick, Kim, Rubin, and Torres have received consulting fees and/or honoraria from Gilead, distributor of Flolan (epoprostenol). Dr. de Lemos had no disclosures.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (www.chestjournal.org/misc/reprints.shtml).


This work was performed at University of Texas Southwestern and University of California, San Diego.

This work was performed at University of Texas Southwestern and University of California, San Diego.

Drs. Chin, Channick, Kim, Rubin, and Torres have received consulting fees and/or honoraria from Gilead, distributor of Flolan (epoprostenol). Dr. de Lemos had no disclosures.

Drs. Chin, Channick, Kim, Rubin, and Torres have received consulting fees and/or honoraria from Gilead, distributor of Flolan (epoprostenol). Dr. de Lemos had no disclosures.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (www.chestjournal.org/misc/reprints.shtml).

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (www.chestjournal.org/misc/reprints.shtml).


Chest. 2009;135(1):130-136. doi:10.1378/chest.08-1323
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Background:  Thrombocytopenia develops in some patients with advanced pulmonary arterial hypertension (PAH) while receiving IV epoprostenol therapy. In this study, we evaluate whether epoprostenol use, other PAH medication use, hemodynamics, or PAH etiology are associated with thrombocytopenia in PAH.

Methods:  Platelet counts were evaluated in 47 PAH patients receiving IV epoprostenol, and in 44 patients with an inadequate response to initial therapy with oral agents in a cross-sectional study. Associations between thrombocytopenia (platelet count < 150,000/mL) and epoprostenol use, hemodynamics, PAH etiology, and use of other PAH medications were evaluated in univariable and multivariable analyses.

Results:  PAH subtypes included idiopathic (69%), fenfluramine (18%), connective tissue disease (10%), and congenital heart disease (2%)-associated PAH. Thrombocytopenia was observed in 34% of patients treated with epoprostenol, compared with 15% of patients receiving oral therapy (odds ratio [OR], 2.9; p < 0.05), and the association between epoprostenol and thrombocytopenia remained significant after adjustment for differences in hemodynamics (OR, 5.0; p < 0.05). Right atrial pressure (OR, 1.12 per mm Hg; p < 0.05) and mixed venous oxygen saturation (Svo2) [OR, 0.92 per percentage; p < 0.05] were also associated with thrombocytopenia in univariable analyses; after logistic regression analysis, both the use of epoprostenol and Svo2 were independently associated with thrombocytopenia. In a separate analysis including only patients with current or prior epoprostenol use, epoprostenol dose and right atrial pressure were inversely associated with platelet count.

Conclusion:  Epoprostenol use and severity of hemodynamic abnormalities are associated with thrombocytopenia in PAH, and these effects appear to be independent and additive.

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