Chest
Original ResearchPulmonary Arterial HypertensionHemodynamics and Epoprostenol Use Are Associated With Thrombocytopenia in Pulmonary Arterial Hypertension
Section snippets
Materials and Methods
This study included current and former epoprostenol-treated PAH patients seen over a 12-month period as well as a comparison group of PAH patients receiving oral therapy. Patients were required to have undergone right-heart catheterization while receiving treatment and have a platelet count within 1 month of catheterization. In order to minimize potential bias related to the severity of PAH, oral therapy patients were included only if they had had an “inadequate response” to their current
Results
A total of 93 patients with PAH were studied, including 47 patients currently receiving epoprostenol, 6 patients who had previously received epoprostenol, and 40 patients receiving oral therapy with plans to add on an oral, inhaled, or IV agent. Patients had idiopathic PAH (69%), and PAH associated with fenfluramine use (18%), connective tissue disease (10%), or congenital heart disease (2%). Frequency of PAH subgroups was similar among patients receiving epoprostenol compared with those
Discussion
The results of this study suggest that abnormal right-heart hemodynamics and use of epoprostenol are associated with thrombocytopenia in patients with severe PAH, and that higher doses of epoprostenol are associated with lower platelet counts than lower doses of epoprostenol. The effects of hemodynamic abnormalities and epoprostenol were independent and additive, with the highest rates of thrombocytopenia seen among patients with both severe hemodynamic abnormalities and use of epoprostenol.
References (28)
- et al.
Human endothelial cells inhibit platelet aggregation by stimulating cAMP and cGMP
Eur J Pharmacol
(1989) - et al.
Effect of intentional hemodilution on platelet survival in secondary pulmonary hypertension
Chest
(1989) - et al.
Epoprostenol for treatment of pulmonary hypertension in patients with systemic lupus erythematosus
Chest
(2000) - et al.
Epoprostenol for treatment of pulmonary hypertension in patients with systemic lupus erythematosus
Chest
(2000) - et al.
Thrombocytopenia associated with chronic intravenous epoprostenol therapy [abstract]
Chest
(2004) - et al.
Expression of prostacyclin receptor in human megakaryocytes
Blood
(1997) - et al.
The effect of prostacyclin agonists on the differentiation of phorbol ester treated human erythroleukemia cells
Prostaglandins Other Lipid Mediat
(2007) - et al.
Transition from IV to subcutaneous prostacyclin: premature withdrawal?
Chest
(2007) - et al.
A comparison of continuous intravenous epoprostenol with conventional therapy in primary pulmonary hypertension
N Engl J Med
(1996) - et al.
Activation of cGMP stimulated phosphodiesterase by nitroprusside limits cAMP accumulation in human platelets: effects on platelets aggregation
Biochem J
(1997)
Aerosolized iloprost induces a mild but sustained inhibition of platelet aggregation
Eur Respir J
Drug-induced thrombocytopenia: an updated systematic review
Ann Intern Med
Frequency and pathogenesis of thrombocytopenia in cardiac failure [in German]
Dtsch Med Wochenschr
Measurement of spleen size and its relation to hypersplenism and portal hemodynamics in portal hypertension due to hepatic cirrhosis
Am J Gastroenterol
Cited by (0)
This work was performed at University of Texas Southwestern and University of California, San Diego.
Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (www.chestjournal.org/misc/reprints.shtml).
- 1
Drs. Chin, Channick, Kim, Rubin, and Torres have received consulting fees and/or honoraria from Gilead, distributor of Flolan (epoprostenol).
- 2
Dr. de Lemos had no disclosures.