Hemodynamics and epoprostenol use are associated with thrombocytopenia in pulmonary arterial hypertension.
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 (Svo(2)) [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 Svo(2) 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.


CONCLUSIONS
Epoprostenol use and severity of hemodynamic abnormalities are associated with thrombocytopenia in PAH, and these effects appear to be independent and additive.
Chin
Kelly M
KM
Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX. Electronic address: kelly.chin@utsouthwestern.edu.
Channick
Richard N
RN
Department of Internal Medicine, University of California, San Diego, CA.
de Lemos
James A
JA
Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX.
Kim
Nick H
NH
Department of Internal Medicine, University of California, San Diego, CA.
Torres
Fernando
F
Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX.
Rubin
Lewis J
LJ
Department of Internal Medicine, University of California, San Diego, CA.
D000284:Administration, Oral; D000959:Antihypertensive Agents / Q000008:administration & dosage*; D015331:Cohort Studies; D003430:Cross-Sectional Studies; D011464:Epoprostenol / Q000008:administration & dosage*; D005260:Female; D006439:Hemodynamics / Q000502:physiology*; D006801:Humans; D006976:Hypertension, Pulmonary / Q000188:drug therapy* / Q000209:etiology / Q000503:physiopathology*; D007262:Infusions, Intravenous; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D015995:Prevalence; D012307:Risk Factors; D013921:Thrombocytopenia / Q000453:epidemiology*; D055815:Young Adult
D000959:Antihypertensive Agents; D011464:Epoprostenol