What is the clinical evidence from this study?

Study design: Observational. Population: Idiopathic Pulmonary Arterial Hypertension (IPAH) (n=16). Intervention: High-dose epoprostenol therapy vs. Baseline values. Primary outcome: Change in mean pulmonary artery pressure (mPAP) and pulmonary vascular resistance (PVR) (p=<0.001).

January 1, 2010Open Access

Marked Hemodynamic Improvements by High-Dose Epoprostenol Therapy in Patients With Idiopathic Pulmonary Arterial Hypertension

Q: What are the key findings of this study?

High-dose epoprostenol therapy significantly reduced mean pulmonary artery pressure by 30% (P<0.001) and pulmonary vascular resistance by 68% (P<0.001) from baseline in patients with IPAH.

Key Result

High-dose epoprostenol therapy significantly reduced mean pulmonary artery pressure by 30% (P<0.001) and pulmonary vascular resistance by 68% (P<0.001) from baseline in patients with IPAH.

Study Design

Type

Observational (n=16)

Structured PICO

Does high-dose epoprostenol monotherapy improve hemodynamics in patients with idiopathic pulmonary arterial hypertension?

Population

16 consecutive patients with idiopathic pulmonary arterial hypertension (IPAH) (14 assessed), mean age 28 ± 10 years, 5 men and 9 women. Baseline WHO functional class III (n=8) or IV (n=6).

Intervention

High-dose epoprostenol monotherapy (>40 ng/kg/min), mean dosage 107 ± 40 ng/kg/min (range 54-190 ng/kg/min), administered for a mean duration of 1,355 ± 627 days.

Outcome

Changes in cardiopulmonary hemodynamic parameters (mean pulmonary artery pressure [mPAP] and pulmonary vascular resistance [PVR]) from baseline to final evaluation (mean 1,355 days).surrogate

High-dose epoprostenol monotherapy (>40 ng/kg/min) significantly improves hemodynamics, including marked reductions in mPAP and PVR, in patients with severe idiopathic pulmonary arterial hypertension.

Main Result

p-value: p=<0.001

Abstract

BACKGROUND: The appropriate dose range of epoprostenol is thought to be 25-40 ng · kg(-1) · min(-1) based on the results of previous studies showing that epoprostenol therapy reduced mean pulmonary artery pressure (mPAP) by 12-22% and pulmonary vascular resistance (PVR) by 32-53% compared with baseline values in patients with idiopathic pulmonary arterial hypertension (IPAH). However, the efficacy of treatment of IPAH patients with epoprostenol >40 ng · kg(-1) · min(-1) has not been determined and this was the aim of the present study. METHODS AND RESULTS: The study group comprised 16 consecutive patients, none of whom died; 2 dropped out because they could not be titrated up as needed to the highest effective epoprostenol dose. Hemodynamics were evaluated in 14 IPAH patients who received high-dose epoprostenol monotherapy. The mean epoprostenol dosage was 107 ± 40 ng · kg(-1) · min(-1) (range, 54-190 ng · kg(-1) · min(-1)) and the mean duration of high-dose epoprostenol therapy was 1,355 ± 627 days (range, 582-2,410 days). Significant decreases from baseline values were seen in mPAP (from 66 ± 16 to 47 ± 12 mmHg, P<0.001) and PVR (from 21.6 ± 8.3 to 6.9 ± 2.9 Wood units, P<0.001). Compared with the baseline state, high-dose epoprostenol therapy reduced mPAP by 30% and PVR by 68%. CONCLUSIONS: The present study suggests high-dose epoprostenol therapy is a new treatment strategy for IPAH.

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