Improvement in pulmonary hemodynamics during intravenous epoprostenol (prostacyclin): A study of 15 patients with moderate to severe portopulmonary hypertension
✍ Scribed by Michael J. Krowka; Robert P. Frantz; Michael D. McGoon; Cathy Severson; David J. Plevak; Russell H. Wiesner
- Publisher
- John Wiley and Sons
- Year
- 1999
- Tongue
- English
- Weight
- 125 KB
- Volume
- 30
- Category
- Article
- ISSN
- 0270-9139
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✦ Synopsis
Pulmonary hypertension associated with increased pulmonary vascular resistance (PVR) and occurring in the setting of portal hypertension is referred to as ''portopulmonary hypertension.'' Intravenous epoprostenol (prostacyclin) is a potent pulmonary and systemic vasodilator with antithrombotic properties. It can decrease PVR and pulmonary artery pressure in patients with primary (idiopathic) pulmonary hypertension. Using right-heart catheterization, we evaluated the acute pulmonary hemodynamic effects of intravenous epoprostenol in patients with moderate to severe pulmonary hypertension (mean pulmonary artery pressure [MPAP] H35 mm Hg) associated with clinical manifestations of portal hypertension. Effects of long-term infusion of epoprostenol were also evaluated. We studied 15 consecutive patients with portopulmonary hypertension; 14 underwent acute administration of epoprostenol, and no significant side effects were noted. Ten patients received continuous epoprostenol (range, 8 days-30 months). Acute changes in PVR (؊34% ؎ 18%), MPAP (؊16% ؎ 10%), and cardiac output (CO) (؉21 ؎ 18%), were statistically significant (P F .01). Long-term use of epoprostenol further lowered PVR (؊47% ؎ 12% from baseline and ؊31% ؎ 22% from the acute change; P F .05) in the 6 patients restudied by right-heart catheterization. Death occurred in 6 of 10 (60%) of those receiving long-term epoprostenol. In moderate to severe portopulmonary hypertension, intravenous epoprostenol resulted in a significant improvement (both acute and long-term) in PVR, MPAP, and CO. Potential adverse effects on portal hypertension and implications for orthotopic liver transplantation (OLT), however, require further study. (HEPATOLOGY 1999;30:641-648.)
Pulmonary hypertension is defined as a mean pulmonary artery pressure (MPAP) Ͼ 25 mm Hg at rest determined by Abbreviations: MPAP, mean pulmonary artery pressure; CO, cardiac output; PCWP, pulmonary capillary wedge pressure; PVR, pulmonary vascular resistance; OLT, orthotopic liver transplantation.