A comparison of the acute hemodynamic effects of prostacyclin and hydralazine in primary pulmonary hypertension

Groves, Bertron Μ.; Rubin, Lewis J.; Frosolono, M.F.; Cato, Allen; Reeves, John Τ.

doi:10.1016/0002-8703(85)90013-4

Cited by 44 publications

(12 citation statements)

References 14 publications

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“…Although the choice of a threshold to define acute pulmo-nary vasodilator response varies in the literature, decreases in both a measure of PVR and MPAP are desired to reflect a significant effect on the pulmonary vasculature. [13][14][15][16][17][18][19][20] The acute responses to intravenous epoprostenol in this study compared with changes reported in patients with primary pulmonary hypertension are shown in Table 4. As a group, mean changes noted in both PVR and MPAP in patients with portopulmonary hypertension were slightly better than those changes seen in patients with primary pulmonary hypertension.…”

Section: Discussionmentioning

confidence: 99%

Improvement in pulmonary hemodynamics during intravenous epoprostenol (prostacyclin): A study of 15 patients with moderate to severe portopulmonary hypertension

et al. 1999

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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 right-heart catheterization. 1 Patients with portal hypertension have multiple factors that contribute to the development of pulmonary arterial or venous hypertension. Such factors include an arterial hyperdynamic circulatory state (increased cardiac output [CO]), increased central venous volume (associated with an elevated pulmonary capillary wedge pressure [PCWP]) and pulmonary artery vasoconstriction/ obliteration (increased pulmonary vascular resistance with a normal PCWP). [2][3][4] In the setting of portal hypertension, the development of a vasoconstrictive/obliterative process affecting the pulmonary arterial bed causing increased pulmonary vascular resistance (PVR) has been described as ''portopulmonary hypertension. '' 4,5 Histopathology of the pulmonary arterial lesions associated with portal hypertension is indistinguishable from that seen in primary pulmonary hypertension.

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Section: Discussionmentioning

confidence: 99%

Improvement in pulmonary hemodynamics during intravenous epoprostenol (prostacyclin): A study of 15 patients with moderate to severe portopulmonary hypertension

et al. 1999

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“…This observation underscores the great variability in the course of thisdisease and serves to emphasize the need to individualize the approach to therapy for each patient. 75 Prostacyclin is not commercially available in the United States at the present time; alternatives which may be suitable for testing acute reactivity include acetylcholine, prostaglandin E 1, and adenosine. 72 The approach taken in many centers is to use a potent, short acting, titratable vasodilator such as immediate intravenous infusion of prostacyclin {prostaglandin IJ during right-sided heart catheterization to determine the potential and magnitude of vasoreactivity.…”

Section: Vasodilatorsmentioning

confidence: 99%

Primary Pulmonary Hypertension

Rubin¹

1993

Chest

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301

100

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“…Additional evidence comes from a study that showed that the hemodynamic effects of hydralazine and PGI 2 were strikingly similar, and suggested that PGI 2 responsiveness (e.g. to iloprost, a synthetic prostacyclin analog) could be used to predict a patient's response to hydralazine [45].…”

Section: Discussionmentioning

confidence: 99%

Mechanism of hydralazine-induced relaxation in resistance arteries during pregnancy

Maille

Gokina

Mandalà

et al. 2016

Vascular Pharmacology

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A comparison of the acute hemodynamic effects of prostacyclin and hydralazine in primary pulmonary hypertension

Cited by 44 publications

References 14 publications

Improvement in pulmonary hemodynamics during intravenous epoprostenol (prostacyclin): A study of 15 patients with moderate to severe portopulmonary hypertension

Improvement in pulmonary hemodynamics during intravenous epoprostenol (prostacyclin): A study of 15 patients with moderate to severe portopulmonary hypertension

Primary Pulmonary Hypertension

Mechanism of hydralazine-induced relaxation in resistance arteries during pregnancy

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