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J Am Coll Cardiol, 1999; 34:1184-1187
© 1999 by the American College of Cardiology Foundation
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CLINICAL STUDIES

The effects of chronic prostacyclin therapy on cardiac output and symptoms in primary pulmonary hypertension

Stuart Rich, MD, FACCa and Vallerie V. McLaughlin, MD, FACCa

a Department of Medicine, Section of Cardiology, Rush University Medical College, Chicago, Illinois, USA

Manuscript received October 14, 1998; revised manuscript received May 4, 1999, accepted June 11, 1999.

Reprint requests and correspondence: Dr. Stuart Rich, Professor of Medicine, Rush Heart Institute, Center for Pulmonary Heart Disease, Rush–Presbyterian–St. Luke’s Medical Center, Suite 020, 1725 West Harrison Street, Chicago, Illinois 60612
srich{at}rush.edu

OBJECTIVES

This study evaluated the response to prostacyclin dose reduction in patients with primary pulmonary hypertension (PPH) who developed high cardiac outputs.

BACKGROUND

Patients on prostacyclin require chronic upward dose titration to overcome tolerance to the medication. No upper limit of effective dose has been described.

METHODS

We studied 12 patients with PPH treated with chronic prostacyclin therapy who presented in high cardiac output states. Each patient underwent prostacyclin dose reduction under hemodynamic guidance targeted to reduce the cardiac index to ≤4 liter/min/M2, unless rebound pulmonary hypertension occurred. Following dose reduction, patients were observed for changes in the effectiveness of the prostacyclin.

RESULTS

Patients were treated for 39 ± 20 months, resulting in a 71% reduction in pulmonary vascular resistance compared to baseline. At the time of their most recent evaluation their cardiac outputs were increased to 10.1 ± 2.3 liter/min. The patients underwent a 39% dose reduction (range 12% to 78%) resulting in a change of mean PAP from 45 to 46 mm Hg (p = NS), cardiac index from 7.4 ± 1.4 to 4 ± 0.74 liter/min/M2 (p = 0.01), and pulmonary vascular resistance from 3.7 ± 1.7 to 4.7 ± 1.5 units (p < 0.001). In no instance did rebound pulmonary hypertension occur. However, the patients all retained their clinical benefit without a return of tolerance.

CONCLUSIONS

Excessive prostacyclin in PPH can lead to a high cardiac output state, suggesting it has important positive inotropic effects. In this circumstance, reducing the dose can allow the cardiac output to return to normal without worsening the clinical state.

Abbreviations and Acronyms
  ANOVA = analysis of variance
  IV = intravenous
  NYHA = New York Heart Association
  PPH = primary pulmonary hypertension




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