How prostacyclin improves cardiac output in right heart failure in conjunction with pulmonary hypertension

Kerbaul, François;Brimioulle, Serge;Rondelet, Benoît;Dewachter, Céline;Naeije, Robert;et.al.
(2007) American Journal of Respiratory and Critical Care Medicine — Vol. 175, n° 8, p. 846-850 (2007)

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Authors
  • Kerbaul, FrançoisULB
    Author
  • Brimioulle, SergeErasme University Hospital
    Author
  • Author
  • Dewachter, CélineULB
    Author
  • Naeije, RobertULB
    Author
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Abstract
Rationale: Prostacyclin therapy improves patients with pulmonary arterial hypertension, but whether this is attributable to an improved inotropic state of the right ventricle in addition to a decreased pulmonary arterial pulmonary vascular resistance remains unclear. Objectives: We measured the effects of prostacyclin on loadindependent measurements of right ventricular contractility in a model of load-induced acute right ventricular failure. Methods and Results: Persistent right ventricular failure was induced in dogs by a transient (90 min) pulmonary arterial constriction. After constriction release and stabilization, intravenous prostacyclin (epoprostenol) was given at doses of 6 and 12 ng/kg/minute for 30 minutes. Pulmonary vascular resistance was assessed by pressure-flow relationships and right ventricular afterload by effective pulmonary arterial elastance. Right ventricular contractility was estimated by end-systolic elastance and right ventriculoarterial coupling efficiency by the ratio of these elastances. Transient pulmonary arterial constriction persistently increased pulmonary vascular resistance, increased arterial elastance from 1.00 ± 0.07 to 2.86 ± 0.26 mm Hg/ml, decreased end-systolic elastance from 1.11 ± 0.07 to 0.54 ± 0.02 mm Hg/ml, decreased the ratio of elastances from 1.14 ± 0.08 to 0.20 ± 0.02, and cardiac output from 4.6 ± 0.1 to 2.3 ± 0.1 L/min (p < 0.05). Epoprostenol did not affect end-systolic elastance; however, it decreased arterial elastance to 1.84 ± 0.33 mm Hg/ml, and increased the ratio of elastances to 0.46 ± 0.17 and cardiac output to 3.4 ± 0.3 L/min (p < 0.05). Conclusions: In this model of afterload-induced right ventricular failure, prostacyclin improves right ventriculoarterial coupling and cardiac output because of vasodilating effects.
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Citations

Kerbaul, F., Brimioulle, S., Rondelet, B., Dewachter, C., Hubloue, I., & Naeije, R. (2007). How prostacyclin improves cardiac output in right heart failure in conjunction with pulmonary hypertension. American Journal of Respiratory and Critical Care Medicine, 175(8), 846-850. https://doi.org/10.1164/rccm.200611-1615OC (Original work published 2007)