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[Treatment of pulmonary arterial hypertension by endothelin receptor antagonists in 2008]

Author(s): Cacoub P, Amoura Z, Langleben D

Affiliation(s): Service de medecine interne, AP-HP, hopital Pitie-Salpetriere, 47-83, boulevard de l'Hopital, 75013 Paris, France. patrice.cacoub@psl.aphp.fr

Publication date & source: 2008-04, Rev Med Interne., 29(4):283-9. Epub 2008 Feb 19.

Publication type: English Abstract; Review

PURPOSE: Pulmonary arterial hypertension (PAH) is a progressive disease characterized by an elevation of pulmonary-artery pressure and pulmonary-vascular resistance, leading to right-ventricular failure and death. Conventional therapy for PAH may include anticoagulation, digoxin, diuretics, supplemental oxygen and less often calcium-channel blockers. Protaglandins and sildenafil improve exercise capacity and hemodynamics. CURRENT KNOWLEDGE AND KEY POINTS: Endothelin-1 (ET-1) has been recognized as a major mediator in the pathogenesis of PAH. ET-1 receptor antagonists have been recently developed. Selective ET(A) receptor antagonists, which preserve endothelial ET(B) receptor vasodilatory and clearance activity, may offer more benefit than nonselective ET(A) plus ET(B) antagonists. Two ET-1 receptor antagonists, orally active, can be used: bosentan (ET(A)/ET(B)=20) is nonselective and sitaxentan (ET(A)/ET(B)=6500) is highly selective. In short-term studies, these two treatments showed similar efficacy. In the Sitaxentan To Relieve ImpaireD Exercise-2X (STRIDE-2X) one-year trial, which compared the two treatments, sitaxentan caused less liver toxicity and showed trends to higher efficacy than bosentan. FUTURE PROSPECTS AND PROJECTS: Individualized treatment for PAH should take into account the type of PAH, the comorbidities (liver disease), treatment interactions, and long-term efficacy.

Page last updated: 2008-06-22

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