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Endothelin receptor antagonists in pulmonary arterial hypertension

Richard N. Channick, MD^*,*, Olivier Sitbon, MD, Robyn J. Barst, MD, Alessandra Manes, MD and Lewis J. Rubin, MD^*

^* Pulmonary and Critical Care Division, University of California, San Diego, California, USA
Division of Pulmonary and Critical Care Medicine, University of Paris-Sud, Paris, France
Division of Pediatric Cardiology, Columbia–Presbyterian Hospital, New York, New York, USA
Institute of Cardiology, University of Bologna, Bologna, Italy

View larger version (29K): [in a new window]   Figure 1 Hemodynamic effects of bosentan versus placebo at 12 weeks. Significant improvements in cardiac index (CI), pulmonary vascular resistance (PVR), and mean pulmonary arterial pressure (mPAP) were all noted. The placebo group worsened over the 12-week period. Adapted from Channick et al. (27)—original work. Control group is shown in blue; bosentan group is shown in green. Significant improvement versus baseline; *Significant decline versus baseline.

View larger version (23K): [in a new window]   Figure 2 Six-minute walk distance improvement seen in study of 213 patients demonstrating significant treatment effect of bosentan. (From Rubin et al. [28]).

View larger version (21K): [in a new window]   Figure 3 Delay in clinical worsening in bosentan-treated patients. Clinical worsening was defined as death, premature withdrawal from study, hospitalization for worsening pulmonary arterial hypertension, or initiation of epoprostenol. (From Rubin et al. [28]).

View larger version (18K): [in a new window]   Figure 4 Six-minute walk distance improvement seen in study of 178 patients demonstrating significant treatment effect of sitaxsentan. (From Barst et al. [37]).