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Bosentan (Tracleer) Improves Symptoms in Patients With Eisenmenger's Syndrome: Presented at CHEST

By Ed Susman

MONTREAL, CANADA -- November 1, 2005 -- The dual endothelin receptor antagonist bosentan helped improve symptoms among patients suffering from pulmonary arterial hypertension caused by congenital heart defects in a study presented here at CHEST 2005, the American College of Chest Physicians Annual Meeting.

The study was the first placebo-controlled trial to show benefits in Eisenmenger's syndrome -- the development of a severe form of pulmonary arterial disease due to malformation of the heart's anatomy.

"Bosentan was well tolerated and improved exercise-induced capacity and haemodynamics without compromising peripheral oxygen saturation," said Nazzareno Galie, MD, professor of medicine, University of Bologna, Bologna, Italy.

"Bosentan may be an important new treatment option for patients with Eisenmenger's physiology, a disease with poor prognosis," Dr. Galie said.

In the BREATHE-5 study, researcher demonstrated that 16 weeks of treatment with bosentan (Tracleer) allowed patients to walk further in timed tests and decreased pulmonary vascular resistance in these patients, who were not amenable to any other therapy, including surgery.

The study's primary endpoint was to show that mean oxygen saturation was unaffected by treatment with bosentan. Subjects treated with bosentan showed a slight increase in oxygen operation, fulfilling the endpoint requirement that use of the drug did not worsen oxygen saturation.

Dr. Galie and associates evaluated the drug in 54 patients, with 37 being randomised to receive bosentan and 17 to placebo. After 16 weeks, mean pulmonary vascular resistance was reduced, showing a drop of 472 dyn sec cm-5 from baseline, a change that was considered statistically significant at the P = .04 level. Patients were also able to walk an average of 34 m longer on the 6-minute walk test (P = .02).

Two patients in each group discontinued due to adverse events.

"Patients with Eisenmenger's syndrome have a reduced life expectancy and a limited functional capacity," Dr. Galie said. "It is extremely encouraging that in this disease finally a drug has shown an improvement in exercise capacity and haemodynamics."

Michael Landzberg, MD, director, Boston Adult Congenital Heart Service, Children's Hospital and Brigham & Women's Hospital, Boston, Massachusetts, United States, commented, "In this area of high unmet medical need, bosentan may be a new treatment option for patients with Eisenmenger's syndrome."

Eisenmenger's syndrome is a progressive heart condition that occurs in people who have a congenital heart defect or "hole in the heart." Prior to the development of Eisenmenger's syndrome, the heart defect allows blood to flow from the left ventricle to the right, which increases blood flow through the lungs. Over time, damage to the pulmonary vessels causes pulmonary hypertension, leading to a reversal of the shunt, with blood flowing from the right to the left side. This phenomenon of pulmonary hypertension and right-to-left shunting is termed "Eisenmenger's syndrome," or "Eisenmenger's physiology."

This flow of blood from the right to the left causes the most recognizable symptom of Eisenmenger's syndrome, a blue tinge to the skin resulting from low blood oxygen concentration. The poor oxygenation of their blood severely limits a person's physical activity. In addition, Eisenmenger's syndrome is associated with organ damage and a higher likelihood of premature death.

Currently, no intervention significantly improves the clinical status of patients with Eisenmenger's syndrome.

BREATHE-5, in a series of bosentan clinical studies, was sponsored by Actelion, Allschwil/Basel, Switzerland.


[Presentation title: Breathe-5 Bosentan Improves Hemodynamics and Exercise Capacity in the First Randomized Placebo-Controlled Trial in Eisenmenger Physiology.]

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