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Drug Effective Against Heart-Lung Disorder

Bosentan slowed decline linked to pulmonary arterial hypertension, study found


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THURSDAY, June 19 (HealthDay News) -- The drug bosentan reduced clinical decline in patients with early-stage pulmonary arterial hypertension (PAH), Italian researchers report.

PAH is a progressive disease in which increased pulmonary resistance in the lungs causes structural damage to the heart, eventually leading to heart failure and death.

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Previous studies have shown that bosentan improves exercise capacity and pulmonary vascular resistance (PVR) and slows clinical decline in patients with later stages of PAH.

This new study included 185 people, ages 12 and over, with early-stage PAH who were divided into two groups. One group received bosentan, and the other group received a placebo. The patients' PVR and distance they could walk in six minutes were measured at the start of the study and again six months later.

After six months, the mean PVR improved at a significant rate for those on bosentan versus those on placebo, wrote Professor Nazzareno Galie, of the Institute of Cardiology at the University of Bologna, and colleagues.

The mean six-minute walk distance also increased 11.2 meters in the bosentan group from 438 meters at baseline, compared to a decrease from 431 meters to 423 meters in the placebo group. However, these changes in distance weren't clinically significant.

Three percent of patients in the bosentan group and 14 percent of those in the placebo group experienced clinical worsening events, such as symptomatic progression of PAH, hospitalization and death. This difference was statistically significant.

Thirteen percent of patients in the bosentan group and 9 percent of those in the placebo group reported serious adverse events. Fainting was the most common adverse event in the bosentan group, and right ventricular failure was the most common in the placebo group.

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-- Robert Preidt

Copyright © 2008 ScoutNews, LLC. All rights reserved.
Last updated 6/19/2008

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SOURCE: The Lancet, news release, June 20, 2008


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