Study Validates Alternative Stress Agent in Asthma, COPD


PHILADELPHIA – Individuals with asthma or chronic obstructive pulmonary disease can tolerate the imaging agent regadenoson well if they need to undergo cardiac stress testing, a study has shown.

Dr. Bruce Prenner, a San Diego allergist, reported on findings from a multicenter trial involving 999 patients who received either regadenoson or a placebo. “Regadenoson has a greater affinity for the A2B receptors and the other types of receptors, and thus the risk of bronchospasm and bronchoreactive events should be quite low,” he said at the meeting.

The risks of adenosine inducing breathing problems in individuals with asthma and COPD have been well documented. This study set out to determine how regadenoson affected forced expiratory volume in 1 second (FEV1) in 999 study subjects, 532 with asthma and 467 with COPD. About half of the patients received the placebo. The primary end point was a greater than 15% decrease in forced expiratory function from baseline within 2 hours of the dose being administered, Dr. Prenner said.

“In the asthma group, 1.1% of [regadenoson] patients had an FEV1 decrease greater than 15%, and 2.9% of patients on placebo,” had such a reduction, he said. Among patients with COPD, 4.2% receiving regadenoson and 5.4% on placebo met the primary end point, he said.

Respiratory problems such as wheezing, dyspnea, obstructive airwaves disorder and tachypnea were more common with regadenoson than placebo: 13% vs. 2%, respectively, in the asthma group; and 19% vs. 4% in the COPD patients. “The asthma patients had less frequency in terms of previous studies,” Dr. Prenner said. He said the variation between regadenoson and placebo was driven by dyspnea, a known side effect of A2A agonists.

However, within 1 day of injection, use of short-acting bronchodilators was similar for those who received both regadenoson and placebo, Dr. Prenner reported. In subjects with asthma, 1.4% of the regadenoson group and 1.1% of the placebo group used the inhalers. Among those with COPD, inhaler the rates were 1.6% and 1.3%, respectively, for the regadenoson and placebo cohorts.

The study showed no clinically meaningful differences between treatments in pulmonary function tests in either group, Dr. Prenner said. While the incidence of adverse events was higher with regadenoson, the adverse event profile was similar to that in previous regadenoson trials in nonasthmatic COPD patients. Of six serious adverse events with regadenoson, three were considered treatment related.

“This information should be very useful in considering the selection of regadenoson as a bottom-line stress agent for myocardial perfusion imaging in these types of patient populations,” Dr. Prenner said.

Dr. Prenner is a scientific adviser to Astellas, the manufacturer of regadenoson, and serves on its speakers bureau.

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