Inflammation-Fighting Drug Fails in Heart Trial

But researchers think the approach could one day pay dividends

TUESDAY, Jan. 2, 2007 (HealthDay News) -- An inflammation-fighting drug has failed to improve the survival of people who had stents implanted after suffering a heart attack, researchers report.

But the idea of fighting inflammation to help such patients remains alive, said Dr. Christopher B. Granger, associate professor of medicine and director of the cardiac care unit at Duke University, a member of the team that tested the drug, pexelizumab, in a large-scale study.

"I think most of us believe, and I do, that there still is promise for the general approach, but this particular drug did not turn out to be effective," Granger said.

The drug had shown promise in some earlier trials, he said. In one study, "it reduced some of the markers of inflammation, such as C-reactive protein and interleukin-6, and that reduction in markers appeared to be associated with better clinical outcomes," Granger said.

But in the larger study, reported in the Jan. 3 issue of the Journal of the American Medical Association, use of pexelizumab made no difference.

The trial included 5,745 people treated for acute ST-elevation myocardial infarction -- a certain pattern on an electrocardiogram following a heart attack. All had stents implanted after undergoing artery-opening angioplasty. Half were given pexelizumab before angioplasty and for 24 hours afterward; the other half got a placebo, an inactive substance.

The 30-day death rate was almost identical for the two groups -- 3.92 percent for those getting a placebo, 4.06 percent for those getting the drug. The numbers were similar for the combination of death, cardiac shock or heart failure in the following 30 days -- 9.19 percent for placebo, and 8.99 percent with pexelizumab.

Other inflammation-fighting drugs are being investigated, Granger said, "and there are also others that have failed."

The general idea, he said, is to "inhibit inflammation and improve the metabolic health of the cell."

But the problem is that "inflammation is a nonspecific response, and there are so many redundant pathways for it that coming up with a specific treatment is difficult," Granger said.

Dr. Paul W. Armstrong is professor of medicine at the University of Alberta, in Edmonton, Canada, and lead author of the report. He said, "The science of this [behind the study] remains very attractive. We know that inflammation is an important player in heart attack and acute coronary conditions caused by narrowing. Reducing inflammation is desirable. The challenge is how you make it happen in the clinic."

Still, Armstrong said, "there are other agents and other approaches" to reducing inflammation. He described the study result as "obviously disappointing," but added that "in some ways, it opens the field to other pretenders to the throne."

More information

The U.S. National Institutes of Health has more on heart bypass surgery.

Related Stories

No stories found.
logo
www.healthday.com