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Gout Drug May Treat Heart Failure

Small study finds it improves blood flow

MONDAY, June 17, 2002 (HealthDayNews) -- People with heart failure may improve their blood flow by using a drug that's widely prescribed to treat another ailment: gout.

Blood flow increased by nearly 50 percent in heart failure patients given allopurinol, a standard medication for gout, says a report from Scottish researchers in tomorrow's issue of Circulation.

It was a small study, involving only 11 patients, and what is needed is a much larger trial to see whether allopurinol can extend the lives of patients with heart failure, says study co-author Dr. Allan D. Struthers, a professor of cardiovascular medicine at Ninewells Hospital and Medical School in Dundee.

Such a study "would be a very big trial," Struthers says, and it's not likely to be done because "allopurinol is a very old drug, and therefore no drug company could make money from it." Without drug company backing, he says, a large-scale study is highly unlikely.

Struthers got the idea for the heart failure study by looking at the molecular activity of allopurinol in gout, a painful condition that happens when excess uric acid in the blood is converted to sodium urate, a solid crystal that forms deposits in the joints and other tissues.

Allopurinol stops formation of that crystal by inhibiting the activity of an enzyme called xanthine oxidase. That enzyme works by producing nasty molecules called superoxide radicals. Those free radicals, Struthers notes, are involved in an artery-damaging process called oxidative stress. Stop that stress and you can help the arteries, he reasons.

He and his colleagues tried the theory on 11 patients with mild to moderate heart failure. Some of them got allopurinol, while some got a placebo. All got acetylcholine, a drug that increases blood flow by widening arteries. After one month, the treatment was switched, so the people who had been getting allopurinol then got a placebo. In this double-blind, crossover study, the gold standard for medical evidence, increased blood flow was found only when the patients got allopurinol.

Struthers has begun another trial to extend that finding. "We are near the end of it, to see if allopurinol reduces breathlessness during exercise," he says. However, all he can do about a larger trial is hope.

The evidence so far is not enough to change the way heart failure is treated, Struthers says. "I think the drug shows promising signs, but cardiologists legitimately want more than just promising signs before they burden patients with another drug," he says.

Dr. Ann F. Bolger, an associate professor of medicine at the University of California, San Francisco, and a spokeswoman for the American Heart Association, agrees.

"It is a very interesting first step, but we always need to realize that a lot of things we can't anticipate will change the way a medication works in actual human patients," she says.

Because "this is a very old drug, there is not a lot of interest in funding for a trial from commercial sources," Bolger adds.

Cardiologists and their patients would be helped a lot if allopurinol could effectively stop oxidative stress, Bolger says, because nothing now available does the job. There were high hopes for antioxidants, but large-scale studies gave disappointing results.

On a practical level, strong evidence of effectiveness would be needed to get the drug into common clinical treatment of heart failure because "one of our most life-limiting problems is patient compliance," Bolger says. "Patients have to keep straight all the complicated regimens, taking certain medications at certain times. It's not that they don't try; it's that it can be extraordinarily complicated."

What To Do

You can learn about heart failure and its treatment from the American Heart Association. Meanwhile, learn more about allopurinol from Medline.

SOURCES: Allan D. Struthers, M.D., F.R.C.P., professor, cardiovascular medicine, Ninewells Hospital and Medical School, Dundee, Scotland; Ann F. Bolger, M.D., associate professor, medicine, University of California, San Francisco; June 18, 2002, Circulation
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