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Viagra may reduce heart failure - study
(Agencies)
Updated: 2005-01-24 09:18

Viagra tablets are seen at Brooks Pharmacy in Montpelier, Vt., in thisApril 6, 1999 file photo. Tests opn animals show the pill, used to restore sexual function, may be used to help treat enlarged hearts. (AP Photo/Toby
Viagra tablets are seen at Brooks Pharmacy in Montpelier, Vt., in thisApril 6, 1999 file photo. Tests opn animals show the pill, used to restore sexual function, may be used to help treat enlarged hearts. [AP]
Viagra may aid in the treatment of enlarged hearts that can result from high blood pressure, tests on animals indicate. Plans are under way for a trial to determine if similar results occur in humans given the drug widely used to treat erectile dysfunction.

The drug, known generically as sildenafil citrate, blocked and even reversed some of the heart enlargement in mice with blood pressure stress, said researchers led by Dr. David A. Kass of the Johns Hopkins University School of Medicine.

"A larger-than-normal heart is a serious medical condition, known as hypertrophy, and is a common feature of heart failure that can be fatal," Kass said.

He said the findings "suggest possible therapies in the future, including sildenafil, which has the added benefit of already being studied as safe and effective for another medical condition" — male sexual dysfunction.

The report, in Sunday's online edition of Nature Medicine, came as no surprise to Dr. William B. White, head of the hypertension section of the University of Connecticut Health Center.

White, who was not part of Kass' research team, noted that sildenafil originally was discovered by researchers studying blood pressure and heart disease.

The drug, however, is effective only for a short time, he said. It would need to be longer acting to be useful in treating heart enlargement, White said.

Dr. Richard Devereux of Weill Cornell Medical College in New York agreed that sildenafil is too short acting to be a practical medication for heart enlargement in humans.

"But this still constitutes a clue that I personally find very exciting and potentially important," he said in a telephone interview.

The finding can propel a search for compounds related to sildenafil that are longer acting and have similar heart benefits, said Devereux, who did not participate in the new research.

Kass said sildenafil blocks the action of an enzyme called PDE5A, which helps break down a molecule known as cyclic GMP. This molecule helps the heart resist stresses and enlargement, researchers said, so protecting it from being broken down allows it to continue the heart-healthy work.

Sildenafil has proved useful in erectile dysfunction because PDE5A also is involved in the relaxation of blood vessels in the penis.

In one experiment cited in Nature Medicine, the Hopkins team induced heart pressure stress in mice by constricting the main artery carrying blood from the heart.

After as long as nine weeks, scientists found that the mice that consumed sildenafil in their food developed only about half as much heart enlargement as those that did not get the drug.

Researchers also found that the mice receiving sildenafil developed 67 percent less fibrous tissue in their hearts and that the treated mice had smaller hearts with better heart function.

In a different experiment, mice that already had enlarged hearts were given sildenafil for two weeks. The researchers said the muscle growth nearly disappeared in those mice, while the hearts continued to enlarge in animals that were not given the drug. Heart function in the mice improved after the treatment.

In both cases, the mice were given 100 milligrams of sildenafil per kilogram of weight per day. The researchers said that produced blood levels similar to those in doses given to humans.

The researchers stressed that the makers of Viagra had no involvement in the design or support of the research.

Their work was funded by the National Institutes of Health, the Peter Belfer Laboratory for Heart Failure Research, Uehara Memorial Foundation, American Heart Association, American Physiological Society and Bernard Family Foundation.



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