American Heart Association Comment: Tirofiban -- The Platelet Receptor Blocker For Heart Attack

May 20, 1998

Two new studies in the New England Journal of Medicine on tirofiban (Aggrastat) show that the drug may be useful in the treatment of heart attack.

"Tirofiban is a novel drug that will open the door to new treatments for the preceding stages of heart attack or the heart attack itself," says Valentin Fuster, M.D., Ph.D., president-elect of the American Heart Association, commenting on two studies.

Tirofiban is a member of a class of drugs called "platelet glycoprotein receptor blockers." As the name suggests, the drug blocks the action of platelets, cells that clump to help form a blood clot.

The drugs have been used to improve the results of angioplasty -- a blood vessel-opening procedure -- by preventing reclosure of blood vessels, a common problem. But last week the Food and Drug Administration approved tirofiban for individuals with unstable angina (chest pain at rest) and non-Q-wave myocardial infarction (limited heart attack). These conditions result from blood clots that have not totally or persistently blocked the blood vessel feeding the heart, but they may precede complete blockage leading to heart attack.

"People with those conditions often have to have surgical interventions such as angioplasty. Tirofiban may help some patients avoid surgery for a short time or totally," says Fuster. "By postponing angioplasty, one can buy time during which other treatments can be applied to lower blood cholesterol and blood pressure."

The treatment advance has resulted from a better understanding of the causes of heart attack.

"We know that heart attack involves a complex process, but one of the final triggers is a blood clot that blocks the blood vessel. By interfering with clot formation, antiplatelet drugs like tirofiban can help prevent a heart attack," he says.

One study looked at the effect of tirofiban in individuals with unstable angina or non Q-wave myocardial infarction. After seven days, individuals on tirofiban and heparin (a blood thinner) had a 32 percent reduced risk of death, heart attack or ischemia compared to a group who received heparin alone. In the second study, after 48 hours individuals with unstable angina taking tirofiban had a reduced risk of 32 percent compared to those receiving heparin.

How often the drug treatment will replace angioplasty or other treatments to remove blockages and relieve chest pain is still unknown. The study found that the major benefits from the drug came immediately, but after a few months those treated with tirofiban were no better off than those receiving heparin.

"As the author of the accompanying editorial in NEJM suggests, 'short-term therapy appears inadequate for a long-term disease,'" says Fuster. "The drug helps treat the tip of the iceberg, but individuals may need more ways to fight the underlying disease -- atherosclerosis. This means not smoking, keeping blood cholesterol and blood pressure levels down and increasing physical activity.

"The best way is to prevent the blood clot in the first place," says Fuster, who was one of the first scientists to show that blood clots that cause heart attack are derived from platelet clumps on top of the fatty buildup, called plaque, that characterize atherosclerosis. Fuster is director of the Cardiovascular Institute, Mount Sinai Medical Center, New York.

For interviews or more information, please contact Carole Bullock of the AHA's News Media Relations department at (214) 706-1279.
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American Heart Association

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