Clot-Buster Drugs Seem to Halt Heart Attacks : The Medicines Are Still Being Tested; Doctors Hope to Save Thousands of Lives

A clump of jellied blood stuck in the heart’s plumbing is as lethal as a bullet.

These clots are the cause of heart attacks. If only something could quickly and safely flush them away, tens of thousands of people each year might elude death.

At least three new drugs under testing seem to do just that. If they work as well as doctors hope, their impact on the treatment of the nation’s biggest killer could be enormous.

About 1.5 million Americans suffer heart attacks each year. More than a third of them die. The disease takes more lives than anything else, more than cancer and accidents combined.

A heart attack disrupts the branching tree of arteries that carry blood to the heart’s own muscle. As people age, cholesterol and fat often build up on walls of the arteries, and they grow narrow. Disaster strikes when a clot lodges in one of the cramped vessels, choking off the flow of blood.

Damage begins within a few minutes. The section of heart supplied by the artery is starved of food and oxygen. After five or six hours, part of the heart is dead.

The new drugs literally stop a heart attack cold. They dissolve the clot so blood can flow again. One of them, called tissue plasminogen activator, or TPA, has already been tested on several hundred people, and studies are under way on two others. One is known as pro-urokinase, while the other has the unwieldy name of anisoylated plasminogen: streptokinase activator complex, or APSAC.

Widespread Usage Seen

If, as many expect, one or another of these experimental drugs is eventually approved for everyday use, the treatment could quickly become a routine part of emergency care. Doctors would give an injection as soon as a suspected heart attack victim walked into the hospital. Ambulance crews would probably carry the drug as well.

Rhode Island Hospital in Providence is one of several giving TPA in a nationwide experiment. Dr. David O. Williams describes a typical case he treated there recently:

A woman in her 50s arrived at the emergency room suffering her first heart attack. Among her complications was a condition called heart block. Electrical impulses weren’t flowing through her heart properly, so her heart rate was very slow, about 30 beats per minute.

The doctors started an intravenous infusion of TPA. Then they took her to the cardiac lab so they could make X-ray movies of her clogged arteries.

“Before we did the first picture, all of a sudden the heart block went away. Just bingo,” Williams says.

“We looked at each other and said, ‘Maybe she opened up.’ We began to take the pictures, and lo and behold, there are no blocked arteries. We could see the area where we thought the clot was, but it was gone. The artery was open.”

Her electrocardiogram was normal, and, at least in the first hours after the attack, there was no sign of permanent damage.

“Her heart attack basically stopped,” Williams said. “We turned back the hands of the clock to where she was before this happened.”

Of course, not all attempts with TPA go this smoothly. And there are potential problems, such as bleeding and the chance that clots will re-form a few hours later. But initial studies suggest that the medicine will reopen about three-quarters of all shut arteries.

Many people working with the medicine are enthusiastic. But they are also cautious until they can be certain that it truly changes people’s fate. Speed is essential. The longer the heart is deprived of blood, the greater the chance of irreversible damage.

“It dissolves the clot, but that’s not enough,” says Dr. James E. Dalen of the University of Massachusetts Medical School. “Does it, in fact, improve the patients’ outlook? Do they live longer? And are they less symptomatic?”

Linda Miller, a stock analyst at Paine Webber in New York, predicts that TPA will be approved by the Food and Drug Administration next year and will cost between $1,500 and $2,500 per patient.

Occurs Naturally

TPA is likely to have competitors and companions in the clot-dissolving business. Like TPA, pro-urokinase occurs naturally in the body to control clotting.

Pro-urokinase was isolated by Dr. Victor Gurewich of St. Elizabeth’s Hospital in Boston. “My suspicion,” he says, “is in the future we will probably be giving both together. That’s the system that nature designed, and it’s not surprising that they would work very well in concert.”

Dr. Victor J. Marder of the University of Rochester is working with the other contender, APSAC. He says its major advantage is that it can be given as a single injection, not a slow infusion over hours, and this may make it easier and faster to use.

Whether TPA or one of the other drugs eventually proves to be the best clot buster, the potential for this kind of therapy is obvious.

“If it works, it will have a major impact,” predicts Dalen. “The reason is the extraordinary prevalence of myocardial infarction,” or heart attack. “If we decrease the mortality by 10%, that’s a lot of lives.”