By Losing (Molecular) Weight, A Clot-Dissolving Drug May Be In Better Shape To Help People Avoid A Repeat Heart Attack

July 27, 1998

DALLAS, July 28 -- In the future, people who have had mild heart attacks or suffer from chest pain may be able to inject themselves with a drug at home to prevent a heart attack or episodes of chest pain, say scientists.

In a study and editorial in today's Circulation: Journal of the American Heart Association, researchers say that enoxaparin -- a slimmed-down form of the commonly used clot-dissolving drug heparin -- could help stifle a clot-forming protein that enters the bloodstream after the heart is damaged.

The release of clot-inducing proteins into the bloodstream continues months after chest pain or mild heart attacks. Researchers say people affected could one day fight back with a regular therapy of at-home enoxaparin injections. "It seems logical to not only provide effective anti-clotting therapy during the initial episode of chest pain or just after the heart attack, but to also use that therapy in the months following that event," says the editorial's lead author Elliott Antman, M.D., director, Samuel A. Levine Cardiac Unit, Brigham and Women's Hospital in Boston. "In theory, this new research might allow physicians to prescribe relatively unsupervised long-term self-administration of anti-clotting therapy, sort of an insulin-like injection for coronary artery disease."

By using enoxaparin, researchers were able to control von Willebrand factor, a "reactant" protein released into the bloodstream when blood vessels are inflamed or when a person has a heart attack or chest pain. The scientists found enoxaparin to be superior to heparin in controlling von Willebrand factor. When released into the bloodstream, von Willebrand factor plays the role of traffic cop. It directs platelets -- disk-shaped blood particles that help form clots -- to the damaged area of blood vessels, leading to a particle pile-up that can form blood clots. By suppressing von Willebrand factor, potential clots can be avoided.

Scientists studied which of the "reactant proteins" could be predictive of future heart attacks or chest pain. They found high blood levels of von Willebrand factor were a better predictor when compared to levels of other proteins such as C-reactive protein and fibrinogen.

"Our study confirms that the first hours of unstable coronary artery disease are associated with a significant response from certain proteins," says the study's lead author Gilles Montalescot, M.D., Ph.D., of the Pitie-Salpetriere Hospital in Paris. "There is an ongoing inflammatory process despite the use of common clot-dissolving therapies."

Researchers found the levels of von Willebrand factor increased dramatically over the first 48 hours following a heart attack or an episode of chest pain in those people treated with regular heparin. The release of this factor was lessened in people receiving enoxaparin.

In a follow-up 14 days after people had an episode of chest pain or a mild heart attack, nine of the 34 people treated with enoxaparin had another bout of chest pain or a heart attack compared to 17 of 34 people given regular heparin. After 30 days, the numbers were nearly the same (9 vs. 18). In addition, researchers found that the rise of von Willebrand factor over the first 48 hours of treatment after hospital admission was more frequent and more pronounced in the heparin group than in the enoxaparin group.

When von Willebrand factor is released from blood vessels, it looks for a place to congregate. Heparin seeks out the protein and turns off the mechanism which makes the protein come together. Heparin helps keep blood flowing normally through the vessels by preventing proteins such as von Willebrand factor from clogging the vessels.

Enoxaparin was found to be the better "binder," and its superior suppression of von Willebrand factor gives researchers a reason to believe this type of drug treatment could significantly help reduce the risk of blood clots in people after a heart attack.

"Our data do not demonstrate a causal relationship between the changes of von Willebrand levels and the clinical efficacy of enoxaparin in patients with unstable heart disease," says Montalescot. "At the present time we have few good explanations for this excess of efficacy of enoxaparin over regular heparin. But we do believe we have identified a new biological prognosis marker of unstable chest pain."

Co-authors are Francois Philippe, M.D.; Annick Ankri, M.D.; Eric Vicaut, M.D., Ph.D.; Etienne Bearez, M.D.; Jean Ernest Poulard, M.D.; Didier Carrie, M.D.; Albert Dutoit, M.D.; Daniel Flammang, M.D.; Alain Carayon, M.D.; Claude Jardel, Ph.D.; Monique Chevrot, M.D.; Jean Philippe Bastard, Ph.D.; Frederique Bigonzi, M.D.; and Daniel Thomas, M.D. The editorial co-author is Robert Handin, M.D.
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Media advisory: Dr. Handin can be reached by phone at (617) 732-5840. Dr. Montalescot is on vacation until July 28. He can be reached after that date by phone at 331 42 17 67 01, by fax at 331 42 17 68 56 or by e-mail at gilles.montalescot@psl.ap-hop-paris.fr; Dr. Antman is on vacation until July 27. He can be reached after that date by phone at (617) 732-7143 or by e-mail at eantman@bustoff.bwh.harvard.edu. (Please do not publish numbers.)
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American Heart Association

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