DALLAS, Oct. 26 -- A new type of therapy that raises the good form of cholesterol -- and caused a "shrinkage" of atherosclerosis in mice experiments -- may lead to novel treatment approaches for heart disease and stroke, according to a study in today's Circulation: Journal of the American Heart Association.

By injecting mice with apoA-1 -- a gene that makes a key protein involved in forming high-density lipoprotein or HDL, the "good" cholesterol -- researchers were able to shrink artery-blocking deposits that characterize atherosclerosis.

Atherosclerosis occurs when deposits, called plaque, collect on the inside walls of arteries. A blood clot can develop on the plaque, blocking the blood vessel and triggering a heart attack or stroke.

"There has been a tremendous interest in raising HDL cholesterol levels, not only as a way to prevent heart disease, but also to help shrink the existing blockages in blood vessels," says the study's lead author Daniel J. Rader, M.D., director of preventive cardiology at the University of Pennsylvania Health System at Philadelphia.

There are medications called "statins" that lower levels of low-density lipoprotein, LDL, the "bad" cholesterol. However, those drugs raise HDL cholesterol levels only slightly, if at all. There are very few effective treatments to raise HDL cholesterol levels.

The mice used in the study were fed a diet high in cholesterol and saturated fat to induce atherosclerosis. Some of the mice were injected with an inactive virus, while the others were injected with a virus containing the apoA-1 gene.

After four weeks, the mice treated with the apoA-1 gene had significant regression of the pre-existing atherosclerotic lesions as well as a moderate increase in their levels of HDL cholesterol. By comparison, the control animals' atherosclerosis progressed during the four weeks.

Previous studies in animals have shown that apoA-1 can slow progression of
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Contact: Carole Bullock
caroleb@heart.org
214-706-1279
American Heart Association
24-Oct-1999