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Elevated levels of a blood protein can protect against heart disease, a finding that could lead to better treatment for patients with high cholesterol, doctors report.

"This is a major new conceptualization," Dr. H. Bryan Brewer of the National Institutes of Health in Bethesda, Md., said this week."We don't have all the pieces of the puzzle together," Brewer said, but the new research is already helping researchers decide which drugs might be best for patients with high cholesterol.

More importantly, he said, the research suggests that some patients with low levels of the so-called good cholesterol that protects against heart disease might not need drugs at all.

In the new studies, Dr. Edward M. Rubin of the Lawrence Berkeley Laboratory and the University of California genetically engineered mice to contain the human gene for a blood protein called LpA-I. Those mice then produced that protein.

The mice that produced the protein had far lower levels of atherosclerosis, or hardening of the arteries, than did mice without the protein but with identical cholesterol levels, Rubin reported at the science writers' conference of the American Heart Association.

The studies help resolve a problem that has stumped researchers for some time, Rubin said.

Scientists had observed that people with high levels of good cholesterol, designated HDL, seemed to be protected against heart disease.

On the other hand, people with high levels of the so-called bad cholesterol, designated LDL, had a increased risk of heart disease.

But some patients with low levels of good cholesterol, whose heart disease risks should have been high, actually had low risks.

Researchers then examined the components of HDL, one of which is the blood protein that Rubin studied, LpA-I.

It now appears that the level of HDL is not what determines heart disease risk, but rather the level of LpA-I within the HDL.

In Rubin's studies, mice were fed high-cholesterol, high-fat diets. ("Mice like cheese," he explained.)

Among mice engineered to have high levels of LpA-I, only one in 15 began to develop atherosclerosis.

Among mice with lower levels of LpA-I, 14 of 15 developed atherosclerosis, Rubin reported.

Brewer said that some cholesterol-lowering drugs raise LpA-I levels and some do not. The one that does so most effectively is niacin, he said.

But the studies should enable drugmakers to devise even better drugs to protect against heart disease, he said.

Brewer said that laboratories are working to develop a commercially available version of the tests now used by researchers to measure LpA-I levels.