BAR HARBOR, Maine (AP) _ Specially bred mice that develop heart disease have led to the discovery of two genes that could help identify people most likely to suffer from atherosclerosis, or hardening of the arteries, a researcher said Wednesday.

The discovery of the genes provides further evidence that elevated blood levels of HDL cholesterol, the so-called ''good cholesterol,'' will protect against the development of atherosclerosis, said Beverly Paigen of Oakland Children's Hospital in Oakland, Calif.

Paigen, speaking during a gathering of geneticists at the Jackson Laboratory in Bar Harbor, said the two new genes, called Ath-1 and Ath-2, are related to levels of the HDLs, or high-density lipoproteins, in the specially bred mouse strains.

Some of Paigen's findings were published in June in the Proceedings of the National Academy of Sciences, and additional details will be published later this year.

Mice that are highly susceptible to atherosclerosis when fed a high-fat diet have low levels of protective HDL cholesterol and have a form of the Ath gene that is different from the form found in two strains of mice resistant to the development of atherosclerosis. The resistant strains of mice have correspondingly high levels of HDL cholesterol, Paigen said.

Many studies in recent years have suggested that HDL cholesterol protects against heart disease. Paigen said people with very high levels of HDLs frequently live very long lives, presumably because they do not suffer from atherosclerosis.

Heart disease is the nation's leading killer, and atherosclerosis, marked by the build-up of fats and cholesterol in arteries, is one of the most important causes of heart disease.

When atherosclerosis blocks the flow of blood in the coronary arteries that nourish the heart, a heart attack can result. Similar clogging of the arteries that supply the brain can lead to a stroke.

The mouse research is particularly useful in the study of human heart disease because many of the genes that control fat and cholesterol levels in the blood are common to both mice and humans, Piagen said.

Thus Paigen thinks it is possible that the heart-disease genes she has identified in mice may also exist in humans. Evaluation of such genes in humans might one day lead to an ability to accurately predict which individuals are at high risk of heart disease and which are at low risk, Paigen said.

In addition, mice are important in the study of human disease because the genetics of mice have been studied for decades and thus parallels between mice and humans can aid understanding of human genetics.

Paigen said her research suggests that only certain segments of the population are susceptible to heart disease, and that recommendations to lower cholesterol in the diet, for example, might better be targeted at only those with the susceptibility.

If susceptibility genes like those she has found in mice can be found in humans, it should be possible to identify those susceptible segments of the population, she said.

Ath-1, she said, has been found to reside on the mouse chromosome designated as chromosome 1. That chromosome also contains a cluster of three genes that are found on human chromosome 1, suggesting that Ath-1, or a similar heart-disease susceptibility gene, might also lie on human chromosome 1.

The mice might also be useful in testing possible treatments for people especially susceptible to atherosclerosis, Paigen said.