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Another Blood Fat Fuels Heart Attack Risk
Date:6/9/2009

Danish study fingers high levels of lipoprotein(a)

TUESDAY, June 9 (HealthDay News) -- Yet another type of blood fat may be linked to higher cardiac risk, a new study suggests.

A Danish study finds an increased risk of heart attacks in people whose genes give them high blood levels of a cholesterol-related blood fat, lipoprotein(a), but the researchers say more work is needed to justify treatment to reduce those levels.

"We show that those with the 10 percent highest lipoprotein(a) have a two- to threefold increased risk of myocardial infarction [heart attack], similar to that for the highest LDL cholesterol levels," said Dr. Borge G. Nordestgaard, a professor of clinical biochemistry at Copenhagen University, and lead author of a report in the June 10 issue of the Journal of the American Medical Association.

However, a large-scale trial is needed to tell whether drugs aimed at reducing lipoprotein(a) (LPA) levels would lower the risk, Nordestgaard said. One compound, niacin, also known as nicotinic acid or vitamin B3, is known to reduce LPA levels, he said.

"I am not aware of other drugs being developed to lower lipoprotein(a), but I certainly hope that our study will make big pharmaceutical companies interested in developing such drugs," Nordestgaard said.

LPA consists of a molecule of LDL cholesterol, the "bad" kind that clogs arteries, attached to a number of units of protein. The number of protein units attached to the LDL unit can vary widely.

Nordestgaard and his colleagues have been studying the relationship of LPA to heart disease for years. Their latest report uses data from three studies that included more than 40,000 Danes, with follow-up periods as long as 16 years.

"We observed an increase in risk of myocardial infarction with increased levels of lipoprotein(a)," the researchers wrote. The risk was highest in people whose LPA had a smaller number of lipoprotein attachments, they noted.

Caution is needed in interpreting the results because all the people in the studies were white, Nordestgaard said. "People of African descent have the highest lipoprotein(a) levels, while those of European descent and most Asians have similar levels, but lower levels than blacks," he noted.

The studies of LPA levels and heart disease in ethnic groups other than whites have been limited, Nordestgaard said. "It is likely that high lipoprotein(a) levels are also important in other ethnic groups, but we need new and much larger studies to confirm this," he said.

The findings could influence medical efforts to reduce heart attack risk, Nordestgaard said. "People who develop heart attacks despite cholesterol-lowering statin treatment may have high levels of lipoprotein(a)," he said. "Also, in medium-risk individuals, an elevated lipoprotein(a) level may suggest that the patient should be given a statin or niacin."

The new study is "an elegant biological demonstration of the link between lipoprotein(a) and heart attack," said Dr. Christopher J. O'Donnell, associate director of the U.S. National Heart, Lung, and Blood Institute's Framingham Heart Study, and co-author of an accompanying editorial

"But it doesn't alter the balance of evidence that to date doesn't support doing a test on the serum level or a genetic test for LPA," O'Donnell said. "There would have to be some type of evidence that direct treatment of LPA lowers the risk or that a subgroup of people with an elevated risk have their risk lowered in some way."

Such evidence would have to come from a truly large-scale study, O'Donnell said. "We would have to screen an entire population," he said. Meanwhile, there is "no compelling evidence" that LPA-lowering therapy would affect coronary risk, he said.

More information

The means and meaning of testing LPA levels are described by U.S. National Library of Medicine.



SOURCES: Borge G. Nordestgaard, M.D., professor, clinical biochemistry, Copenhagen, Denmark; Christopher J. O'Donnell, M.D., associate director, U.S. National Heart, Lung, and Blood Institute Framingham Heart Study; June 10, 2009, Journal of the American Medical Association


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