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Saturday, January 03, 2009

Millions of people under 40 across the world suffer without knowing from early coronary artery disease, which in many cases leads to heart attacks in later life.

Now researchers believe they have pinpointed a gene or marker that can help predict in advance whether someone is at increased risk.

They believe that this could lead to a test to identify the latent threat of hardened arteries so that patients could be given dietary advice and other treatment before too much damage is done.

"These young patients are a vulnerable population on whom coronary artery disease has a significant long-term impact, but they are particularly hard to identify and therefore to initiate preventive therapies for," said Dr Svati Shah, co-author of the study at Duke University Medical School in North Carolina.

"These and other genetic findings may help us in the future to identify these patients prior to development of coronary artery disease or their first heart attack."

For years, scientists have known that the devastating, early-onset form of the disease was inherited, but they knew little about the genes responsible until now.

In a previous study, a region on chromosome 7 was linked to coronary artery disease.

More recently, the researchers focused on identifying the gene in this region that leads to the higher risk of early-onset coronary heart disease and identified a variation in the protein known that is linked to the condition.

Known as neuropeptide Y (NPY), it is one of the most plentiful and important proteins in the body and is linked to the control of appetite and feeding behaviour, among other things.

The current research, led by Dr Shah and Dr Elizabeth Hauser, found evidence for six related variations in the NPY gene that show evidence of transmission from generation to generation and association across a population of early-onset coronary artery disease patients.

The researchers evaluated 1,000 families for coronary artery disease or evidence of a true heart attack, as part of a larger study put together by Duke University.

They found a strong link between the mutant gene and those with actual heart disease or ancestral history of the disease.

"If you had 1 or 2 copies of this mutant version of the gene, there could be a change in NPY level," Dr Shah said.

"The concept is that small changes over time can promote atherosclerosis (hardening of the arteries) at a very young age."

Experiments on mice subsequently confirmed that the NPY promotes atherosclerosis, according to the report published in the Public Library of Science journal.


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