In what may be the largest global investigation of its kind, scientists have implicated 13 new gene regions in the onset of heart vessel plaque build-up, a condition that often leads to fatal heart attacks.
The discovery doubles the number of gene regions linked to the development of coronary atherosclerosis, which the authors note is the most common cause of death globally.
"I've been waiting my entire life to see the names of these genes," said study co-author Dr Thomas Quertermous, a professor in cardiovascular medicine at Stanford University in Palo Alto. "We are making huge progress, but there is much work left to do."
Meanwhile, Quertermous said, "these new discoveries will allow scientists worldwide to eventually better understand the root causes of coronary atherosclerosis, possibly leading to important new drug therapies that may profoundly reduce the risk of having a heart attack."
The findings stem from an analysis of data collected by more than 150 researchers participating in 14 genomic studies conducted all over the world, including the United States, Iceland, Canada, and Great Britain.
Quertermous and his colleagues report their observations in the journal Nature Genetics. He and his Stanford colleagues reported no conflicts of interest; GlaxoSmithKline supported two of the studies.
To get a better understanding of the genetic underpinnings of heart disease, the authors reviewed the genetic profiles of more than 22,000 men and women, all of European descent and all heart disease patients. In addition, they examined the genetic profiles of another 60,000 healthy individuals.
After poring through enormous quantities of genetic code - a process that Quertermous described as being "like looking for a change in one letter in one word in the Encyclopedia Britannica" - the research consortium finally settled on 13 gene regions linked to atherosclerosis risk.
High risk identified early on
"With such information we should be able to better identify people at high risk early on in life and quickly take the steps to neutralize that excess risk by strongly recommending lifestyle and pharmacological therapies that we already know substantially reduce risk," a study co-author, Dr Themistocles (Tim) Assimes, an assistant professor of medicine at Stanford, noted.
"(But) although we are inching closer to that day, we will probably need to reliably identify many more variants predisposing to heart attacks over the next few years before it becomes useful to perform this genetic profiling in a doctor's office," he cautioned.
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