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Study Seeks Genes Contributing to Early Heart Attack
and Stroke Risk
The researchers will take advantage of data from two large-scale studies
Researchers in the Human Genetics Center of The University of Texas School of Public Health at Houston will participate in a $10 million, multi-year study led by Wake Forest University Baptist Medical Center to identify genes that may contribute to early atherosclerosis.
James E. Hixson, Ph.D.
“If we can identify people in their teens and early adult life that have a genetic predisposition to develop atherosclerosis, we can manage their risk factors for heart disease and stroke sooner and more aggressively,” said David Herrington, M.D., professor of cardiology at Wake Forest and lead investigator.
Funded by the National Heart, Lung and Blood Institute (NHLBI) of the National Institutes of Health, the study – known as SEA (“SNPs and Extent of Atherosclerosis”) – will build on research from two previously funded NHLBI projects. The new study also will benefit from a unique collaboration with Perlegen Sciences, a company that specializes in techniques to uncover the genetic causes of diseases.
Atherosclerosis is the development of fatty deposits in arteries that leads to blood clot formation, angina, heart attack and stroke. This process can begin in childhood and early adult life. Doctors have known that genetic factors contribute to risk for early atherosclerosis but the exact genes involved are not yet known.
The researchers will take advantage of data from two large-scale studies: the Pathobiological Determinants of Atherosclerosis in Youth (PDAY) study and the Multi-Ethnic Study of Atherosclerosis (MESA).
Using DNA data from the PDAY study, scientists will work to pinpoint specific atherosclerosis genes. This autopsy study, which started in 1985, included about 3,000 young people, aged 15 to 34, who died from accidental causes, suicide and homicide.
In Houston, a team led by principal investigator James E. Hixson, Ph.D., professor of human genetics at the UT School of Public Health, will perform detailed molecular studies of tissue samples in the PDAY cohort to determine how particular genetic variants may alter development of atherosclerosis and its risk factors.
“Perhaps the most remarkable thing about the SEA study is the large number of genetic variants that we’re going to investigate,” said Hixson, who also holds an appointment at the UT Graduate School of Biomedical Sciences at Houston. “Using special technology provided by Perlegen Sciences, we will examine more than two million different gene variations.”
In the second part of the study, researchers will work to confirm their findings by seeing if any genetic factors associated with early atherosclerosis in PDAY subjects also predict atherosclerosis in living participants of the 10-year, multi-center MESA study. Since 2000, the MESA study has examined about 6,800 men and women, aged 45 to 84, who had no known heart disease. These participants were screened for atherosclerosis using non-invasive imaging tests.
“We hope that, over the five years or so it will take to complete, the SEA study will give us new understanding about the causes of atherosclerosis, including the discovery of new genes and new pathways that could guide the development of new drug treatments that may be more effective in preventing the development of heart disease,” Hixson said.
The Human Genetics Center was established as a unit within the UT School of Public Health in 1994. Its research projects focus on identifying genes that influence common diseases such as cardiovascular disease, diabetes, hypertension, obesity and eye disorders.
Other participating centers in the SEA study are Cedars Sinai Medical Center, Louisiana State University Health Sciences Center in New Orleans and the University of Washington.
By David R. Bates, Institutional Advancement