FRIDAY, Sept. 23 (HealthDay News) -- Researchers have identified five new genes that play a role in people's risk for heart attack and coronary artery disease -- the most common cause of premature death and disability in the world, according to a new study.
Latest Heart News
The international consortium said their discovery could help scientists predict coronary artery disease (CAD) and develop new treatments for the condition.
In conducting the study, published online Sept. 22 in the open-access journal PLoS Genetics, the researchers examined more than 49,000 genetic variants in nearly 15,600 cases of CAD along with slightly fewer than 35,000 controls, which included people of European descent and South Asian origin. The investigators also duplicated their findings in 17,121 more cases of the disease and 40,473 controls.
"This is one of the first genetic studies of CAD to include a significant proportion of subjects of South Asian origin, an ethnic group that has a higher risk of CAD," John Danesh, the study's co-principal investigator, said in a journal news release. "Our study shows that many of the genes that affect risk of CAD do so similarly in European Caucasians as in South Asians."
The study findings add to the list of more than 30 genes already known to affect people's risk for coronary artery disease and heart attack, the authors pointed out.
"The findings provide new insights into and understanding of the causal biological pathways that cause heart disease, and particularly highlight the role of lipids and inflammation," the study's co-principal investigator, Nilesh Samani, British Heart Foundation professor of cardiology at the University of Leicester, U.K., said in the news release.
The study authors pointed out that although the individual effects of the new genetic variants they found are small, the treatments that are developed as a result of the findings could have a much broader effect.
-- Mary Elizabeth Dallas
Copyright © 2011 HealthDay. All rights reserved.
SOURCE: PLoS Genetics, news release, Sept. 22, 2011