An international research consortium has discovered 13 new genetic markers and confirmed ten previously identified markers associated with heart disease. The study, one of the world's largest, more than doubles the known genetic risk factors for coronary artery disease, a common cause of heart attacks and strokes.
The study is significant because the research suggests that there are important unknown causes for heart disease, opening the door to new avenues for treatment.
'This is a landfall discovery for heart disease prevention. I am confident that it will make a major contribution to preventing and treating heart disease within the next five years', Dr Robert Roberts, principal investigator and Director of the Heart Institute at the University of Ottawa, told BioNews.
Heart disease is the number one killer in the world with heart attacks killing one person every six minutes in Britain alone. Only six of the 23 markers are associated with known risk factors, such as cholesterol.
'What this means is that there are other causes of heart disease that we were totally unaware of until we identified these genes', Dr Roberts explained. This may help to explain why a person can have an apparently healthy lifestyle and still develop heart disease.
How these genes contribute to heart disease is as yet unknown. But future studies will use animal models to look at their function, and a better understanding of this should aid the development of novel drugs and therapies targeting these genes.
Epidemiologists believe that about half of heart disease risk is genetic and half is environmental, such as exercise, lifestyle and diet. Treating known risk factors such as high blood pressure and cholesterol has been shown to decrease heart disease by 30 to 40 percent. With some experts speculating that heart disease will be eliminated in this century through prevention.
A lack of understanding of the genetic components is seen by some scientists as representing a major barrier to comprehensive prevention. Polygenic susceptibility is complex- no single mutation is sufficient or necessary to cause the disease.
The 23 loci only account for a fraction of overall genetic risk but this study offers hope to overcome that barrier, Dr Roberts told BioNews.
The study, conducted by 167 researchers from universities in Europe and North America, including the UK, was extremely large and ranged acoss a number of populations. 'The breadth of the study is second only to the Human Genome Project', Dr Roberts described to BioNews.
The study consisted of 14 genome-wide association studies (GWAS) involving over 140,000 individual genotypes that were scanned with two million markers (one million Hapmap markers inputted retrospectively).
The research was published in Nature Genetics.