London - Arab Today
Researchers found a gene linked to increased risk for heart attack in women, but not in men, according to a newly published study.
The gene, BCAR1, has been indicated in previous studies to encourage the thickening of blood vessel walls, which increases the chance for blockages that can cause heart attacks and strokes. The greater risk for women, researchers believe, results from the gene's combination with estrogen.
"Heart disease is often seen as a disease which predominantly affects men, but this is simply not the case," said Dr. Shannon Amoils, a senior research adviser at the British Heart Foundation, in a press release. "We know that women have a lower overall risk of coronary heart disease compared with men but as this study shows, women do get coronary heart disease, and it is important to find out more about the factors that increase their risk."
Researchers analyzed data from five previous studies on 4,000 men and women, comparing their genes, artery thickness and artery health.
Researchers said, in addition to noting the differences between men and women as a result of naturally-occurring estrogen, the GG version of the gene increases the risk, as opposed to the AA version's lack of increased risk. Men with the GG version of BCAR1 are not effected, based on the research.
Women with the high-risk gene had a 6.1 percent increased risk of heart attack, stroke or diseased blood vessel, as opposed to the 2.5 percent increased risk of women with the lower risk version of the gene.
"We've known for a long time that risk factors for heart disease are different for men and women," Dr. Freya Boardman-Pretty, a researcher at the University College London, told the BBC. "This gene effect seen only in women, could be contributing to this difference, although we expect there are a lot of other factors at play. If we can confirm that this gene is involved, and work out exactly how it leads to an increased risk of heart disease in women, it could become a new target for drugs in the future."
Source: UPL