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London, May 30 (IANS) An international team of researchers has identified new genes that are associated with an increased risk of a type of heart attack primarily affecting young to middle-aged women.
The study, published in Nature Genetics, identified 16 genes that increased the risk of a SCAD -- or Spontaneous Coronary Artery Dissection -- which is most common in women under the age of 60 and is a leading cause of heart attacks around the time of pregnancy.
SCAD occurs when a bruise or bleed occurs in the wall of a coronary artery, cutting off the blood to part of the heart. This leads to a heart attack.
However, people who suffer from SCAD tend to be generally healthy and it can sometimes happen more than once. To date, little is known about why a SCAD happens, often striking out of the blue, meaning that it is currently impossible to prevent.
In the study, the researchers present a genome-wide association meta-analysis involving a total of 1,917 cases of SCAD and 9,292 controls from European ancestry.
The identified 16 genes are involved in processes that determine how the cells and connective tissue hold together, and also how the blood clots when bleeding occurs in tissues.
Interestingly, the researchers found that, while many genes linked to a higher risk of SCAD are shared with risk genes for conventional coronary artery disease (CAD), they have an opposite effect.
This means patients with a SCAD have some genetic protection from the risk of CAD, and is further evidence that these diseases are very different. The only shared risk factor appeared to be genetically elevated blood pressure.
"This research confirms that there are multiple genes involved in determining the risk of a person having a SCAD," said lead author David Adlam, Associate Professor of Acute and Interventional Cardiology at the University of Leicester, UK.
"These genes give us the first key insight into the underlying causes of this disease and provide new lines of enquiry, which we hope will guide future new treatment approaches," he added.
--IANS
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