Scientists discover new causes of irregular heartbeat

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In a new study, researchers found hundreds of new links between people’s DNA and the heart’s electrical activity.

The results could one day lead to advanced screening methods to discern who is at greatest risk of developing the disease, and could help reveal new genetic targets for research and drug development.

The research was led by researchers at the Queen Mary University of London and the Broad Institute of MIT and Harvard.

Over the past 10 years, researchers have identified many genetic factors that contribute to—or protect against—the onset of specific heart diseases.

However, it has been difficult to find genetic factors associated with arrhythmias—one of the most common forms of heart disease where the heart beats abnormally.

In the study, the team of scientists from more than 140 institutions looked at data from 293,051 people across the world.

They study the individual genomes and their measurements on an electrocardiogram—one of the oldest and most widely used heart diagnostic tests.

They specifically studied the length of time between two points on the electrocardiogram read-out known as the “PR interval,” which is linked to a number of common electrical disorders such as atrial fibrillation and other arrhythmias.

The findings report 202 locations in the genome with links to this type of electrical activity in the heart—141 of which had not been previously identified.

This more than triples the number of known genetic regions linked to this type of electrical activity and explains about 62 percent of its heritability.

This is the largest global study to test the genetic basis of the PR interval—a well-established electrocardiogram risk marker for heart disease and mortality.

The insights provide new knowledge on biological processes relating to the heart’s electrical activity and potential avenues of drug research for preventing and treating heart conditions.”

The findings indicate that an individual’s inherited predisposition to heart disease is not the result of single-gene mutations, but rather a cumulative effect of many variants across the genome.

One author of the study is Professor Patricia Munroe from Queen Mary’s William Harvey Research Institute.

The study is published in the journal Nature Communications.

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