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Over 150 genes linked to irregular heart rate conditions

| | Washington
Over 150 genes linked to irregular heart rate conditions

Scientists have identified 151 genes linked to atrial fibrillation, a condition that causes irregular heart rates and puts over 30 million people worldwide at increased risk of stroke, heart failure, and death.

Researchers from the University of Michigan in the US led a large collaborative effort to discover as-yet unknown genetic risk factors for atrial fibrillation.

By performing one large genome-wide association study (GWAS) comprising data from six smaller studies, scientists identified 151 candidate genes for the condition.

Many of the genes identified are important for foetal development of the heart, implying that genetic variation predisposes the heart to atrial fibrillation during fetal development, or, that the genetic variation could reactivate genes in the adult heart that normally only function during foetal development.

The increased understanding the study yields of the biological processes underlying atrial fibrillation could lead to better treatment and prevention.

"We are hopeful that additional molecular biology experiments will determine how to create sustained regular heart rhythms by studying the genes we and others have identified," said Cristen Willer, associate professor at University of Michigan.

If atrial fibrillation is detected early, it is possible to prevent complications such as stroke and heart failure.

Current treatment options for atrial fibrillation are limited, however, include serious side effects, and are rarely curative. The genetic variants uncovered in this study could potentially improve both early detection and treatment.

By identifying genes important for atrial fibrillation, researchers constructed a risk score to help identify high-risk individuals and monitor them accordingly, which "may have important implications for precision health and prevention of cardiovascular disease," said Willer.

Of the 151 genes identified as important for atrial fibrillation, 32 are likely to interact with existing drugs not necessarily developed to treat atrial fibrillation.

"Discovery of novel genetic variants and genes important for atrial fibrillation was only possible because we combined information from multiple biobanks from around the world in a large collaborative effort," said Jonas Bille Nielsen, first author of the study published in the journal Nature Genetics.

"By combining multiple independent data sources, we also found that people with early-onset atrial fibrillation have a higher genetic burden of atrial fibrillation compared with people who develop the disease later in life," said Nielson.

 
 
 
 
 

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