New research uncovers 151 genes linked to A-fib.
The findings of the “big data” international study — now published in the journal Nature Genetics — should improve our understanding of the biology of atrial fibrillation (A-fib) and lead to better treatments.
They could also “have important implications for precision health and prevention of cardiovascular disease,” says co-senior study author Cristen J. Willer, an associate professor of computational medicine and bioinformatics at the University of Michigan in Ann Arbor.
From the genes that they identified, the researchers compiled a genetic “risk score” for helping to pick out individuals at higher risk for A-fib for closer monitoring.
Many of the genes influence heart development in the fetus. The team says that this implies that variants in these genes could instil susceptibility to A-fib before birth.
Another possibility is that they could cause genes that have been inactive since before birth to switch on again in adulthood.
A-fib needs new treatments
Around 2.2 million people in the United States have A-fib, a condition in which the left side of the heart’s upper chamber, or atrium, beats irregularly. This causes blood to pool and raises the likelihood of blood clots.
If a blood clot forms in the atrium, it can travel to the brain and block one of its arteries, giving rise to a stroke. This is why having A-fib raises a person’s risk of stroke by an average of four to six times.
Some people with A-fib experience symptoms such as chest pain, fluttering in the chest, fatigue, fainting, and shortness of breath. Others have none.
The earlier A-fib is detected, the greater the chances of preventing stroke, heart failure, and other complications.
However, there are few current options for treating A-fib, and those that do exist rarely cure it and often result in grave side effects.
Willer and her colleagues claim that it is likely that 32 of the 151 genes that they identified interact with drugs already approved for treating other conditions.
They suggest that their findings provide a foundation for further research into whether or not such drugs can prevent or cure A-fib.
Data from several biobanks
The researchers carried out a genome-wide association study on data pooled from six studies. The datasets came from a number of “biobanks” in different countries. These included datasets from: AFGen Consortium, DiscovEHR, Michigan Genomics Initiative, UK Biobank, deCODE Genetics in Iceland, and the HUNT study in Norway.
By using a collaborative big data approach, the researchers believe that they were able to identify genes that do not emerge from analyses of individual datasets.
They note that many of the risk variants they identified are located near genes where more harmful mutations “have been reported to cause serious heart defects in humans […] or near genes important for striated muscle function and integrity.”
They also discovered that people who develop A-fib early in life carry more of the risk genes than those who develop it later.
The team concludes that, while the findings are significant, further studies now need to confirm them.
“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.”
Cristen J. Willer