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Lifetime risk for AF greater than previously thought
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The lifetime risk for atrial fibrillation is approximately 37% after age 55 years, greater than previous estimates, according to data published in Circulation.
Researchers analyzed 4,606 participants from the Framingham Heart Study who were without AF at age 55 years.
For each individual, the researchers calculated polygenic risk for AF using a score composed of approximately 1,000 single nucleotide polymorphisms associated with AF and clinical risk factor burden for AF consisting of height, weight, systolic BP, diastolic BP, smoking status, antihypertensive medication use, diabetes, history of MI and history of HF.
Participants were stratified into tertiles based on polygenic and clinical risk.
After a median follow-up of 9.4 years (interquartile range, 4.4-14.3), 580 participants developed incident AF.
Lifetime risk for AF after age 55 years was 37.1% and was greatly influenced by polygenic and clinical risk factor burden, Lu-Chen Weng, PhD, from the Cardiovascular Research Center at Massachusetts General Hospital and the Program in Medical and Population Genetics at the Broad Institute of Harvard and MIT, and colleagues wrote.
Prior reports estimated lifetime risk for AF after age 55 years at approximately 25%, according to the researchers.
Those in the lowest tertiles of polygenic and clinical risk had lifetime risk for AF of 22.3% (95% CI, 15.4-29.1), whereas those in the highest tertiles had lifetime risk for AF of 48.2% (95% CI, 41.3-55.1), according to the researchers.
After adjustment for genetic predisposition, lower clinical risk factor burden was associated with later onset of AF (P < .001), Weng and colleagues wrote.
“Nevertheless, the lifetime risk of atrial fibrillation in individuals with high genetic predisposition was substantial, even when the clinical risk factor burden was low,” Weng and colleagues wrote, noting that those with low risk factor burden but high polygenic burden had lifetime risk for AF of 43.6% (95% CI, 35.6-51.6).
“The higher lifetime risk estimates in our study may be related to diminished mortality from competing causes of death, greater follow-up during older ages of life when AF risk is the greatest or enhanced surveillance for AF owing to increased awareness of the arrhythmia,” Weng and colleagues wrote. “We anticipate that the true lifetime risk of AF and attributable morbidity are currently underestimated since undiagnosed AF is common.” – by Erik Swain
Disclosures: One researcher reports he received a grant from Bayer HealthCare. Another researcher reports he received research support from Bayer HealthCare, Biotronik and Boehringer Ingelheim, and has consulted for Quest Diagnostics and St. Jude Medical.
Perspective
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Dan Roden, MD
I think the most intriguing results are, No, 1, that there is an even higher incidence of AF than previously estimated: This might be unique in some way to Framingham, but that seems unlikely. More data in bigger numbers will help nail this down and also the corresponding disability (stroke, HF, mortality) burden. No. 2, while genetic studies of AF have been interesting and hold the promise of unraveling mechanisms or even pointing to new drug development, taking genetics into account hasn’t changed risk prognostication much. This is one of the first studies to suggest that genetics add value in predicting the indices of AF or the age of its onset.
I don’t think these findings can be used in clinical practice yet, if for no other reason than logistics of getting genetic data into the flow of health care is quite daunting. I suppose if I had had my whole genome sequenced, it might be interesting to see if I am at increased risk. But even if I was, I am not sure yet what I would do with that information. Where this may be going is developing ways of identifying people at modest to high risk (through traditional risk factors or traditional risk factors plus genetics) and seeing if intensive monitoring can find AF early and/or if prophylactic anticoagulation will impact stroke risk. All all of this is for the future, but is appealing to think about.
Many questions remain to be investigated. What mechanism(s) are the genetics defining for us? What is special about aging that conspires with genetics and other traditional risk factors to generate AF? Are there subsets of patients at very high genetic risk or subsets who will get AF even in the face of low genetic risk?
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