Health Rounds: Untreated atrial fibrillation can raise risk of dementia, death
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By Nancy Lapid
June 6(Reuters) -Hello Health Rounds Readers! Today we share some important findings for people with the common heart rhythm disorder atrial fibrillation: taking blood thinners that reduce the risk of strokes may also stave off a form of dementia, and lowering the dose of those medicines does not cut the risk of bleeding episodes. We also highlight a potentially important discovery involving the cause of inflammatory bowel disease that could lead to new treatments.
Untreated Afib linked with higher risk of dementia
Patients with the common heart rhythm disorder atrial fibrillation who don’t take blood thinners that reduce the risk of stroke are also at higher risk for dementia and death, a large UK study shows.
Atrial fibrillation, or Afib, significantly increases a patient’s risk of developing blood clots in the heart that can break off, travel to the brain, and cause a stroke.
The blood thinners used to prevent those clots come with their own risks of serious bleeding, so doctors sometimes hold off on prescribing them for patients thought to be at a relatively low risk of a stroke.
But stroke may not be the only outcome to worry about, the research team found.
Even Afib patients with a lower risk of stroke may face an elevated risk of so-called vascular dementia, cognitive problems caused by impaired blood flow to the brain, they wrote on Wednesday in Nature Medicine.
Researchers tracked 36,340 primary care patients with a diagnosis of Afib, no history of stroke, a low perceived risk of stroke based on clinical risk factors and who were not prescribed oral anticoagulants such as Eliquis from Bristol Myers Squibb BMY.N and Pfizer PFE.N. They were compared with 117,298 similar patients without Afib.
With half the patients followed for at least 5 years, and after accounting for individual risk factors, rates of first strokes and of blood clots in arteries were each more than 100% higher in the untreated Afib patients. This group also had a 44% higher risk of death during the study, and a 68% higher risk of developing vascular dementia.
The study was not designed to prove that untreated Afib caused these outcomes, the researchers noted.
Randomized controlled trials are needed to determine whether these “low stroke risk” patients with Afib “could benefit from earlier use of oral anticoagulants to improve their prognosis and prevent cognitive decline,” they said.
A separate study of 1,657 Afib patients published on Thursday in Blood Advances by a different team of researchers found that trying to limit the bleeding risks associated with blood thinners by prescribing a lower-than-usual dose is likely to backfire.
“Patients with Afib who took low doses of blood-thinning medications known as direct oral anticoagulants experienced more bleeding episodes during the first three months of treatment... compared with similar patients who took standard doses of the same medications,” the researchers reported.
Commonly used blood thinners for this patient population include Eliquis and Xarelto from Bayer BAYGn.DE and Johnson & Johnson JNJ.N.
Link to inflammatory bowel disease found in 'gene desert'
A piece of DNA that plays a major role in inflammatory bowel disease (IBD) has been hiding in a mysterious chromosome region known as a “gene desert,” researchers reported on Wednesday in Nature.
Gene deserts, which account for nearly 25% of the human chromosome, were once thought to consist only of “junk,” because they don’t contain genes that make proteins. But in one such region, researchers have discovered a section of DNA that can increase the productivity of nearby genes that do make proteins, known as an enhancer.
This particular enhancer boosts a gene called ETS2, which in higher levels is linked to greater risk for IBD.
Gene editing experiments showed that ETS2 was essential for almost all inflammatory functions in immune cells known as macrophages, including several that directly contribute to tissue damage in IBD.
In fact, simply increasing the amount of ETS2 in resting macrophages turned them into inflammatory cells that closely resembled those seen in IBD patients, the researchers reported.
Many other genes previously linked to IBD are part of the ETS2 pathway as well, they also discovered.
Cancer drugs known as MEK inhibitors can help dampen the ETS2 gene’s inflammatory effects, the researchers found, but they said they hope to develop drugs with fewer side effects that would specifically target the gene.
“IBD and other autoimmune conditions are really complex, with multiple genetic and environmental risk factors, so to find one of the central pathways, and show how this can be switched off with an existing drug, is a massive step forwards,” study leader Christina Stankey of the Francis Crick Institute in London said in a statement.
Inflammatory bowel disease, which includes Crohn's disease and ulcerative colitis, can cause diarrhea, rectal bleeding, abdominal pain, fatigue and weight loss. About 5 million people suffer with IBD worldwide, according to a 2019 study.
Currently available IBD drugs don’t work well in every patient.
Reporting by Nancy Lapid; Editing by Bill Berkrot
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