The heart and brain are closely connected, and treating a heart rhythm problem may have unexpected effects on how the brain ages.
New Swedish research has found that people with Alzheimer’s disease and atrial fibrillation lost cognitive abilities more slowly when they were treated with newer blood thinners.
The medicines are known as NOACs, a group that includes several commonly used anticoagulant drugs. They are primarily prescribed to prevent dangerous blood clots rather than to treat dementia.
Atrial fibrillation causes the upper chambers of the heart to beat in an irregular and poorly coordinated way. Because blood may not move normally through the heart, clots can form and later travel through the bloodstream.
A clot that reaches the brain can cause a stroke. For this reason, preventing clots is one of the most important goals when doctors treat older adults with atrial fibrillation.
Alzheimer’s disease has a different main cause. It involves progressive changes and damage in the brain that gradually affect memory, reasoning and the ability to perform everyday activities.
But Alzheimer’s and blood vessel disease can overlap. A person may have the brain changes of Alzheimer’s while also experiencing small strokes or reduced blood flow, and these additional injuries may make cognitive problems worse.
Scientists have therefore wondered whether anticoagulants might indirectly protect cognition by preventing some blood vessel damage. Earlier studies suggested that blood-thinning treatment might be associated with a lower risk of developing dementia, but less was known about people who already had Alzheimer’s.
A team at Karolinska Institutet used Sweden’s national dementia quality register to investigate the question. They identified 7,308 people living with both Alzheimer’s disease and atrial fibrillation.
Participants were compared in three matched groups based on treatment. Some used newer NOAC blood thinners, some took the older anticoagulant warfarin, and others were not receiving anticoagulant medication.
The researchers followed changes in cognition using the Mini-Mental State Examination. The MMSE is a short clinical test that measures several basic thinking abilities and produces a score that can be tracked over time.
People receiving NOACs declined more slowly than the other groups. On average, the difference was slightly more than 0.2 MMSE points each year compared with people taking warfarin or no anticoagulant.
This effect is modest and would probably not be obvious from one appointment to the next. But Alzheimer’s develops over years, so researchers are interested in whether small annual differences could accumulate into a meaningful change over a longer period.
NOAC treatment was also linked with other favorable outcomes. Patients taking these medicines had lower risks of death, stroke, blood clots and fractures than patients who received no anticoagulant treatment.
Warfarin also appeared to protect against death, stroke and blood clots. The trade-off was a higher risk of major bleeding, which is a known danger of medicines that interfere with blood clotting.
Newer anticoagulants have changed atrial fibrillation care because they are easier to use for many patients than warfarin. Warfarin requires careful monitoring and can be affected by diet, other medicines and changes in health, while NOACs generally have more predictable dosing.
The research was led by Professor Maria Eriksdotter at Karolinska Institutet, with Nanbo Zhu and other colleagues. The study was published in the European Heart Journal.
The study provides useful real-world evidence because it included thousands of people with two conditions that commonly occur together in later life. It also examined both cognitive decline and major medical outcomes rather than looking only at stroke prevention.
But there is an important reason for caution. This was not a randomized clinical trial, so doctors had already chosen each patient’s treatment, and those choices may have been influenced by health differences that also affected later outcomes.
For example, patients who were frailer, had a greater bleeding risk or had other illnesses may have been less likely to receive certain anticoagulants. Statistical matching can reduce these differences but cannot guarantee that every important factor has been removed.
The study also cannot show that NOACs directly affect the biological process that causes Alzheimer’s disease. A more likely possibility is that better prevention of strokes and smaller blood vessel injuries helps protect the brain from additional damage on top of the dementia.
Overall, the findings strengthen the case for carefully managing cardiovascular health in people with Alzheimer’s disease. They also provide a reason to investigate in clinical trials whether the choice of blood thinner can make a meaningful long-term difference to cognition, daily functioning and quality of life.
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Source: Karolinska Institutet
