Artery widening, rather than fatty plaque, has been strongly linked to lacunar stroke and may help explain why preventive treatments often fail.
The findings may explain why aspirin and other antiplatelet medicines have had limited success in preventing this common type of stroke.
Antiplatelet drugs make blood cells called platelets less likely to stick together and form clots.
Joanna Wardlaw, professor of applied neuroimaging at the University of Edinburgh’s Institute for Neuroscience and Cardiovascular Disease and group leader at the UK Dementia Research Institute, said: “This study provides strong evidence that lacunar stroke is not caused by fatty blockage of larger arteries, but by disease of the small vessels within the brain itself.
“Recognising this distinction is crucial, because it explains why conventional treatments like antiplatelet drugs are not as effective for this type of stroke and highlights the urgent need to develop new therapies that target the underlying microvascular damage.”
Researchers from the University of Edinburgh, the UK Dementia Research Institute and international collaborators studied 229 people who had experienced either a lacunar stroke or a mild non-lacunar stroke.
Lacunar stroke develops when the brain’s smallest blood vessels are damaged by a condition known as small vessel disease. It is linked to disability, cognitive decline, dementia and a higher risk of further strokes.
Participants completed clinical and cognitive assessments and had MRI brain scans shortly after their stroke and again one year later.
The scans helped researchers identify the type of stroke, assess signs of small vessel disease and detect new areas of brain injury that developed over time.
The team compared two types of blood vessel change: fatty narrowing in larger arteries and the widening and lengthening of arteries inside the brain.
Narrowing of the larger arteries was not linked to lacunar stroke or small vessel disease.
Although narrowing was more common in people with other types of stroke, it did not predict new brain damage on follow-up scans.
In contrast, people with enlarged arteries were more than four times as likely to have experienced a lacunar stroke.
Artery widening was also linked to more severe small vessel disease, faster progression of brain damage and a greater chance of developing new silent strokes.
Silent strokes are small areas of brain damage caused by an interruption to the blood supply and may occur without noticeable symptoms.
More than one in four participants developed silent strokes during the study despite receiving standard treatments intended to prevent further strokes.
The findings suggest that future treatments should focus on damage to the brain’s small blood vessels rather than fatty plaque in larger arteries.
The results are helping to guide the LACunar Intervention Trial 3, known as LACI-3, which is testing treatments designed to support and protect small blood vessels in the brain.
The trial is studying cilostazol and isosorbide mononitrate to assess whether the existing medicines can help protect the brain, reduce further strokes and limit longer-term problems involving memory, mobility and dementia after lacunar stroke.
