New research published in the journal Circulation indicates that lacunar ischemic stroke is not primarily caused by fatty plaque building up inside arteries, but by changes in the brain’s blood vessels, specifically the enlargement and widening of arteries. This finding challenges assumptions and explains why standard antiplatelet treatments often have limited success in preventing this specific type of stroke.
Why Standard Stroke Prevention Often Fails
Medical protocols for stroke prevention have focused on treating the buildup of fatty plaque in the body’s larger arteries. However, these conventional approaches, including the use of aspirin and other antiplatelet medications, have shown limited effectiveness in preventing lacunar strokes.
According to research from the University of Edinburgh, the UK Dementia Research Institute, and international collaborators, lacunar stroke develops when the brain’s tiniest blood vessels are damaged by a condition known as small vessel disease.
The Role of Artery Widening
The study, which examined 229 participants who experienced either a lacunar or mild non-lacunar stroke, utilized MRI scans to monitor vascular health over one year. Researchers compared two specific vascular phenomena: the fatty narrowing of larger arteries and the widening and elongation of arteries within the brain.
The data revealed a clear distinction:
- Large Artery Narrowing: This was not associated with lacunar stroke and did not predict future brain damage.
- Artery Widening: Patients with enlarged arteries were more than four times more likely to have experienced a lacunar stroke.
This widening is linked to more severe small vessel disease, faster progression of brain damage, and a higher frequency of "silent" strokes—small areas of brain tissue damage caused by interrupted blood supply that can occur without obvious symptoms. Notably, more than one in four participants in the study experienced these silent strokes despite being on standard treatments intended to prevent additional strokes.
Future Directions in Treatment
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, emphasizes that distinguishing this pathology is essential for developing effective therapies.
Current clinical investigations, such as the LACI-3 (LACunar Intervention Trial 3), are testing whether medications like cilostazol and isosorbide mononitrate can help protect the brain, lower the risk of additional strokes, and reduce long-term problems involving memory, mobility, and dementia.
Key Takeaways for Patients and Clinicians
- Pathology: Lacunar stroke is caused by small vessel disease, characterized by the widening and elongation of arteries within the brain.
- Limitations of Care: Traditional antiplatelet medications have had limited success for this condition.
- Ongoing Research: The LACI-3 trial is currently evaluating new drug strategies designed to protect and support the brain’s smallest blood vessels.
- Silent Strokes: Patients remain at risk for silent strokes, which can occur even when standard preventive measures are in place.
The research was supported by the UK Dementia Research Institute, the Leducq Foundation, the Stroke Association, British Heart Foundation, Scottish Government’s Chief Scientist Office, Row Fogo Charitable Trust, Wellcome Trust, and other national funding agencies, involving international collaborators from China and Mexico.