Nirali Vora, MD
We recommend carotid endarterectomy (CEA) in symptomatic, high-grade carotid stenosis to avoid a high risk of early, recurrent stroke. What do those arteries and the plaque look like under the microscope? Can the pathology clue us into better medical therapies for stroke prevention?
Marnane et al. attempted to answer this question by reviewing the histopathology of carotid plaque resected during CEA in patients who had recently had a TIA or stroke. They had a small population of 44 patients with typical distribution of vascular risk factors and symptomatic carotid stenosis, with the majority high-grade >70% stenosis. Stroke recurrence prior to CEA occurred among 27% patients. All strokes were confirmed with DWI positivity on MRI. CEA took place within a mean of 10 days from most recent event.
Among patients who had recurrent stroke between initial presentation and CEA (versus those that simply had a single event), the plaque had significantly increased inflammation with denser macrophages and lower fibrous tissue content. This was true even when adjusting for age or severity of carotid stenosis.
It’s unclear to me if this association is the result of the recurrent stroke or an underlying feature of plaque in high-risk carotids? Either way, it seems reasonable to target therapy with drugs that can reduce macrophage infiltration. Traditionally, we think of statin therapy as having some “anti-inflammatory” effect. The patients in both arms did receive equal amount of statins (and anti platelets). What is another therapy we can use to target this macrophage inflammation, either acutely or for prevention? Let us know what you are studying!
