ArticleFrontiers in neurology
Hyperintense acute reperfusion marker (HARM) and thrombus analysis in acute ischemic stroke.
Article in Frontiers in neurology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Mechanical thrombectomy allows thrombus analysis in acute ischemic stroke. The extravasation of contrast material into the cerebrospinal fluid (CSF) on fluid-attenuated inversion recovery (FLAIR) imaging is referred to as a hyperintense acute reperfusion marker (HARM), which indicates deterioration of the blood-brain barrier (BBB). In this study, we aimed to examine the relationship between the histopathological features of thrombi and HARM in acute ischemic stroke. A total of 56 patients who underwent mechanical thrombectomy (MT) were included in the study. Procedural data, including the number of passes, techniques used, and recanalization scores based on the modified Thrombolysis in Cerebral Infarction (mTICI) scale, were documented. FLAIR imaging was performed 24 h after contrast administration. The presence of contrast extravasation into the cerebral sulci was defined as a positive HARM. A total of 52 thrombi were successfully retrieved and analyzed. Thrombus sections were stained with hematoxylin and eosin (H&E) to evaluate their fibrin and erythrocyte composition. Immunohistochemical staining using CD3, CD20, and CD45 antibodies was performed to identify T lymphocytes, B lymphocytes, and total leukocytes, respectively. In our study, it was found that clinical outcomes-measured by National Institutes of Health Stroke Scale (NIHSS) scores at 24 h and modified Rankin Scale (mRS) scores at 90 days-were significantly worse in HARM-positive patients. A histopathological analysis revealed that thrombi from HARM-positive patients were predominantly rich in fibrin, suggesting a potential association between thrombus composition and BBB disruption. Future studies incorporating more detailed thrombus characterization alongside advanced radiological markers may yield valuable insights into stroke pathophysiology.
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