4.6 Article

Evaluation of clinical relevance and underlying pathology for hemodynamic compromise in acute small subcortical infarction using MRI-based neuroimaging markers

Journal

BIOMEDICAL JOURNAL
Volume 46, Issue 2, Pages -

Publisher

ELSEVIER
DOI: 10.1016/j.bj.2022.03.014

Keywords

Perfusion defect; Single subcortical infarction; Small vessel disease; MRI; Early neurological deterioration

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This study aimed to evaluate the clinical relevance and underlying pathology of hemodynamic compromise in acute small subcortical infarction (SSI) using MRI-based neuroimaging markers. The results showed that hemodynamic compromise was highly related to early neurological deterioration (END), basal ganglia EPVS, and branch atheromatous disease.
Background: Hemodynamic compromise has been observed in patients with acute small subcortical infarction (SSI), and it may play a critical role in the development of early neurological deterioration (END). This study aimed to evaluate the clinical relevance and underlying pathology of hemodynamic compromise in SSI using MRI-based neuroimaging markers. Methods: We retrospectively analyzed data and imaging of previous prospective studies. Patients with acute SSI in penetrating artery territories were recruited, all of whom underwent perfusion MRI within 24 h of stroke onset. We examined the relationships among perfusion defects and neuroimaging markers of small vessel disease, including white matter hyperintensities, cerebral microbleeds, enlarged perivascular spaces (EPVSs) and lacunes. Results: One hundred and seven patients were recruited, of whom 21 (19.6%) had END and 55 (51.4%) had visible perfusion defects. Patients with perfusion defects were associated with a higher rate of END (34.5% vs. 3.8%; p < 0.001), higher initial National Institutes of Health Stroke Scale scores (5.4 vs. 3.4, p < 0.001), higher rate of branch atheromatous disease (61.8% vs. 34.6%, p = 0.005) and higher rate of poor outcome at 3 months (40.0% vs. 5.4%; p = 0.005). In multiple logistic regression, perfusion defects were significantly associated with basal ganglia EPVS scores (adjusted odds ratio [aOR]: 3.93; 95% confidence interval [CI]: 1.76-8.77; p = 0.001) and branch atheromatous disease (aOR: 2.64; 95% CI: 1.06-6.60; p = 0.037). Conclusion: Hemodynamic compromise in acute SSI was highly related to the development of END, basal ganglia EPVS and branch atheromatous disease, suggesting the correlation with underlying pathologies of hypertensive arteriopathy and atherosclerosis.

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