Abstract P314: Mechanisms of Intracranial Atherosclerotic Disease Drive Hypoperfusion Patterns
Background: In patients with symptomatic intracranial atherosclerotic disease (ICAD), borderzone infarct pattern and perfusion mismatch have each been shown to independently predict recurrent strokes, which may reflect the shared underlying mechanism of hypoperfusion distal to the intracranial atherosclerosis. As such, we hypothesized that perfusion volumes and patterns may correlate with various ICAD subtypes. Methods: A retrospective, 5-year analysis of consecutive ICAD patients with perfusion imaging for acute strokes (0-24 hours) due to sub-occlusive (50-99%) stenosis was conducted. The following subtypes were assigned based on the infarct pattern seen on the diffusion-weighted imaging (DWI): perforator, borderzone, and thromboembolic. Core volume on MRI and perfusion parameters on CT or MR perfusion, obtained concurrently or within 12 hours of MR DWI, were studied in each group. Results: 42 patients (57% women, mean age 71±13 years old) with acute strokes received MRI imaging upon initial presentation. 15 were found with borderzone, 12 perforator, and 15 with thromboembolic pattern on DWI. Across all ICAD subtypes, median core volume (ADC <620) was 0 mL (0[0-6], 0[0-3], 0[0-7], p =0.95). Hypoperfusion with Tmax >4s and Tmax >6s delay volumes was significantly higher in the thromboembolic and borderzone infarct patterns compared to the perforator subtype ( Figure 1 ). The volume difference between Tmax >4s and Tmax >6s (Δ Tmax>4s - Tmax>6s) was higher in the borderzone subtype compared to thromboembolism when analyzed pairwise. Conclusion: Core volume in ischemic strokes secondary to symptomatic ICAD is minimal. TMax>4 and TMax>6 parameters vary across the different ICAD patterns, with significantly large Tmax>4 delay volumes in the borderzone profile. Perfusion mapping may further elucidate hemodynamic mechanisms underlying ICAD.