Abstract
Introduction: ICAS confers the greatest risk of stroke, but the pathophysiology of stroke mechanismremains unclear. Essentially, plaque rupture is a physical process of structural failuredue to destructive biomechanics, and hypoperfusion is due to low perfusion pressure,which act as 2 major stroke mechanisms in sICAS. Notably, blood pressure (BP)plays key role in determining both biomechanics and perfusion of ICAS. Hypothesis: ICAS could result in significant BP change which may further influence strokemechanism. High local pressure gradient across ICAS may cause plaque rupture andthe subsequent artery-to-artery embolism, whereas low perfusion pressure atpost-stenosis area may restrict perfusion and induce the subsequent borderzoneinfarcts (Fig) . Method: A total of 339 sICAS patients due to 50-99% stenosis in MCA or ICA were includedfrom CNSR3. By Newton-Krylov-Schwarz method, CFD models were built based onTOF-MRA (Fig) . Translesional pressure ratio (PR) across ICAS was calculated as:pressurepoststenotic/pressureprestenotic. SBP gradient was calculated as: SBPх(1-PR),indicating the SBP drop across ICAS. Perfusion pressure at post-stenosis area wascalculated as: MAPхPR. Results: After adjustment, high SBP gradient and low perfusion pressure was shown tocorrelate with cortical infarcts (p=0.041) and borderzone infarcts (borderlinesignificant, p=0.059) (Fig) . Between the 2 parameters, Pearson correlation coefficient=-0.854, p <.0001. The cutoff of SBP gradient and perfusion pressure for the above 2stroke mechanisms was 14.4mmHg and 94.4mmHg, respectively. Conclusions: We demonstrated the hemodynamic hypothesis of stroke mechanism in sICAS thatartery-to-artery embolism and hypoperfusion could be attributed to the combinedeffect of blood pressure and translesional PR. Accordingly, a double-edged role of high BP level in sICAS may further surface, which can induce destructivebiomechanics but relieve hypoperfusion simultaneously.
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