Background and Purpose- In unilateral moyamoya disease, altered endothelial shear stress on the intact-side terminal internal carotid artery might trigger the progression to bilateral disease. We analyzed the endothelial shear stress parameters of the normally appearing terminal internal carotid artery in unilateral moyamoya disease and its association with the progression to bilateral disease. Methods- This retrospective cohort study included patients diagnosed with unilateral moyamoya disease by cerebral angiography and followed-up with regular magnetic resonance imaging/magnetic resonance angiography evaluations for >1 year. Endothelial shear stress parameters acquired were mean and maximum signal intensity gradients (SIG) and SIG SD at the vessel boundary in time-of-flight sequences in initial brain magnetic resonance imaging/magnetic resonance angiography. Contralateral disease progression defined as the detection of newly developed vessel steno-occlusion with an magnetic resonance angiography steno-occlusive stage of ≥2, in the previously intact side of the brain on follow-up magnetic resonance imaging/magnetic resonance angiography evaluation. Results- Among 146 patients (66 males [45.2%] and 80 females [54.8%]; 76 pediatric [52.1%]), contralateral disease progression was detected in 43 patients (29.5%) after a mean follow-up of 4.3±2.4 years. Multivariate analysis showed that SIG SD was significantly associated with this progression (odds ratio, 13.001 [95% CI, 1.764-95.794], =0.012). In receiver operating characteristic curve analysis, SIG SD predicted the contralateral progression with area under the curve values of 0.803 (95% CI, 0.726-0.880, <0.001). The regression model was reproduced in the external cohort of 31 patients. Conclusions- Increased spatial variability of the endothelial shear stress around the normally appearing terminal internal carotid artery, as measured by SIG SD in time-of-flight sequences, may predict the contralateral progression of unilateral moyamoya disease.

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http://dx.doi.org/10.1161/STROKEAHA.119.028117DOI Listing

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