Introduction: EDAS generates new collateral vessels from the external carotid artery to the cerebral circulation in patients with moyamoya disease (MMD) and intracranial atherosclerotic disease (ICASD). The mechanisms involved in this neoangiogenesis process are not well understood. We hypothesize that, if angiogenesis is the leading mechanism, the angioarchitecture of EDAS neovascularization should have greater complexity, manifesting as higher fractal connectivity when compared to native collaterals formed by arteriogenesis. Contrary to arteriogenesis, angiogenic mechanisms involve local hypoxia, sprouting, and splitting of vascular structures.
Methods: Pre and postoperative digital subtraction angiograms (DSA) were analyzed in patients enrolled in a prospective trial of EDAS surgery. Images were processed using the Fraclac plugin of ImageJ. LCFD provides an index of complexity by measuring changes in connectivity with varying scales, allowing quantification of non-Euclidean geometric patterns. Log transformations were used for skewed data. High connectivity was defined as LCFD = 1.2. Comparison of means was performed using 2-way unpaired t-test and 2-way paired t-test for matched samples.
Results: 73 angiograms (27 baseline, 46 post-operative) were analyzed. Study population included 42 patients (69% female), age 4-84 (mean 35, SD 19.2). ICASD and MMD groups had 21 patients each. Both ICASD and MMD groups had significantly higher mean LCFD peaks on the postoperative collaterals (ICASD: 1.12 vs 1.22, P<0.001; MMD: 1.20 vs 1.25 P=0.04). The proportion of high connectivity in the matched groups was significantly higher in postoperative angiograms for both ICASD group (P<0.001) and MMD group (P=0.01). The observed reduction in low connectivity and increase in high connectivity was greater in the ICASD group (P=0.01) when compared with MMD cases.
Conclusions: Collaterals formed after EDAS have higher local connected fractal dimension (LCFD) compared to innate collaterals in ICASD and MMD patients. Higher LCFDs are consistent with the greater complexity expected in vascular sprouting and splitting associated with angiogenesis.
Patient Care: A better understanding of the patterns of growth of vessels after EDAS surgery is key to potentially target that neovascularization for enhancement in individuals at risk for stroke.
Learning Objectives: To differentiate anatomical characteristic of native versus surgical collaterals
To gain insight in the mechanism of vessel formation after EDAS