Performance of Aneurysm Wall Enhancement Compared with Clinical Predictive Scales: PHASES, ELAPSS, and UIATS.

OBJECTIVE: To correlate the presence of objectively measured wall enhancement on high-resolution vessel wall imaging (HR-VWI) with the clinical predictive scales PHASES, ELAPSS, and UIATS. METHODS: Patients with unruptured intracranial aneurysm (UIAs) prospectively underwent HR-VWI on a 3-T magnetic resonance imaging scanner at diagnosis. Aneurysmal wall enhancement was objectively quantified on T1 postcontrast magnetic resonance imaging using signal intensity values adjusted for the pituitary stalk to calculate a contrast ratio (CRstalk). UIAs with CRstalk ≥0.60 were considered "enhancing." Patients' demographics, comorbidities, and aneurysm morphology were reviewed to calculate PHASES, ELAPSS, and UIATS scores. Pearson coefficients were applied for statistical correlation. Univariable and multivariable logistic regressions were performed to assess for confounders. RESULTS: One-hundred and twenty-three patients harboring 178 UIAs underwent HR-VWI. A total of 101 patients with 135 UIAs were analyzed. Enhancing UIAs were larger (8.4 ± 5.5 mm vs. 5.5 ± 2.3 mm; P < 0.001), had higher aspect ratio (2.3 ± 1.5 vs. 1.8 ± 0.7; P = 0.008), higher size ratio (3.0 ± 1.8 vs. 2.4 ± 1.1; P = 0.016), scored higher on PHASES (5.6 ± 3.9 vs. 4.4 ± 2.6; P = 0.04) and ELAPSS (19.4 ± 8.9 vs. 15.4 ± 7.3; P = 0.006) compared with nonenhancing UIAs. Treatment allocation as defined by UIATS was measured independently to enhancement status. No significant differences were found for UIATS between enhancing and nonenhancing UIAs (P = 0.63). Multivariable regression showed that size was the only independent factor significantly associated with UIA enhancement (odds ratio, 1.76; P = 0.005). CONCLUSIONS: Enhancing UIAs score higher in PHASES and ELAPSS scales. This association is largely explained by aneurysm size, aspect, and size ratios. Morphologic UIA features should be accounted for in clinical predictive scales of aneurysm instability.

Insights into the pathogenesis of cerebral fusiform aneurysms: high-resolution MRI and computational analysis.

BACKGROUND: Intracranial fusiform aneurysms are complex and poorly characterized vascular lesions. High-resolution magnetic resonance imaging (HR-MRI) and computational morphological analysis may be used to characterize cerebral fusiform aneurysms. OBJECTIVE: To use advanced imaging and computational analysis to understand the unique pathophysiology, and determine possible underlying mechanisms of instability of cerebral fusiform aneurysms. METHODS: Patients with unruptured intracranial aneurysms prospectively underwent imaging with 3T HR-MRI at diagnosis. Aneurysmal wall enhancement was objectively quantified using signal intensity after normalization of the contrast ratio (CR) with the pituitary stalk. Enhancement between saccular and fusiform aneurysms was compared, as well as enhancement characteristics of fusiform aneurysms. The presence of microhemorrhages in fusiform aneurysms was determined with quantitative susceptibility mapping (QSM). Three distinct types of fusiform aneurysms were analyzed with computational fluid dynamics (CFD) and finite element analysis (FEA). RESULTS: A total of 130 patients with 160 aneurysms underwent HR-MRI. 136 aneurysms were saccular and 24 were fusiform. Fusiform aneurysms had a significantly higher CR and diameter than saccular aneurysms. Enhancing fusiform aneurysms exhibited more enhancement of reference vessels than non-enhancing fusiform aneurysms. Ten fusiform aneurysms underwent QSM analysis, and five aneurysms showed microhemorrhages. Microhemorrhage-positive aneurysms had a larger volume, diameter, and greater enhancement than aneurysms without microhemorrhage. Three types of fusiform aneurysms exhibited different CFD and FEA patterns. CONCLUSION: Fusiform aneurysms exhibited more contrast enhancement than saccular aneurysms. Enhancing fusiform aneurysms had larger volume and diameter, more enhancement of reference vessels, and more often exhibited microhemorrhage than non-enhancing aneurysms. CFD and FEA suggest that various pathophysiological processes determine the formation and growth of fusiform aneurysms.