Myriam Edjlali1, Jean-Christophe Gentric2, Christine Régent-Rodriguez2, Denis Trystram2, Wajih Ben Hassen2, Stéphanie Lion2, François Nataf2, Jean Raymond2, Oliver Wieben2, Patrick Turski2, Jean-Francois Meder2, Catherine Oppenheim2, Olivier Naggara2. 1. From the Departments of Radiology (M.E., C.R.-R., D.T., W.B.H., S.L., J.F.M., C.O., O.N.) and Neurosurgery (F.N.), Université Paris Descartes Sorbonne Paris Cité, INSERM S894, Centre Hospitalier Sainte-Anne, Paris, France; Department of Interventional Neuroradiology, University of Montreal, CHUM Notre-Dame Hospital, Montreal, Quebec, Canada (J.-C.G., J.R.); and the Departments of Medical Physics and Radiology (O.W., P.T.), University of Wisconsin, Madison. m.edjlali@ch-sainte-anne.fr. 2. From the Departments of Radiology (M.E., C.R.-R., D.T., W.B.H., S.L., J.F.M., C.O., O.N.) and Neurosurgery (F.N.), Université Paris Descartes Sorbonne Paris Cité, INSERM S894, Centre Hospitalier Sainte-Anne, Paris, France; Department of Interventional Neuroradiology, University of Montreal, CHUM Notre-Dame Hospital, Montreal, Quebec, Canada (J.-C.G., J.R.); and the Departments of Medical Physics and Radiology (O.W., P.T.), University of Wisconsin, Madison.
Abstract
BACKGROUND AND PURPOSE: Arterial wall enhancement on vessel wall MRI was described in intracranial inflammatory arterial disease. We hypothesized that circumferential aneurysmal wall enhancement (CAWE) could be an indirect marker of aneurysmal wall inflammation and, therefore, would be more frequent in unstable (ruptured, symptomatic, or undergoing morphological modification) than in stable (incidental and nonevolving) intracranial aneurysms. METHODS: We prospectively performed vessel wall MRI in patients with stable or unstable intracranial aneurysms. Two readers independently had to determine whether a CAWE was present. RESULTS: We included 87 patients harboring 108 aneurysms. Interreader and intrareader agreement for CAWE was excellent (κ=0.85; 95% confidence interval, 0.75-0.95 and κ=0.90; 95% confidence interval, 0.83-0.98, respectively). A CAWE was significantly more frequently seen in unstable than in stable aneurysms (27/31, 87% versus 22/77, 28.5%, respectively; P<0.0001). Multivariate logistic regression, including CAWE, size, location, multiplicity of aneurysms, and daily aspirin intake, revealed that CAWE was the only independent factor associated with unstable status (odds ratio, 9.20; 95% confidence interval, 2.92-29.0; P=0.0002). CONCLUSIONS: CAWE was more frequently observed in unstable intracranial aneurysms and may be used as a surrogate of inflammatory activity in the aneurysmal wall.
BACKGROUND AND PURPOSE: Arterial wall enhancement on vessel wall MRI was described in intracranial inflammatory arterial disease. We hypothesized that circumferential aneurysmal wall enhancement (CAWE) could be an indirect marker of aneurysmal wall inflammation and, therefore, would be more frequent in unstable (ruptured, symptomatic, or undergoing morphological modification) than in stable (incidental and nonevolving) intracranial aneurysms. METHODS: We prospectively performed vessel wall MRI in patients with stable or unstable intracranial aneurysms. Two readers independently had to determine whether a CAWE was present. RESULTS: We included 87 patients harboring 108 aneurysms. Interreader and intrareader agreement for CAWE was excellent (κ=0.85; 95% confidence interval, 0.75-0.95 and κ=0.90; 95% confidence interval, 0.83-0.98, respectively). A CAWE was significantly more frequently seen in unstable than in stable aneurysms (27/31, 87% versus 22/77, 28.5%, respectively; P<0.0001). Multivariate logistic regression, including CAWE, size, location, multiplicity of aneurysms, and daily aspirin intake, revealed that CAWE was the only independent factor associated with unstable status (odds ratio, 9.20; 95% confidence interval, 2.92-29.0; P=0.0002). CONCLUSIONS: CAWE was more frequently observed in unstable intracranial aneurysms and may be used as a surrogate of inflammatory activity in the aneurysmal wall.
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