Post-contrast HR-MRI was imaged after the intravenous injection of gadolinium diethylenetriamine penta-acetic acid (GdDTPA Magnevist Bayer Schering Pharma, Berlin, Germany) for about 6 minutes at a dose of 0.1 mmol/kg.īased on the pre- and post-contrast HR-MRI images, the existence of AWE was determined by 2 experienced neuroradiologists (with >4 years’ experience in neurovascular imaging) who were blinded to the patients’ clinical data and other sequences except for 3D TOF-MRA.
Furthermore, pre- and post-contrast HR-MRI were performed using a 3D black-blood T1-weighted volumetric isotropic turbo spin echo acquisition (3D T1-VISTA) sequence with a variable flip angle ( 24), and the other imaging parameters were as follows: TR/TE =800/21 ms, FOV =200×180×40 mm 3, and voxel size =0.6×0.6×0.6 mm 3. Then, 4D-flow MRI was acquired using a free-breathing, peripheral pulse-gated, multi-shot turbo filed echo sequence, and the scan parameters were as follows: TR/TE =8.0/3.6 ms, FOV =160×160×30 mm 3, voxel size =1×1×1 mm 3, flip angle =20°, and velocity encoding (VENC) =120 cm/s for all 3 directions. The imaging parameters for 3D TOF-MRA were as follows: repetition time/echo time (TR/TE) =25/3.5 ms, field of view (FOV) =160×160×60 mm 3, voxel size =0.8×0.8×0.8 mm 3, and flip angle =20°. First, the 3D time-of-flight MRA (3D TOF-MRA) was acquired, and the aneurysm was located. We present the following article in accordance with the STROBE reporting checklist (available at ).Īll MRI scans were conducted on a 3.0T MR scanner (Achieva TX, Philips, Best, The Netherlands) with a 32-channel head coil. We aimed to provide new insights into the relationship between hemodynamics and inflammation processes in UIAs. In this study, taking advantage of HR-MRI and 4D-flow MRI, the relationship between distribution of AWE and hemodynamic parameters on aneurysmal wall was studied from a pixel-level perspective for each specific patient. However, all of these studies compared groups of aneurysms they did not reflect the spatial distribution correlation between aneurysmal wall inflammation and hemodynamics at the individual-patient level. One study used four-dimensional flow MRI (4D-flow MRI), which allows direct in vivo and reliable hemodynamic measurement of UIAs ( 21, 22), to explore the relationship between hemodynamics and AWE and also found that low WSS was independently associated with high AWE grade ( 23). With the same methods, another study showed that the association between AWE and hemodynamics seemed to depend on the location of the AWE region ( 20). Based on computational fluid dynamics (CFD) and HR-MRI, several studies found that AWE regions were associated with lower wall shear stress (WSS), which is the most highlighted hemodynamic parameter, and WSS was found to be an independent predictor of AWE ( 17- 19). Previous studies have hypothesized a pathogenetic link between hemodynamics and inflammatory vessel wall alteration leading to the development and rupture of UIAs, and many studies have explored this association ( 13- 16). These findings did not refute the clinical value of HR-MRI, but hinted that studies of AWE should be carefully conducted, with measures taken to reduce the impact of low-flow patterns. In 2 other phantom studies, it was demonstrated that near-wall slow flow mimicked wall enhancement in HR-MRI ( 11, 12). Recent studies have found that several factors could contribute to AWE except wall inflammation, particularly low-flow patterns, which could lead to pseudo-enhancement of the aneurysm wall ( 9, 10). Aneurysm wall enhancement (AWE) on high-resolution magnetic resonance imaging (HR-MRI) has been used as an indicator of wall inflammation and weakening of the aneurysm wall ( 7, 8).
Histopathological evidence from human and animal studies has suggested that the inflammatory processes in the aneurysmal wall may play a role in the formation, growth, and rupture of the aneurysm ( 5, 6). Once ruptured, UIAs can cause intracranial subarachnoid hemorrhage, which has a mortality rate of up to 50% ( 4). In a study including 11,660 aneurysm-years, the annual rupture risk was reported to be 0.95% ( 3). The prevalence of UIAs is 3–7% in the adult population worldwide ( 1, 2). Unruptured intracranial aneurysms (UIAs) are local dilatations on the wall of intracranial arteries.
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