Bart M. W. Cornelissen, Eva L. Leemans, Bram F. Coolen, Eva S. Peper, René van den Berg, Henk A. Marquering, Cornelis H. Slump and Charles B. L. M. Majoie
MR vessel wall imaging (VWI) is increasingly performed in clinical settings to support treatment decision-making regarding intracranial aneurysms. Aneurysm wall enhancement after contrast agent injection is expected to be related to aneurysm instability and rupture status. However, the authors hypothesize that slow-flow artifacts mimic aneurysm wall enhancement. Therefore, in this phantom study they assess the effect of slow flow on wall-like enhancement by using different MR VWI techniques.
The authors developed an MR-compatible aneurysm phantom model, which was connected to a pump to enable pulsatile inflow conditions. For VWI, 3D turbo spin echo sequences—both with and without motion-sensitized driven equilibrium (MSDE) and delay alternating with nutation for tailored excitation (DANTE) preparation pulses—were performed using a 3-T MR scanner. VWI was acquired both before and after Gd contrast agent administration by using two different pulsatile inflow conditions (2.5 ml/sec peak flow at 77 and 48 beats per minute). The intraluminal signal intensity along the aneurysm wall was analyzed to assess the performance of slow-flow suppression.
The authors observed wall-like enhancement after contrast agent injection, especially in low pump rate settings. Preparation pulses, in particular the DANTE technique, improved the performance of slow-flow suppression.
Near-wall slow flow mimics wall enhancement in VWI protocols. Therefore, VWI should be carefully interpreted. Preparation pulses improve slow-flow suppression, and therefore the authors encourage further development and clinical implementation of these techniques.
Eva L. Leemans, Bart M. W. Cornelissen, Miran Said, René van den Berg, Cornelis H. Slump, Henk A. Marquering and Charles B. L. M. Majoie
Previous studies have shown a relation between growth and rupture of intracranial aneurysms. Additionally, several morphological characteristics are frequently measured to estimate rupture risk. Little is known about how the rupture risk is associated with morphological characteristic changes during growth. The aim of this study was to provide insights into how morphological characteristics, associated with rupture, change during an aneurysm’s growth.
The authors retrospectively identified patients with longitudinal MRA images of unruptured growing aneurysms. The MRA images had an in-plane resolution of 0.2–0.5 mm and a slice thickness of 0.2–0.75 mm. Therefore, growth was defined as an increase of at least 0.5 mm in two directions or 1 mm in one direction. Using the MRA images, the authors semiautomatically segmented the aneurysm and the perianeurysmal vasculature. Twelve morphological characteristics were automatically measured. These characteristics were related to size (diameter, height, width, neck diameter, volume, surface area, aspect ratio, height-width ratio, and bottleneck factor) and shape (ellipticity index, nonsphericity index, and undulation index) of the aneurysm. Morphological characteristics before and after growth were compared using the Wilcoxon signed-rank test.
The authors included 31 patients with 38 growing aneurysms. The aneurysms’ growth was detected after a mean of 218 weeks (range 23–567 weeks). A significant increase was seen in all size-related characteristics, and the bottleneck factor also significantly increased (from a median of 1.00 [IQR 0.85–1.04] to 1.03 [IQR 0.93–1.18]), while the ellipticity index decreased (from a median of 0.26 [IQR 0.25–0.28] to 0.25 [IQR 0.24–0.26]). The changes in size ratios and shape indices varied largely among patients. Larger aneurysms more often showed an increase in shape ratios.
Although aneurysm growth, size-related characteristics, bottleneck factor, and ellipticity index changed significantly during growth, most size ratios and shape indices showed inconsistent changes among aneurysms. This suggests that, for an accurate rupture prediction, morphological parameters need to be reassessed after growth.
Bart M. W. Cornelissen, Eva L. Leemans, Cornelis H. Slump, Henk A. Marquering, Charles B. L. M. Majoie and René van den Berg
For patients with subarachnoid hemorrhage (SAH) and multiple intracranial aneurysms, it is often challenging to identify the ruptured aneurysm. Some investigators have asserted that vessel wall imaging (VWI) can be used to identify the ruptured aneurysm since wall enhancement after contrast agent injection is presumably related to inflammation in unstable and ruptured aneurysms. The aim of this study was to determine whether additional factors contribute to aneurysm wall enhancement by assessing imaging data in a series of patients.
Patients with symptoms of SAH who subsequently underwent VWI in the period between January 2017 and September 2018 were eligible for study inclusion. Three-dimensional turbo spin-echo sequences with motion-sensitized driven-equilibrium preparation pulses were acquired using a 3-T MRI scanner to visualize the aneurysm wall. Identification of the ruptured aneurysm was based on aneurysm characteristics and hemorrhage distributions on MRI. Complementary imaging data (CT, DSA, MRI) were used to assess potential underlying enhancement mechanisms. Additionally, aneurysm luminal diameter measurements on MRA were compared with those on contrast-enhanced VWI to assess the intraluminal contribution to aneurysm enhancement.
Six patients with 14 aneurysms were included in this series. The mean aneurysm size was 5.8 mm (range 1.1–16.9 mm). A total of 10 aneurysms showed enhancement on VWI; 5 ruptured aneurysms showed enhancement, and 1 unruptured but symptomatic aneurysm showed enhancement on VWI and ruptured 1 day later. Four unruptured aneurysms showed enhancement. In 6 (60%) of the 10 enhanced aneurysms, intraluminal diameters appeared notably smaller (≥ 0.8 mm smaller) on contrast-enhanced VWI compared to their appearance on multiple overlapping thin slab acquisition time of flight (MOTSA-TOF) MRA and/or precontrast VWI, suggesting that enhancement was at least partially in the aneurysm lumen itself.
Several factors other than the hypothesized inflammatory response contribute to aneurysm wall enhancement. In 60% of the cases in this study, enhancement was at least partially caused by slow intraaneurysmal flow, leading to pseudo-enhancement of the aneurysm wall. Notwithstanding, there seems to be clinical value in differentiating ruptured from unruptured aneurysms using VWI, but the hypothesis that we image the inflammatory cell infiltration in the aneurysm wall is not yet confirmed.