scholarly journals Wall enhancement segmentation for intracranial aneurysm

2020 ◽  
Vol 6 (1) ◽  
Author(s):  
Annika Niemann ◽  
Naomi Larsen ◽  
Bernhard Preim ◽  
Sylvia Saalfeld
Keyword(s):  
Intracranial Aneurysm ◽  
Intracranial Aneurysms ◽  
Automatic Segmentation ◽  
Black Blood ◽  
Manual Segmentation ◽  
Lower Intensity ◽  
Black Blood Mri

AbstractWe present a tool for automatic segmentation of wall enhancement of intracranial aneurysms in black blood MRI. The results of the automatic segmentation with several configurations is compared to manual expert segmentations. While the manual segmentation includes some voxels of lower intensity not present in the automatic segmentation, overall the volume of the automatic segmentation is higher.

scholarly journals Pseudo‐Enhancement in Intracranial Aneurysms on Black‐Blood MRI : Effects of Flow Rate, Spatial Resolution, and Additional Flow Suppression

2021 ◽  
Author(s):  
Mariya S. Pravdivtseva ◽  
Franziska Gaidzik ◽  
Philipp Berg ◽  
Carson Hoffman ◽  
Leonardo A. Rivera‐Rivera ◽  
...  
Keyword(s):  
Spatial Resolution ◽  
Flow Rate ◽  
Intracranial Aneurysms ◽  
Black Blood ◽  
Black Blood Mri

scholarly journals Associations between haemodynamics and wall enhancement of intracranial aneurysm

2021 ◽  
pp. svn-2020-000636
Author(s):  
Miaoqi Zhang ◽  
Fei Peng ◽  
Xin Tong ◽  
Xin Feng ◽  
Yunduo Li ◽  
...  
Keyword(s):  
Blood Flow ◽  
High Resolution ◽  
Ordinal Regression ◽  
Parent Artery ◽  
Black Blood ◽  
4D Flow Mri ◽  
4D Flow ◽  
Unruptured Intracranial Aneurysms ◽  
Black Blood Mri ◽  
Flow Mri

Background and purposePrevious studies have reported about inflammation processes (IPs) that play important roles in aneurysm formation and rupture, which could be driven by blood flow. IPs can be identified using aneurysmal wall enhancement (AWE) on high-resolution black-blood MRI (BB-MRI) and blood flow haemodynamics can be demonstrated by four-dimensional-flow MRI (4D-flow MRI). Thus, this study investigated the associations between AWE and haemodynamics in unruptured intracranial aneurysms (IA) by combining 4D-flow MRI and high-resolution BB-MRI.Materials and methodsBetween April 2014 and October 2017, 48 patients with 49 unruptured IA who underwent both 4D-flow MRI and high-resolution BB-MRI were retrospectively included in this study. The haemodynamic parameters demonstrated using 4D-flow MRI were compared between different AWE patterns using the Kruskal-Wallis test and ordinal regression.ResultsThe results of Kruskal-Wallis test showed that the average wall shear stress in the IA (WSSavg-IA), maximum through-plane velocity in the adjacent parent artery, inflow jet patterns and the average vorticity in IA (vorticityavg-IA) were significantly associated with the AWE patterns. Ordinal regression analysis identified WSSavg-IA (p=0.002) and vorticityavg-IA (p=0.033) as independent predictors of AWE patterns.ConclusionA low WSS and low average vorticity were independently associated with a high AWE grade for IAs larger than 4 mm. Therefore, WSS and average vorticity could predict AWE and circumferential AWE.

scholarly journals High-Resolution Black-Blood MRI of the Carotid Vessel Wall Using Phased-Array Coils at 1.5 and 3 Tesla1

2005 ◽  
Vol 12 (12) ◽  
pp. 1521-1526 ◽  
Author(s):  
SeshaSailaja Anumula ◽  
Hee Kwon Song ◽  
Alexander C. Wright ◽  
Felix W. Wehrli
Keyword(s):  
High Resolution ◽  
Vessel Wall ◽  
Phased Array ◽  
Black Blood ◽  
Black Blood Mri ◽  
Carotid Vessel Wall ◽  
Phased Array Coils ◽  
Array Coils ◽  
Carotid Vessel

Abstract W MP47: Roles of Macrophage PPARγ on Intracranial Aneurysmal Rupture

Stroke ◽  
2015 ◽  
Vol 46 (suppl_1) ◽  
Author(s):  
Masaaki Korai ◽  
Kenji Shimada ◽  
Hajime Furukawa ◽  
Kosuke Wada ◽  
Yuan Wei ◽  
...  
Keyword(s):  
Intracranial Aneurysm ◽  
Inflammatory Cytokines ◽  
Intracranial Aneurysms ◽  
Peroxisome Proliferator ◽  
Protective Effects ◽  
Knock Out ◽  
Aneurysmal Rupture ◽  
Clodronate Liposome ◽  
Pparγ Agonist ◽  
Knock Out Mice

Background and Purpose: Peroxisome proliferator-activated receptor gamma (PPARγ) plays a role in regulating not only lipid and glucose metabolism but also atherosclerosis and inflammation which are associated with intracranial aneurysmal rupture. It has been suggested that PPARγ is present in various kinds of cell types including macrophages which we reported to contribute to intracranial aneurysm formation. In addition, macrophage PPARγ regulates inflammatory cytokines negatively. Therefore we hypothesized that macrophage PPARγ is protective against intracranial aneurysmal rupture. We tested this hypothesis by using our own established mouse model of intracranial aneurysm. Methods: Intracranial aneurysms were induced in male mice using a combination of a single injection of elastase into the cerebrospinal fluid and the deoxycorticosterone acetate (DOCA) salt hypertension. Six days after aneurysm induction, we started 2-week treatment with vehicle or PPARγ agonist (pioglitazone:PGZ) or clodronate liposome. PPARγ antagonist (GW9662) was added to PGZ treatment. We induced aneurysms to macrophage-specific PPARγ knockout mice and treated them with vehicle or PGZ with the same protocol mentioned above. Aneurysmal rupture was detected by neurological symptoms and confirmed by the presence of intracranial aneurysms with subarachnoid hemorrhage. Results: Both PGZ and depletion of macrophage by clodronate liposome reduced the incidence of ruptured aneurysms and rupture rate. PGZ treatment decreased the inflammatory cytokines that were increased in cerebral arteries of mice with aneurysm induction compared to mice without aneurysm induction. To examine whether the macrophage PPARγ is associated with intracranial aneurysmal rupture, we administered PGZ to macrophage-specific PPARγ knock out mice. PGZ did not have protective effect against aneurysmal rupture in macrophage-specific PPARγ knock out mice although it exerted protective effects in wild type mice. Conclusion: PPARγ activation is protective against intracranial aneurysmal rupture by suppressing inflammatory cytokines and macrophage PPARγ is associated with this protective effects.

Abstract 147: Role of Nicotine in the Development of Intracranial Aneurysm Rupture

Stroke ◽  
2017 ◽  
Vol 48 (suppl_1) ◽  
Author(s):  
Yoshinobu Kamio ◽  
Hajime Furukawa ◽  
Kimihiko Yokosuka ◽  
Masaaki Korai ◽  
Kazuha Mitsui ◽  
...  
Keyword(s):  
Intracranial Aneurysm ◽  
Tobacco Smoke ◽  
Intracranial Aneurysms ◽  
Aneurysm Rupture ◽  
Alpha7 Nicotinic Acetylcholine Receptor ◽  
Acetate Salt ◽  
Nicotine Receptors ◽  
Aneurysm Wall ◽  
Salt Hypertension

Background: Nicotine is one of main chemicals of tobacco smoke and promotes atherosclerosis and stroke. Tobacco smoke is considered an independent risk factor for intracranial aneurysm formation, growth, and rupture. There are mainly 5 subtypes of nicotine receptors. Roles of alpha7 nicotinic acetylcholine receptor (α7nAChR) in inflammation and vascular remodeling are diverse and context-dependent. Notably, endothelial α7nAChR is considered to mediate nicotine-induced inflammation. Activation of endothelial α7nAChR by nicotine may promote aneurysm rupture by increasing the aneurysm wall inflammation. Using a mouse model of intracranial aneurysm, we examined effects of nicotine in aneurysm rupture. Moreover we investigated potential roles of α7nAChR stimulation by nicotine in the pathophysiology of intracranial aneurysms. Methods: Intracranial aneurysms were induced by a combination of elastase injection into the cerebrospinal fluid and deoxycorticosteron acetate-salt (DOCA-salt) hypertension in male mice. Mice were treated with (1) nicotine (5 mg/kg/day, n=25); (2) saline sc (n=22) for three weeks after aneurysm induction. To investigate the effect of α7nAChR, mice were treated with (1) saline sc + saline ip (n=11); (2) saline sc + α7nAChR antagonist (Methyllycaconitine, MLA 5mg/kg/day) ip (n=13); (3) nicotine (5 mg/kg/day, sc, 28 days) + saline ip (n=18); (4) nicotine sc + MLA ip (n=18). Results: Nicotine alone significantly increased aneurysmal rupture compared with saline treatment (89% vs 46%, p=0.009). While α7nAChR antagonist did not affect the incidence of aneurysm or rupture rates, the α7nAChR antagonist significantly reduced the deleterious effect of nicotine as indicated by the reduction of the rupture rates (41% vs 100%: nicotine sc + MLA ip group vs nicotine sc + saline ip group, p=0.027). Conclusion: Our data indicate the promotion of aneurysm rupture by nicotine may be mediated by its stimulation of alpha7nAChR.

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