Comprehensive morphomechanical analysis of brain aneurysms.

OBJECTIVE: Brain aneurysms comprise different compartments that undergo unique biological processes. A detailed multimodal analysis incorporating 3D aneurysm wall enhancement (AWE), computational fluid dynamics (CFD), and finite element analysis (FEA) data can provide insights into the aneurysm wall biology. METHODS: Unruptured aneurysms were prospectively imaged with 7 T high-resolution MRI (HR-MRI). 3D AWE color maps of the entire aneurysm wall were generated and co-registered with contour plots of morphomechanical parameters derived from CFD and FEA. A multimodal analysis of the entire aneurysm was performed using 3D circumferential AWE (3D-CAWE), wall tension (WT), time-averaged wall shear stress (TAWSS), wall shear stress gradient (WSSG), and oscillatory shear index (OSI). A detailed compartmental analysis of each aneurysm's dome, bleb, and neck was also performed. RESULTS: Twenty-six aneurysms were analyzed. 3D-CAWE + aneurysms had higher WT (p = 0.03) and higher TAWSS (p = 0.045) than 3D-CAWE- aneurysms. WT, TAWSS, and WSSG were lower in areas of focal AWE in the aneurysm dome compared to the neck (p = 0.009, p = 0.049, and p = 0.040, respectively), whereas OSI was higher in areas of focal AWE compared to the neck (p = 0.020). When compared to areas of no AWE of the aneurysm sac (AWE = 0.92 vs. 0.49, p = 0.001), blebs exhibited lower WT (1.6 vs. 2.45, p = 0.010), lower TAWSS (2.6 vs. 6.34), lower OSI (0.0007 vs. 0.0010), and lower WSSG (2900 vs. 5306). Fusiform aneurysms had a higher 3D-CAWE and WT than saccular aneurysms (p = 0.046 and p = 0.003, respectively). CONCLUSIONS: Areas of focal high AWE in the sac and blebs are associated with low wall tension, low wall shear stress, and low flow conditions (TAWSS and WSSG). Conversely, the neck had average AWE, high wall tension, high wall shear stress, and high flow conditions. The aneurysm dome and the aneurysm neck have different morphomechanical environments, with increased mechanical load at the neck.

Analysis of Cerebral Aneurysm Wall Tension and Enhancement Using Finite Element Analysis and High-Resolution Vessel Wall Imaging.

Biomechanical computational simulation of intracranial aneurysms has become a promising method for predicting features of instability leading to aneurysm growth and rupture. Hemodynamic analysis of aneurysm behavior has helped investigate the complex relationship between features of aneurysm shape, morphology, flow patterns, and the proliferation or degradation of the aneurysm wall. Finite element analysis paired with high-resolution vessel wall imaging can provide more insight into how exactly aneurysm morphology relates to wall behavior, and whether wall enhancement can describe this phenomenon. In a retrospective analysis of 23 unruptured aneurysms, finite element analysis was conducted using an isotropic, homogenous third order polynomial material model. Aneurysm wall enhancement was quantified on 2D multiplanar views, with 14 aneurysms classified as enhancing (CRstalk≥0.6) and nine classified as non-enhancing. Enhancing aneurysms had a significantly higher 95th percentile wall tension (µ = 0.77 N/cm) compared to non-enhancing aneurysms (µ = 0.42 N/cm, p < 0.001). Wall enhancement remained a significant predictor of wall tension while accounting for the effects of aneurysm size (p = 0.046). In a qualitative comparison, low wall tension areas concentrated around aneurysm blebs. Aneurysms with irregular morphologies may show increased areas of low wall tension. The biological implications of finite element analysis in intracranial aneurysms are still unclear but may provide further insights into the complex process of bleb formation and aneurysm rupture.

Does elevated wall tension cause aortic aneurysm rupture? Investigation using a subject-specific heterogeneous model.

OBJECTIVE: To investigate whether peak wall tension in abdominal aortic aneurysm occurs at the site of rupture to test for a causative relationship. METHODS: Four ruptured and nine unruptured AAA were harvested whole from cadavers, followed by regional measurements of wall thickness, elastic parameters and failure tension. Finite element models were developed with subject-specific load-free AAA morphology and heterogeneous properties interpolated using a geodesic distance weighted approach from the measurements. The wall tension under uniform pressure and tension to failure tension ratio as an index of susceptibility to rupture were computed. As a secondary aim, the peak wall tension using this heterogeneous model approach was compared to the traditional homogeneous model approach in order to evaluate the reliability of the latter. RESULTS: The average peak wall tension in the ruptured group was 43% higher than in the unruptured group without statistical significance even though it was 54% larger in diameter. The site of peak wall tension was in the vicinity of the site of rupture in two ruptured AAA. The peak tension did not breach failure tension at the rupture site in any of the AAA. The traditional population-wide homogeneous model approach overestimated peak wall tension by just 3% compared to the subject-specific heterogeneous model approach. CONCLUSION: We failed to find adequate evidence of a causative relationship between peak wall tension and AAA rupture. The findings are not conclusive owing to study limitations such as ignoring intraluminal thrombus, sparse distribution of specimens procured and small study population.

Extracardiac Fontan operation after late bidirectional Glenn shunt.

The outcomes of 33 consecutive extracardiac Fontan operations performed between 1999 and 2008 in patients who mostly had initial Glenn shunts beyond infancy were reviewed. Preoperatively, the median oxygen saturation was 76.2% and mean pulmonary artery pressure was 10.5 mm Hg. The median age was 4.1 years at Glenn shunt procedure and 10 years at Fontan operation. The duration of chest tube drainage was longer in these patients than in series where Glenn shunts were created at a younger age. All patients received warfarin for 1 year, then warfarin and/or aspirin. At follow-up (median, 14 months), there was no significant ventricular dysfunction. Median oxygen saturation at the last follow-up was 92%. All patients in sinus rhythm preoperatively continued in this status. There was no Fontan failure or mortality. All patients were in New York Heart Association class I or II, although objective cardiopulmonary exercise evaluation in 8 patients showed impaired exercise tolerance. Despite a trend towards prolonged pleural effusion, there was no adverse outcome in the short or intermediate term. Long-term follow-up is required to see whether delayed creation of a Glenn shunt is associated with late disadvantages.