Image-based Hemodynamics and Wall Enhancement in a Superior Basilar Aneurysm: Growth to Rupture

doi:10.21203/rs.3.rs-1615089/v1

Background: High-resolution magnetic resonance imaging (HR-MRI) could be used to evaluate the inflammatory process of tissue remodeling via aneurysm wall enhancement (AWE), however, due to the lack of longitudinal evidence, its relationship to the flow pattern has not been fully understood. In this study, HR-MRI and computational hemodynamics were synchronously analyzed on a longitudinal case, from growth to rupture, to reveal the biomechanical and pathological development of intracranial aneurysm (IA).

Methods: One patient with superior basilar aneurysm was strictly examined. The growing process and the rupture event of the IA was captured via longitudinal HR-MRI examinations. The signal intensity, thickness of enhancement region, and spatial growth of IA were quantified. In addition, computational fluidic analysis was applied on the patient-specific model at each time points. Precise voxel-based comparison was conducted among the morphological, hemodynamic and enhancement data.

Results: There was a significant difference in the flow pattern between enhancement and non-enhancement areas. The time-averaged wall shear stress was negatively correlated with the radial growth of IA (r=-0.413). Enhancement areas were found consistent to the presentations of low flow velocity. Peak signal intensity occurred in the area where displacement index or its rate were in positive values.

Conclusions: Based on this growth to rupture longitudinal study, the relationship between hemodynamic patterns to AWE features was confirmed. The rupture site of IA was likely to occur in the junction between the growing and the non-growing interface of the aneurysm wall.

Hemodynamics

aneurysm growth

rupture

aneurysm wall enhancement

Intracranial aneurysms (IAs) are lesions or injuries of the intracranial arterial wall, resulting in locally pathological dilatations^[1]. Rupture of IAs may lead to spontaneous subarachnoid hemorrhage, which was reported to be with high morbidity and mortality rate[2]. The prevalence of unruptured intracranial aneurysms in the general population is approximately 3%, which might be underestimated because most IAs are asymptomatic and the detection rate is continuously increasing due to the development of imaging technique[3–5]. In order to balance the risk of preventive interventions and rupture in follow-up periods, assessment of aneurysm growth and rupture risk is drawing increasing attention.

Previous retrospective studies indicated that aneurysm growth was associated with the increased rupture risk[6] and wall inflammation played a key role in IA formation, growth, and rupture[7]. Furthermore, in the context of other histological findings, the aneurysm wall which presents a higher inflammation degree will show a higher rupture risk[8, 9]. High-resolution magnetic resonance imaging (HR-MRI) is capable to provide distinguished visualization of the arterial wall, revealing a range of pathological conditions. Previous studies have suggested that intracranial aneurysm wall enhancement (AWE) could be used to assess inflammatory infiltration or vasculopathy process of the arterial wall and had the potential to be a surrogate marker to determine the rupture risk of intracranial aneurysms[9–12]. Additionally, aneurysm rupture was believed to be associated with endothelial inflammatory dysfunction resulted from an abnormal hemodynamic environment[13, 14]. Recent evidence suggested that computational fluid dynamics (CFD) was an effective tool to reveal hemodynamic characteristics of IA, such as wall shear stress (WSS) and oscillatory shears index (OSI), which were reported to relate to aneurysm rupture[15–18]. Previous studies found that AWE regions tend to have lower WSS and OSI compared with non-enhanced regions[19]. Similarly, another study found that AWE in different regions, such as body dome and neck, on the same aneurysm presented different hemodynamic states[20]. However, all of these studies lack of longitudinal follow-up evidence, to demonstrate the actual relationships between hemodynamics and AWE.

This study reported a rare case of a superior basilar aneurysm with twice HR-MRI examinations presenting the aneurysm growth and then rupture. We thoroughly investigated the flow-derived characteristics, importantly, the contrast enhancement presentation, including AWE signal intensity and thickness, and the spatial growth of the aneurysm were quantified. The enhancement and IA models were registered by reference to the aneurysm sac to achieve the voxel-based comparison analysis. In the current study, we aimed to detect typical indices prompting the growth or rupture of the aneurysm.

Patient

This study was approved by the Ethics Committee at Beijing Tiantan Hospital. A 31-year-old male patient presented with sudden posterior headache without any apparent cause. The first HR-MRI examination was performed and revealed a superior basilar aneurysm with Grade-1 of the aneurysmal wall enhancement. Considering the relatively high risk of endovascular treatment for this case, conservative treatment was applied. After seven months, the patient came for re-examination with progressive headache, and Grade-2 of AWE with obvious IA enlargement were found. Unfortunately, in one month, the aneurysm ruptured. All of the imaging examinations were performed via a 3.0-T MR scanner (Achieva TX, Philips, Netherlands) . The legal representatives of the participant gave their informed consent.

Reconstruction of Aneurysms and Enhancement Sections and Model co-registration

The patient-specific aneurysm models were reconstructed based on the TOF MRI images and the enhancement regions were extracted based on the T1-Vista sequence, via a semi-automatic image processing tool, MIMICS (Materialize, Leuven, Belgium). The lumen profiles of the aneurysm and the segmented enhancement regions were confirmed by two experienced neurointerventional experts. Aneurysm/enhancement models at the first and follow-up examinations, denoted as A-T₁/E-T₁ and A-T₂/E-T₂ models, were thus confirmed (Figure 1A). The longitudinal models were registried via the reference point system alignment method. Optimal fit alignment of two models was achieved by a three-dimensional transformation matrix shown in Figure 1B. In this matrix, A_ij, i, j=1,2,3 controls the rotation of the 3D model, [P_x P_y P_z]^Tis the perspective transformation matrix, [t_x t_y t_z] denotes the translation and S is the overall scale factor with a default value of 1. Furthermore, due to the various scanning resolution, medical images showing enhancement regions contain 6 slices and 34 slices for E-T₁ and E-T₂ model, respectively (Figure 1C and D).

Morphological Features and Growth Quantification

Imaging follow-ups facilitate morphological analysis on growing aneurysms. However, the hemodynamic and pathological mechanism that promotes aneurysm growth is still unclear. To precisely quantify the aneurysm growth by digital representation, two quantitative indices, Displacement Index (DI) and Area Stretch Ratio (ASR)[21], were calculated. DI represented the Eulerian distance between two aneurysm models in the direction of the normal vector at each voxel on A-T1 model. The ASR provided a more sophisticated descriptor of aneurysm growth compared to DI and the growth was considered as the stretching of the A-T₁ surface over time. This parameter was quantified as the ratio of the A-T₂ surface area to that at A-T₁, which was a function of the displacement between the A-T₁ and A-T₂ surfaces.

Hemodynamics Modeling

The reconstructed aneurysm geometries were meshed in ICEM CFD with tetrahedron elements in the core region surrounded by 5-layer prismatic elements to reinforce the grid resolution near the vessel wall. Hemodynamic computations were conducted on A-T₁ and A-T₂ models after 3D registration. The blood flow was assumed as laminar, incompressible and Newtonian flow with a constant viscosity of 0.0035 Pa.s and constant density of 1066 kg/m^-3. The property of arterial wall was set as rigid and non-slip boundary. The unstructured mesh was imported into ANSYS CFX 19.2 (ANSYS Inc. Canonsburg, PA, USA) to solve the flow governing Naviér-Strokes equation. This specific boundary condition was extracted from the software @neufuse which possesses the database of a 1D model of human vascular tree[22]. Computations were conducted for three cardiac cycles to guarantee the numerical stability and the results of last cardiac cycle were applied for further data analysis.

Signal Intensity Standardization of Enhancement

Jorge A. Roa et al. demonstrated three measurement methods of the signal intensity (SI) normalization and revealed that the SI value of aneurysm enhancement scandalized by pituitary stalk achieved higher sensitivity and specificity, and allowed enhancement measurements standardization in HR-MRI [23]. In the currently study, the SI of E-T₁ and E-T₂models were extracted and compared with the pituitary stalk to standardize the SI of enhancement area, which were defined in Equation 1, where SI-ave-pi denoted the average SI of pituitary stalk.

stanSI =SI-en / SI-ave-pi (1)

The E-T₁ and E-T₂ models were mapped with stanSI to obtain the enhanced 3D model with SI for subsequent visualizations.

Thickness and SI Quantification of Enhancement on Single Layer

To explore the correlation between hemodynamic and enhancement characteristics (Aim 1), i.e. SI and thickness, hemodynamic results on aneurysm lumen and enhancement features on each slice were extracted (40 slices). Furthermore, six new slices of enhancement in the post-registered E-T₂model were extracted aligned with the enhancement layers in the E-T₁model, which aims to investigate the effective markers for aneurysm local growth (Aim 2). Therefore, a total of 46 slices were enrolled for Aim 1 and only 6 slices were included for Aim 2 due to the limited layers in the E-T₁model.

To satisfy the analysis requirements of above two aims, the key procedure is the quantification of the thickness and SI of enhancement regions and the establishment of voxel-based match of hemodynamics and enhancement. Firstly, the 3D coordinates of enhancement region on slice 17 were selected to determine the origin of the local coordinate system because of its medial position. By using the principal component analysis (PCA) method, two largest principal components that were mutually orthogonal were calculated as the X/C₁-axis and Y/C₂-axis of the local coordinate system (Figure 2A). For each single slice, the localized origin O_(n) was determined as the mean value of the coordinates on the outline of the aneurysm lumen. Taking the positive Y-axis as the starting direction, the outline of aneurysm lumen was clockwise discretized into 200 intersection points with an interval of = /100. Hemodynamic information, i.e. time averaged wall shear stress (TAWSS), OSI, gradient oscillatory number (GON), aneurysm formation index at middle diastole (AFI^md), pressure at systole (P^s), at all points were extracted. Along with each direction, the enhancement thickness, maximum gray value and average gray value were also calculated.

Statistical Analysis

Significance and correlation test for all statistical data were conducted using SPSS (IBM, Armonk, New York, USA). Mann-Whitney test was performed to analyze the differences of hemodynamic variables between AWE patterns. P <0.05 was considered statistically significant. Shapiro-Wilk test was performed to verify whether the parameters conform to normal distribution. For nonnormally distributed parameters, Spearman correlation coefficient was performed to analyze the correlation between hemodynamic variables and AWE.

3.1 Quantification of Hemodynamics and Growth

Hemodynamic computation was performed on two aneurysm models and significant characteristics were plotted in Figure 3. The streamline traces were plotted in Figure 3(A) where the white arrows indicate the inflow direction and the variable range was limited to 0-0.1m/s in order to clearly reflect the velocity gradient due to the extremely low velocity inside aneurysm. Two stages of the flow environment were compared and it showed that the flow inside the A-T₂aneurysm presented more spiral patterns with slower flow close to the inner wall. Figure 3B displays the WSS distribution at systole and the color bar was restricted in the range of 0 to 0.2 Pa similarly. It was explicitly shown that the area of low WSS enlarged from the middle to top region and the high OSI (>0.2) distributed at a similar location (Figure 3C). Aneurysm formation indicator (AFI) and gradient oscillatory number (GON) are two WSS- derivative parameters. AFI investigates the risk derived from the strength of eddies that contribute to the formation of stagnation zone as a result of formation of aneurysm GON represents the fluctuation of tension/compression forces acting on endothelial cells which were also invented for exploring the aneurysm formation risk. Figure 3D-E displays the increased areas of low AFI and high GON focusing on the aneurysm roof, reflecting the highly disturbed flow. All unfavorable hemodynamic features are located closely or partially overlapped, i.e. aneurysm roof, which might be the reasons leading to the ultimate rupture. In terms of the growth quantification, here we employed the DI and ASR to depict the enlargement extent and plotted in Figure 3F. Interestingly, locations with these unfavorable hemodynamic characteristics are in accordance with the junction between low DI and high DI regions (arrow).

3.2 Slice-based Enhancement and Hemodynamic characteristics

The enhancement features of the inflammation were extracted and one typical slice of the T1 model was shown in Fig 4A. The enhancement thickness value was extracted in the clockwise direction (arrows) which were visualized in Figure 4B. Both the enhancement features of AWE and the hemodynamics parameters of the lumen were extracted from all layers. The relationship among those parameters was explored and shown in Table 1 and Table 2.

Table 1. Significance Analysis of Significant Hemodynamic Indices and Enhancement

	Mann-Whitney test
Variable	TAWSS	OSI	Pressure	AFI	GON	RRT
E-T₁model	0.000	0.979	0.010	0.041	0.043	0.000
E-T₂model	0.000	0.000	0.000	0.000	0.000	0.000
All slices	0.000	0.000	0.000	0.000	0.000	0.000

Values are presented as mean±SD unless otherwise indicated.

*Mann–Whitney U tests were used to calculate P- values due to non- normally distributed data.

Table 2. Correlation between Hemodynamic Characteristics and Quantitative Evaluations of Enhancement

	Spearman test
Variable	TAWSS	OSI	Pressure	AFI	GON	RRT
Thickness	-0.187	0.305	0.198	-0.248	0.269	0.290
stanSI_max	-0.415	0.415	0.232	-0.307	0.326	0.528
stanSI_mean	-0.413	0.422	0.236	-0.311	0.333	0.516

Note:——r: correlation coefficient

Table 1 revealed the significant variation in hemodynamic characteristics caused by the presence of AWE under the Mann-Whitney test (p<0.05). Compared with the E-T2 model, the E-T1 model presented a lower significance value (E-T1 model: AFI: p=0.041, GON: p=0.043, OSIfield=0.979; E-T2 model: AFI: p=0.000, GON: p=0.000, OSIfield=0.000). This situation may resulted from the long-term impact of the abnormal hemodynamic status, which may aggravate the abnormal expression of inflammation. Meanwhile, the worse contrast effect of the E-T1 model image sequence may also contribute to this result.

The correlation between the hemodynamic characteristics and the enhancement quantitative parameters were detected (Table 2). OSI was positively correlated with stanSI_mean and the thickness (r=0.305, r=0.415). RRT showed a high positive correlation with stanSI_max (r=0.528), which indicated the possibility of thrombosis in AWE. There was a certain negative correlation between TAWSS with stanSI_mean. Totally speaking, the thickness showed less sensitive than the stanSImax.

3.3 Correlation between Growth and Enhancement

The DI on the aneurysm lumen, the enhancement SI of the inflammation, and the flow velocity in the sac were all plotted in Figure 5. The intravascular velocity was limited in the range of 0 ~ 0.3m/s for showing flow patterns. Enhancement areas were found consistent to the presentations of low flow velocity. The peak of SI frequently occurred in the area where DI or DI_rate always displayed positive values. A hypothesis was proposed that the aneurysm sac corresponding to the inflammation area has obvious growth changes. To verify our observations, the change rate of DI was quantified in Figure 6.

The extracted data was represented in the direction displayed in Fig 4. DI_rate is defined as the change rate of DI and SI_refwas the normalized SI. These two parameters were plotted in different ways. Totally speaking, DI or DI_rate always displayed positive values in the enhancement area. The results pointed out the hypothesis that enhancement area can be associated with the IAs growth.

In this study, HR-MRI was used to visualize aneurysm wall inflammation, and CFD was used to calculate hemodynamic characteristics of the aneurysm, the combination of HR-MRI and CFD was used to investigate the potential mechanisms associated with hemodynamics and aneurysmal wall inflammation in aneurysm growth and rupture. Our retrospective study supports the notion that there are correlations between aneurysm rupture and AWE, in which abnormal hemodynamic conditions in the AWE region may suggest wall degeneration. Our research provided new insights into IA instability and rupture. To the best of our knowledge, this is the first study in exploring the relationship between aberrant hemodynamic features and enhancement characteristics in a growth model.

4.1 Association between hemodynamic characteristics and AWE

Previous studies have found that AWE regions tend to have abnormal hemodynamics compared with non-AWE regions, which may result in IAs’ formation, growth, and rupture[7, 13, 14]. Low WSS and low flow usually occupied an important position in the region with the characteristic of atherosclerotic and hyperplastic which might influence the progression of the aneurysm wall[9, 12]. In this study, the difference in hemodynamics between the AWE region and the non-AWE region was also compared. TAWSS was significantly lower in AWE regions in our case. The low flow environment may potentially lead to low TAWSS, which can damage the wall endothelium. These results were consistent with previous studies that low WSS may increase vascular permeability[24], which may lead to the loss of endothelial cells and the differential expression of inflammatory cytokines in AWE regions[9, 25]. In addition, there was a positive correlation between the thickness and stanSI _mean of the AWE regions with RRT, which may result from leukocyte transmigration into the wall which will increase blood residence time and cause aneurysm growth[9, 26]. Therefore, we proposed the degree of wall inflammation is related to the exposure time under disordered hemodynamic conditions in IAs. Namely, the longer the exposure to disordered hemodynamics, the greater wall inflammation will present, thus cause aneurysm growth and rupture.

4.2 Potential mechanisms associated with hemodynamics and AWE in a growth model

Previous hemodynamic studies of aneurysm growth have proved that high and low WSS may drive different mechanobiological pathways of the aneurysm. Low WSS and high OSI may trigger inflammatory cells, leading to the growth and rupture of large atherosclerotic aneurysms, while high WSS combined with positive WSSG may trigger mural cells leading to the growth and rupture of small or secondary bubble aneurysm[26]. In our study, the enhancement area often corresponded to the area with low flow velocity and TAWSS when we compared hemodynamics in different layers under the same model. It is reported that in the regions with low WSS, vascular permeability may be increased which corresponds to local AWE[19]. Our research found that the stanSI_max frequently occurred in the transitional area where the low and high values of DI connected. Moreover, low flow area was often found to be associated with a high value of DI which corresponds to obvious growth (Fig. 5). To confirm our findings, the scatter points were generated by the PCA method and shown in Fig. 6. In the enhancement area, DI or DI_rate always displayed as positive and DI showed a positive and increasing trend. In conclusion, in a growth model, low WSS and high signal intensity of AWE may promote aneurysm growth.

Kataoka et al. found that thick intima-like walls are mostly unruptured, while very thin and degenerated walls with hyaline deposits are mostly ruptured[27]. The aneurysm wall thickness will be different in the area where the aneurysmal sac presented a greater variation in growth, similarly in the organizational strength of the aneurysm wall. In our study, the high signal intensity of AWE frequently occurred at the region with the high value of DI or DI_rate, which may correspond to the rupture site of the aneurysm. Therefore, our study provided a new perspective that the junction between growing and non-growing of the aneurysm wall might be the rupture site that corresponds with the junction on the strongest and weakest tissue, and the AWE could be found in this area. Unfortunately, pathology specimens were not available as the patient was transferred to the local hospital for treatment after follow-up examination. Future histological studies can be supplemented to verify our hypothesis.

4.3 Method innovation

In our study, how to quantify the enhancement of IAs and accurately match the follow-up data is the key point of our technology. Our registration is based on the reference point system alignment method, which achieved the best fit alignment of the two models through a three-dimensional conversion matrix. Optimal fit alignment of two models was achieved by a three-dimensional transformation matrix, in which we evaluated the rotation and translation changes of the model. Meanwhile, visualizing and quantifying the enhancement region in sequences will contribute to our study. We standardized the SI of aneurysm enhancement based on the pituitary stalk for higher sensitivity and specificity in HR-MRI[23].

In summary, our retrospective study provides strong support to the correlation between aneurysm growth rupture and AWE, in which abnormal hemodynamics conditions in the AWE region may suggest wall degeneration. Our findings also highlight the potential role of HR-MRI in the prediction of aneurysm rupture and suggest that AWE should be considered when establishing the growth model of UIAs. In addition, We also intend to rich assessment models with morphology, hemodynamics, and aneurysm wall characteristics in subsequent studies to further improve the accuracy of clinical aneurysm rupture prediction. It is also necessary for us to conduct prospective studies with a great number of cases to confirm our findings that can be used in a clinical tool for treatment decisions.

4.4 Strengths and Limitations

This study has some limitations. First of all, our sample is based on one single superior basilar aneurysm, and our research is limited to six layers of comparative study between the follow-up data due to the limitation of the MR images at the first examination. Our retrospective design and the small sample size may affect the data collection and statistical analysis producing deviations. Secondly, we made some approximations in CFD studies. The blood flow was assumed as Newtonian, the blood vessel wall as rigid, and physiological pulsating blood flow conditions were used from the healthy group, all of these may lead to small inaccuracy error in the calculation of hemodynamic parameters. Third, there may be image artifacts in T1-Vista sequence caused by slow-moving blood, which makes it difficult to confirm the AWE area in MR images and have an effect on quantifying the enhancement IAs.

There was a significant difference in AFI, GON and OSI between enhancement and non-enhancement areas. The thickness of enhancement region is less sensitive than the stanSImax in our study. There was a moderate correlation between high OSI, low TAWSS and AWE and the enhancement areas were found to correspond to Low flow velocity areas. Abnormal flow pattern could be used to evaluate the expression intensity of inflammatory response in tumor wall. Meanwhile, DI or DI_rate always displayed positive values in the enhancement area. The intensity of inflammatory infiltration in aneurysm wall is related to abnormal blood flow pattern in aneurysm sac, aneurysm growth and rupture. Our study provided a new perspective that the rupture site might occurred in the junction between growing and non-growing area of aneurysm wall.

The research leading to these results received funding from the Beijing Natural Science Foundation under Grant Agreement Z190014 and the National Natural Science Foundation of China under Grant Agreement 82001938, 81970404.

The authors have no competing interests to declare that are relevant to the content of this article.

Patient gave informed consent priorto their inclusion in the study.

Conflict of interest

The authors report no conflicts of interests.

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GraphicalAbstract.png

Image-based Hemodynamics and Wall Enhancement in a Superior Basilar Aneurysm: Growth to Rupture

Status:

Version 1

Abstract

Figures

Introduction

Methods

Results

Discussion

4.1 Association between hemodynamic characteristics and AWE

4.2 Potential mechanisms associated with hemodynamics and AWE in a growth model

4.3 Method innovation

4.4 Strengths and Limitations

Conclusion

Statements And Declarations

References

Additional Declarations

Supplementary Files

Status:

Version 1