Article Figures & Data
Figures
- Fig 1.
Tissue samples were harvested after aneurysm clipping by cutting through the aneurysm dome distal to the clip, as demonstrated in A (black line represents the estimated site of cut). B, The tissue samples obtained varied significantly in size (from small, approximately 2 × 1 mm tissue samples to half domes with a >10-mm radius). In addition to variation in size, many of the aneurysm samples had local variation in the appearance of the wall (B) with translucent areas (asterisk) and thicker wall regions (hash tag). C, In histology, endothelium (CD31+ luminal cells with endothelial cells morphology) was present in only 3/10 of the studied aneurysm walls. D, In 8/20 aneurysms, the luminal surface was instead covered by thrombus, and in 7/20 aneurysms, some degree of thrombus organization was observed (hematoxylin-eosin staining). E, Loss of endothelium and organizing luminal thrombosis were associated with inflammatory cell infiltration (CD45+) in the aneurysm wall. F, Many of the inflammatory cells were macrophages (CD68+). Immunostaining protocol for CD68 is described by Ollikainen et al.17 Scale bars represent a 50-μm scale. Negative control for immunostaining is given for CD45 staining (Neg). The black arrows indicate positive cells.
- Fig 2.
A, Infiltration of inflammatory cells (CD45+) associated with rupture and high mean wall shear stress. B, WSS grouping is as follows: mean WSS of < 4.5 dyne/cm2 = low; 4.5 < mean WSS < 18 dyne/cm2 = mid; mean WSS > 18 dyne/cm2 = high. Bars display means, and error bars, standard error of mean.
- Fig 3.
A–F, Three aneurysms from the high WSS group with substantial wall inflammation. A–C, CD45 immunostaining and inflammatory cells in brown along with 3 aneurysms from the low WSS group (G–L) with little wall inflammation (J–L, negative CD45 immunostaining).
- Fig 4.
Flow conditions in the 6 sample aneurysms (Fig 3) with high or no inflammation in the wall. The visualizations show the following: the inflow jet at peak systole (A–C, J–L), the flow pattern at peak systole (D–F, M–O), and vortex core lines at 3 instances during the cardiac cycle (G–I, P–R), to illustrate both the complexity of the flow pattern and its change during the cycle (instability). An aneurysm with inflammation (upper panel) had a strong inflow jet impacting the aneurysm dome and producing complex (but somewhat stable) flow structures and associated WSS distributions with regions of high WSS and regions of low WSS near the outflow. In contrast, aneurysms with no inflammation had more diffuse inflows entering the aneurysms at lower velocity and diffusing into a simpler but more variable (unstable) flow pattern, with associated WSS distribution characterized by a fairly uniformly low WSS.
Tables
Hemodynamic Variable Wall Type A B C P Values ICI 2.24 (1.92–2.56) 0.62 (0.11–2.91) 0.36 (0.22–1.67) pAB = .119, pAC = .04,b pBC = .334 Q 1.71 (1.22–2.19) 0.67 (0.52–2.32) 0.52 (0.31–0.95) pAB = .081, pAC = .041,b pBC = .291 Corelen 5.56 (4.31–6.81) 1.48 (0.00–3.11) 0.46 (0.03–4.80) pAB = .021,b pAC = .088, pBC = .476 Podent 0.55 (0.37–0.74) 0.24 (0.13–0.54) 0.19 (0.13–0.44) pAB = .034,b pAC = .088, pBC = .334 OSImax 0.47 (0.46–0.49) 0.36 (0.26–0.46) 0.28 (0.10–0.44) pAB = .034,b pAC = .041,b pBC = .213 OSI 0.044 (0.03–0.05) 0.02 (0.01–0.03) 0.01 (0.00–0.03) pAB = .021,b pAC = .041,b pBC = .427 Note:—ICI indicates inflow concentration index; Q, inflow rate into the aneurysm; corelen, vortex core line length, a measure of flow complexity; podent, proper orthogonal decomposition entropy, a measure of flow instability.
↵a Median and range are given for the hemodynamic variables in each wall type group, and corresponding P values for comparisons between groups are given. pAB = P value (A vs B), pAC = P value (A vs C), pBC = P value (B vs C). Group A is defined by an intact-looking wall with linearly organized smooth muscle cells and intact endothelium; group B, by smooth muscle cell hyperplasia; and group C, by loss of smooth muscle cells and endothelial cells complemented by degeneration of the extracellular matrix and luminal thrombosis.
↵b Significant.
- Table 2:
Association of damage to the sIA wall endothelium (assessed through presence of CD31+ luminal cells with endothelial cell morphology) with wall inflammation (CD45+ cells), hemodynamics, and geometry of the sIAa
Variables Condition of the Endothelium P Value Intact Damaged Histology CD45+ cells 13 (7–8) 30 (12–279) .034b Hemodynamics VO 41.2 (38.9–72.3) 191.8 (47.3–317.8) .034b VD 23.2 (15.9–45.6) 291.1 (35.0–1027.6) .020b SR 28.2 (27.7–51.3) 129.1 (41.5–231.9) .034b OSImax 0.30 (0.04–0.41) 0.18 (0.01–0.47) .034b Geometry Size 15 mm (10–21 mm) 7 mm (4–12 mm) .020b Nsize 9 mm (7–13 mm) 5 mm (4–9 mm) .020b UI 0.13 (0.04–0.13) 0.25 (0.10–0.35) .034b EI 0.24 (0.24–0.24) 0.26 (0.25–0.30) .011b
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