Figure 4
From: Modeling lamellar disruption within the aortic wall using a particle-based approach
Stress concentrations near a pool of cells undergoing apoptosis and replacement with GAGs. (a) Pools of intra-lamellar particles defined by four angular extents (2°, 4°, 8°, and 20°) are assumed to lose contractility and matrix stiffness (step I), be replaced with GAGs having reduced tensile stiffness (step II), and gain Gibbs-Donnan type swelling (step III; see red arrows for sequence), thus changing the maximum circumferential stress in the (b) nearest elastic lamella, (c) nearest intra-lamellar space, (d) second nearest intra-lamellar space, and (e) second nearest elastic lamella (all shown in (a)). The horizontal dashed lines show the baseline stress before disease. Loss of contractility and reduction of stiffness (steps I and II) create a stress concentration in the nearby particles that increases with distending pressure (left-to-right) but decreases with the size of the pool. GAG swelling (step III) increases the stress in the nearest elastic lamella while not affecting distant locations. Once the nearest elastic lamellae rupture (step IV, lamellar disruption), stress in the intra-lamellar regions increases dramatically (c,d), suggesting a greater chance of further SMC damage in these areas. Also note the jump in stress in the second nearest elastic lamella following disruption of the nearest elastic lamella (e), with damage within an intra-lamellar space propagating radially. Overall, these results suggest a feedback loop between cell apoptosis and lamellar disruption, which, independent of the initiating event, can lead to catastrophic damage within the wall (shown in (a)).
