Figure 1:

Figure 1a: The arterial geometry is approximated as a nonlinear elastic cylinder with unloaded radius R and thickness H (left) which is pressurized and axially pre-stretched to mimic in vivo conditions (right). Figure 1b: Diameters, internal pressures and constituent stretches at different phases of our model of vasospasm. In the pre-vasospasm phase (1), arterial diameter at systolic blood pressure is 2.9mm, VSMC stretch equals its attachment stretch. In the early phase of vasospasm (2), the constriction is chemically driven and VSMCs haven’t remodelled yet. Following remodelling (3), VSMCs have returned to their attachment stretch while elastin hasn’t remodelled so its stretch hasn’t changed from phase (2). Finally, if a stent provides enough pressure to exceed a critical value, a dilatation threshold (4) is reached at which VSMCs are brought to mechanical failure and incapacity to bear the pressure load. This signifies successful treatment of CVS.