Effects of stent design and atherosclerotic plaque composition on arterial wall biomechanics

Abstract

Purpose: To examine the solid mechanical effects of varying stent design and atherosclerotic plaque stiffness on the biomechanical environment induced in a diseased artery wall model.

Methods: Computational modeling techniques were employed to investigate the final radius of the lumen and artery wall stresses after stent implantation. Two stent designs were studied (one stiff and one less stiff). The stenotic artery was modeled as an axisymmetrical diseased vessel with a 20% stenosis by diameter. The material properties of the diseased tissue in the artery models varied. Atherosclerotic plaques half as stiff (0.5x), of equal stiffness (1.0x), or twice as stiff (2.0x) as the artery wall were investigated.

Results: Final lumen radius was dependent on stent design, and the stiffer stent deformed the artery to an approximately 10% greater radius than the more compliant design. Alternatively, circumferential stress levels were dependent on both stent design and plaque material properties. Overall, the stiffer stent subjected the artery wall to much higher stress values than the more compliant design, with differences in peak values of 0.50, 0.31, and 0.09 MPa for the 2.0x, 1.0x, and 0.5x stiff plaques, respectively.

Conclusion: Evidence suggests that a judicious choice of stent design can minimize stress while maintaining a patent lumen in stenotic arteries. If confronted with a rigid, calcified plaque, stent design is more important, as design differences can impose dramatically different stress fields, while still providing arterial patency. Alternatively, stent design is not as much of an issue when treating a soft, lipid-laden plaque, as stress fields do not vary significantly among stent designs.

Figure 1

♦ Illustrations of the stent designs employed in this investigation. The 1Z1 design has a high radial stiffness and induces high radial displacement and stress on the artery wall. The 2B3 design has a lower radial stiffness and places less radial displacement and stress on the artery wall.

Figure 2

♦ Undeformed geometry of the diseased models used in this investigation: vessel radius (r_v), stenosis radius (r_s), vessel length (l_v), stenosis length (l_s). The white region denotes healthy arterial tissue and the dark region denotes the atherosclerotic plaque. The stent was “deployed” only in the diseased region

Figure 3

♦ Unloaded stenosis geometries. Due to the variation in plaque material properties, the unloaded geometries of the stenosed arteries varied (unloaded in B, stretched in C, stretched and pressurized at 80 mmHg in A) to ensure that each model had the same radial dimensions at diastolic pressure (∼20% stenosis by diameter). The lines represent plaque stiffness relative to the artery wall: the dashed lines are 0.5×, the solid lines are 1.0×, and the dotted lines are 2.0×

Figure 4

♦ Material responses used to describe the arterial wall and atherosclerotic plaque. The strain energy function constants were scaled to model plaques that were half as stiff (0.5×, dashed), of equal stiffness (1.0×, solid), or twice as stiff (2.0×, dotted) as the artery wall

Figure 5

♦ Final inner radial positions (lumen radius). Deformed radial position values were determined by averaging around the circumference of the vessel at diastolic pressure along the vessel axis. The final radial position was dependent only on stent design and not plaque material properties. The stiffer (1Z1) and more compliant (2B3) stent designs propped open the artery to ∼2.47 and 2.27 mm, respectively, despite the change in plaque material properties

Figure 6

♦ Artery wall hoop stress values (averaged over the circumference) at the internal elastic lamina (IEL) were dependent on both stent design and plaque material properties. Highest stress values were observed for the stiffest plaque (2.0×) and most rigid stent (1Z1), while the smallest values were seen for the least stiff plaque (0.5×) and more compliant stent design (2B3). Note high circumferential stress values at the IEL are most likely to disrupt this structure, provoking neointimal growth leading to restenosis.,