A stent strut that protrudes into the lumen acts like a small step in the flow. Downstream of each strut the boundary layer separates and a recirculation ("wake") bubble forms, briefly reversing near-wall flow before it reattaches. Low and oscillating wall shear stress (WSS) inside that bubble is a well-established trigger for endothelial dysfunction and smooth-muscle proliferation — the core mechanism of in-stent restenosis.
Baseline (Poiseuille) wall shear stress:
τ₀ = 8μV / D
Reattachment (wake) length behind a strut of height h:
L_r ≈ k·h, k ≈ 5 (typical for coronary strut CFD studies)
Local WSS behind a strut, distance x downstream (0 ≤ x ≤ L_r):
τ(x) = τ₀ · [ -0.4 + 1.4·smoothstep(x / L_r) ]
τ(x) = τ₀ for x ≥ L_r
- Strut protrusion h — taller struts (worse malapposition, or a thicker bare-metal strut) create a longer, deeper recirculation zone and lower minimum WSS.
- Strut spacing — when spacing is shorter than the reattachment length, adjacent wakes overlap and the wall never recovers to healthy WSS: a chronic low-shear zone along the whole stented segment.
- Velocity & viscosity — both set the baseline τ₀ = 8μV/D through Poiseuille flow; higher flow raises baseline shear and can partially offset a strut's wake.
- The wall color map and flow particles show this qualitatively: red/purple bands mark low or reversed WSS behind each strut, blue/teal marks healthy shear. Particle motion is slowed for legibility — the τ readouts use the real input velocity, not the animation speed.
- Clinically, sustained WSS below roughly 1–1.5 Pa is associated with an atherogenic, pro-proliferative endothelial phenotype, which is why the risk readout tracks the fraction of stented wall length below that threshold.