Finding in literature, both for coronary and carotid arteries show that plaque rupture occurs predominately at the proximal (upstream region) part of the plaque.
Dirksen et al. showed in longitudinal cross-sections of plaques a different distribution for both MF and SMCs upstream versus downstream. This indicates a higher matrix degradation by MFs and lower possible synthesis by SMCs at the upstream region compared with the downstream region. But why is not understood yet. Maybe there is a link with the Ecs. Tricot et al. showed in longitudinal cross-sections a higher cell apoptosis downstream compared with upstream. This could indicate that the endothelial cells at the upstream region have regained their functionality and response inflammatory to the high shear stress.
Zooming in at the advanced plaque, we notice a high shear stress region at the upstream part and a low shear stress region at the downstream part of the plaque, both previously located at the inner curve and thus at a low shear stress region.
Plaque rupture proximal of minimal lumen
Fujii, et al. Circulation 2003
Lovett and Rothwell, Cerebrovasc Dis 2003
Dirksen et al., Circulation 1998
Masawa, Pathology International 1994
Direct mechanical effect of shear stress Gertz and Roberts, Editorial Am J Card, 1990
Biological effect of shear stress on cap stability
Slager et al., Nat Clin Pract Card 2005
Biological observations related to flow
Dirksen et al., Circ. 1998
High density Low density High densityLow density
Tricot et al., Circ. 2000
Macrophages Flow Smooth muscle cells
2.7% 18.8 %
Endothelial cells in apoptosis
Shear stress distribution over
High shear stress
Low shear stress