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1. Plaque rupture proximal of minimal lumen
Coronary artery
Fujii, et al. Circulation 2003
Carotid artery
Lovett and Rothwell, Cerebrovasc Dis 2003
Dirksen et al., Circulation 1998
Masawa, Pathology International 1994
Reason(s)?
Direct mechanical effect of shear stress Gertz and Roberts, Editorial Am J Card, 1990
Biological effect of shear stress on cap stability
Hemodynamics Laboratory
Thoraxcenter Rotterdam
Slager et al., Nat Clin Pract Card 2005
2. Biological observations related to flow
direction
Dirksen et al., Circ. 1998
Flow
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
Flow
Hemodynamics Laboratory
Thoraxcenter Rotterdam
3. Shear stress distribution over
advanced plaque
High shear stress
Cap
Blood
flow
Lipid core
Low shear stress
Hemodynamics Laboratory
Thoraxcenter Rotterdam
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.