Morphologic bases for establishing end-points for early plaque detection and plaque instability

Abstract

The artery wall responds to changes in wall shear stress or tensile stress with modeling reactions which assure wall stability and continued adequate flow. The intima participates in these reactions and the adaptive processes continue during atherogenesis. The lumen tends to remain circular and the lesion is sequestered from the lumen by a fibrous cap. The artery enlarges, tending to preserve an adequate lumen cross-sectional area. Since lesions form initially in regions of low wall shear stress, early detection by methods such as ultrasonography must take into account circumferential and axial plaque distribution in relation to flow patterns. For the carotid bifurcation, for example, flow and maximum intimal thickening follow a helical path from the near wall at the distal common carotid artery to the far wall at the bifurcation and in the proximal internal carotid. Large plaques are complex with juxtaposition of regions of different composition and complex lesions tend to become complicated by disruption, thrombosis and plaque hemorrhage. Features which suggest manifest or imminent plaque disruption include thinning, absence or erosion of the fibrous cap in apposition to lipid pools or calcifications, and lumen irregularities or cavitations. Regions of contrasting density and/or extensive regions of low density, particularly in large plaques suggest vulnerability to disruption. Disruption of plaques are associated with hemodynamic stresses and plaque strains associated with marked stenosis, elevated heart rate and rapid excursions of pressure.