ABSTRACT
Coronary Atherosclerosis Blood vessels are very sensitive structures which respond to hemodynamic changes. Thus
endothelial nuclear shape and orientation e.g., elongated, flow-direction oriented nuclei in segments with stable flow; round, less ordered nuclei in segments with unsteady, turbulent flow and possibly the density of endothelial nuclei depend upon stresses secondary to flow dynamics (Flaherty et al, 1972). In general, the architecture of a vessel wall is proportionate to the latter (Burton, 1954) and may change according to the nature of variations in flow dynamics (Rodbard, 1971). Types of stresses which act on the vessel wall are compressional with a radial direction, tensile with circumferential and longitudinal directions; and shearing, which depends on flow velocity and viscosity and is caused by the drag of flowing blood acting parallel to the vascular surface (Fry, 1969)). When stresses reach a critical point, structural changes in the vessel wall can be expected (Langille, 1991). In particular, an increase in shear stress stimulates vasodila tion in normal coronary arteries, limiting this stress at the endothelial surface. This is in con trast to atherosclerotic arteries in which vasodilation is reduced and major shear stress is likely (Vita et al, 1989).
