The mechanisms of plaque destabilization (fissuring and rupture, followed by thrombus formation) are not fully understood. Study of plaques in the coronary arteries that have undergone fissuring indicate that the majority are composed of eccentrically situated lipids (i.e., located in an area where the vessel bifurcates) that do not have an internal lattice of collagen supporting the cap of the plaque.
The vulnerability of such a structure to fissuring appears to be related to circumferential stress on the plaque cap in systole, as well as infiltration of the cap tissue with foam cells (with reduction of total collagen content and a concomitant fall in tensile strength) [Davis MJ, 1994]. It is unclear whether foam cells weaken the tissue by passively distorting the spatial arrangement of the connective tissue matrix or by actively destroying connective tissue matrix protein by lytic mechanisms.
Acute Ischemic Stroke: New Concepts of Care
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