Abstract
Atherosclerosis has a long initial phase in which plaques form within the arterial intima, followed by a second episodic phase in which clinical symptoms occur. We are investigating the events that initiate the second phase. It has been established that a major proportion of the acute episodes are thrombotic and that the trigger is exposure to the blood of thrombogenic constituents of the intima when cracks of fissures develop in the cap of atheromatous plaques.
Why plaque fissuring occurs is not know, but it is reasonable to assume it to be due to yielding of tissue in reaction to mechanical forces acting on the structure of the plague. We are working on the hypothesis that there is a sub-population of plagues, probably on a minority, in which there is a propensity for fissuring. This may be caused by structural and physical properties of the most superficial layer of the plague, i.e. the cap; by the presence of liquid-rich pool in the plaque producing a potential space in the intima; or by a combination of these and other factors. We describe here some initial investigations.
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Born, G.V.R., Richardson, P.D. (1990). Mechanical Properties of Human Atherosclerotic Lesions. In: Glagov, S., Newman, W.P., Schaffer, S.A. (eds) Pathobiology of the Human Atherosclerotic Plaque. Springer, New York, NY. https://doi.org/10.1007/978-1-4612-3326-8_27
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DOI: https://doi.org/10.1007/978-1-4612-3326-8_27
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