Abstract
The hypothesis that atheromatous plaques originate as intimai collections of blood components was first advanced by Rokitansky (1). This hypothesis has since been revived by Duguid (2) and others (3, 4). Recent findings in support of this concept include the demonstration that the intimai deposits may consist of platelets as well as fibrin. The presence of high thromboplastic activity in the intimai layer of blood vessels, especially arteries (5), provides a mechanism for fibrin or platelet deposition. Additionally, any increase in the coagulability of the circulating blood would facilitate the process. On the other hand, fibrinolytic activity is high in the vascular intima, though less active in arteries than in veins, and could be important in the removal of mural thrombi.
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Kwaan, H.C. (1978). Possible Effects of Risk Factors on Fibrinolysis. In: Chandler, A.B., Eurenius, K., McMillan, G.C., Nelson, C.B., Schwartz, C.J., Wessler, S. (eds) The Thrombotic Process in Atherogenesis. Advances in Experimental Medicine and Biology, vol 104. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-7787-0_17
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DOI: https://doi.org/10.1007/978-1-4684-7787-0_17
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