Abstract
The rapid closure of coronary arteries as a result of occlusive thrombi is the major cause of acute myocardial infarction, and disrupted (via rupture or erosion) coronary atherosclerotic plaques can trigger a coronary thrombosis. Accumulating evidence indicates that inflammation plays a key role in plaque instability and thrombus formation. Autopsy studies of acute myocardial infarction have revealed that thrombi on disrupted plaques are principally composed of aggregated platelets and a large amount of fibrin with many inflammatory cells. Thrombi from ruptured plaques are significantly richer in fibrin than those on eroded plaques, and more tissue factor and C-reactive protein are expressed in ruptured than eroded plaques. These compounds appear to contribute more to fibrin-rich thrombus formation upon plaque rupture than plaque erosion. On the other hand, plaque disruption does not always result in total thrombotic occlusion because microscopic coronary thrombi are frequent in autopsies of noncardiac death. However, the mechanisms of arterial thrombus propagation in vivo remain unclear. Recent studies have demonstrated that increased vascular wall thrombogenicity together with substantial blood flow alteration is crucial for occlusive thrombus formation. Furthermore, not only plasma von Willebrand factor and vascular wall tissue factor but also intrinsic coagulation factors play important roles in thrombus propagation in vivo.
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Yamashita, A., Asada, Y. (2008). Atherothrombosis and Thrombus Propagation. In: Tanaka, K., Davie, E.W., Ikeda, Y., Iwanaga, S., Saito, H., Sueishi, K. (eds) Recent Advances in Thrombosis and Hemostasis 2008. Springer, Tokyo. https://doi.org/10.1007/978-4-431-78847-8_42
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DOI: https://doi.org/10.1007/978-4-431-78847-8_42
Publisher Name: Springer, Tokyo
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