Abstract
Most acute ischemic syndromes, with totally different clinical presentations such as myocardial infarction, stroke or acute limb ischemia, share a common pathogenetic feature: disruption of an atherosclerotic plaque followed by luminal thrombosis 1-3. Plaque disruptions under these circumstances may vary greatly in extent: from focal erosions of the plaque surface, to deep ruptures throughout the fibrous cap reaching into the soft lipid core of lesions. Discontinuity of the endothelium allows a contact between the blood stream and highly thrombogenic plaque materials (collagen fibrils and lipid debris insulated with Tissue Factor), which initiates activation of the coagulation system with at least some degree of thrombus formation4. The differences in the type and extent of plaque laceration may have implications for the clinical outcome of the rupture event (figure 1). In coronary arteries, the arterial site where plaque rupture has been studied most extensively, a number of correlations have emerged between the morphology of the plaque, the degree of thrombus formation and the clinical syndrome of patients.
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van der Wal, A.C., Becker, A.E. (1998). Stable and Unstable Atherosclerotic Plaques: Plaque Biology in Relation to Acute Events. In: Van Der Wall, E.E., Blanksma, P.K., Niemeyer, M.G., Vaalburg, W., Crijns, H.J.G.M. (eds) Advanced Imaging In Coronary Artery Disease. Developments in Cardiovascular Medicine, vol 202. Springer, Dordrecht. https://doi.org/10.1007/978-94-007-0866-2_1
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DOI: https://doi.org/10.1007/978-94-007-0866-2_1
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