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Figure 3 Acute coronary syndromes typically derive from atherosclerotic plaque disruption. Lipid-rich lesions (A) account for 70% of acute coronary occlusions. The shoulder regions of the plaque often have a thinner fibrous cap that is highly infiltrated with macrophages and are prone to rupture. Mural thrombi on disrupted or ulcerated plaques may progress to occlusive thrombi or be partially lysed and be replaced in the process of organization by the vascular repair response (B).
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