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Carotid atherosclerotic plaque is a pathological accumulation of lipids, inflammatory cells, and connective tissue within the carotid artery wall, resulting in narrowing of the arterial lumen. Plaque formation impedes cerebral blood flow and, if ruptured, may induce ischemic stroke by embolization of plaque fragments. Plaques are characterized by a lipid-rich necrotic core covered by a fibrous cap, surrounded by infiltrating immune cells and occasional calcification. Severity is monitored by imaging modalities (ultrasound, MRI) assessing features such as plaque area, echogenicity, and lumen narrowing. Statins stabilize plaque by reducing lipid content and inflammation. Surgical interventions (endarterectomy, stenting) physically remove or bypass plaque to restore blood flow and decrease stroke risk[1][2][3][4][5].
Statins: decrease LDL-cholesterol and stabilize plaque (anti-inflammatory, lipid-lowering, increases plaque calcification and echogenicity) [2] Antiplatelet agents: reduce thrombotic risk by inhibiting platelet aggregation Antihypertensives: lower blood pressure and decrease hydrodynamic contribution to plaque progression
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