Atherogenesis Sample Clauses

Atherogenesis. Atherosclerotic plaques develop over many years and frequently go unnoticed until a patient develops symptoms of ischaemia. The lesions typically develop in areas where there is a substantial change in blood flow velocity. The first stage of atherosclerosis occurs when serum lipoproteins accumulate within the arterial intima creating a state of chronic inflammation. The intimal cells become increasingly hypoxic as the arterial wall thickness increases. Monocytes are recruited to the subendothelial layer where the initial lesion, known as a fatty streak, develops. The monocytes differentiate into macrophages, which phagocytose the modified lipoproteins, in particular oxidised low-density lipoprotein (oxLDL) and form foam cells. Foam cells accumulate over time and aggregate into a necrotic, atheromatous core within the lesion. The plaque reduces the diameter of the vessel lumen, impairing arterial flow. Hypoxic conditions develop within the plaque and subsequent neovascularisation develops, increasing the likelihood of plaque haemorrhage. As the lesion increases in size, the endothelial shear stress to which it is subjected will rise accordingly. If the plaque ruptures, the lipid-rich contents of the atheromatous core are released and the subendothelial layer is exposed. Both plaque-bound and circulating blood-borne tissue factor bind to, and activate, factor VII, initiating the clotting cascade and thus platelet activation and aggregation. Platelets adhere to the ruptured lesion, enhancing the production of platelet agonists, thrombin and thromboxane A2 (TXA2). Further platelet recruitment occurs and thrombus formation develops along with vasoconstriction of the already compromised vessels. Significant vessel occlusion will result in organ ischaemia and, ultimately, infarction, precipitating events such as stroke and myocardial infarction (MI) 2 3.
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