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Atherosclerosis: Difference between revisions
→Initiation and formation of atherosclerotic plaque
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Atherogenesis can be divided into five key steps, which are 1) endothelial dysfunction, 2) formation of lipid layer within the intima, 3) migration of leukocytes and smooth muscle cells to the vessel wall, 4) foam cells formation and 5) degradation of extracellular matrix. Via these consecutive steps, an atherosclerotic plaque is formed. The formation of the plaque can also be divided into three major stages namely 1) the fatty streak, which represents the initiation 2) plaque progression, which represents adaption and 3) plaque disruption, which represents clinical complications of atherosclerosis.<br /> | Atherogenesis can be divided into five key steps, which are 1) endothelial dysfunction, 2) formation of lipid layer within the intima, 3) migration of leukocytes and smooth muscle cells to the vessel wall, 4) foam cells formation and 5) degradation of extracellular matrix. Via these consecutive steps, an atherosclerotic plaque is formed. The formation of the plaque can also be divided into three major stages namely 1) the fatty streak, which represents the initiation 2) plaque progression, which represents adaption and 3) plaque disruption, which represents clinical complications of atherosclerosis.<br /> | ||
[[File:Figure_7_-_Fatty_streak_formation_revealing_platelet_aggregation_on_the_endothelial_surface.png|right|thumb|Figure 7. Fatty streak formation]] | |||
=== Initiation and formation of atherosclerotic plaque === | === Initiation and formation of atherosclerotic plaque === | ||
The earliest visible signs of atherogenesis are the fatty streak and pre-existing lesions of adaptive intimal thickening. Fatty streak is yellow discoloration on the surface of the artery lumen, which is flat or slightly elevated in the intima and contains accumulations of intracellular and extracellular lipid. At this stage of initiation, the fatty streak doesn’t protrude substantially into the artery wall nor impede blood flow. This process is already visible in most people by the age of 20. At this stage, there are no symptoms and this lesion may even diminish over time. Initiation of fatty streak development is most likely caused by endothelial dysfunction, since it involves entry and modification of lipids within the subintima. This modified layer of lipids creates a proinflammatory environment and initiates the migration of leukocytes and formation of foam cells (Figure 7). Intimal thickening mainly contains smooth muscle cells and proteoglycan-collagen matrix with a few or no infiltrating inflammatory cells.<br /> | The earliest visible signs of atherogenesis are the fatty streak and pre-existing lesions of adaptive intimal thickening. Fatty streak is yellow discoloration on the surface of the artery lumen, which is flat or slightly elevated in the intima and contains accumulations of intracellular and extracellular lipid. At this stage of initiation, the fatty streak doesn’t protrude substantially into the artery wall nor impede blood flow. This process is already visible in most people by the age of 20. At this stage, there are no symptoms and this lesion may even diminish over time. Initiation of fatty streak development is most likely caused by endothelial dysfunction, since it involves entry and modification of lipids within the subintima. This modified layer of lipids creates a proinflammatory environment and initiates the migration of leukocytes and formation of foam cells (Figure 7). Intimal thickening mainly contains smooth muscle cells and proteoglycan-collagen matrix with a few or no infiltrating inflammatory cells.<br /> | ||