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Figure 1: The main features of atherosclerotic pathogenesis. Under nonpathogenic circumstances, an intact arterial endothelium (represented here as dots in light blue) prevents the ingress of atherosclerotic mediators. When normal endothelial function is compromised by factors such as hemodynamic stress and hyperlipidemia, however, the entry of low-density lipoprotein is facilitated. This begins the pathogenic cascade that culminates in the formation of an atherosclerotic lesion. Once formed, these lesions may continue to expand, resulting in cerebrovascular disease by occlusion. Alternatively, if possessed of certain predisposing histological features,[25] they may produce cerebrovascular disease through thrombosis or hemorrhage

Figure 1: The main features of atherosclerotic pathogenesis. Under nonpathogenic circumstances, an intact arterial endothelium (represented here as dots in light blue) prevents the ingress of atherosclerotic mediators. When normal endothelial function is compromised by factors such as hemodynamic stress and hyperlipidemia, however, the entry of low-density lipoprotein is facilitated. This begins the pathogenic cascade that culminates in the formation of an atherosclerotic lesion. Once formed, these lesions may continue to expand, resulting in cerebrovascular disease by occlusion. Alternatively, if possessed of certain predisposing histological features,[25] they may produce cerebrovascular disease through thrombosis or hemorrhage