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Dia-Präsentation von SERVIER
EUROPA-Studie (Perindopril) (60 Abbildungen)
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Zum ersten Bild Abb. 4: KHK - Sekundärprävention Abb. 5: KHK - Sekundärprävention Abb. 6: Endotheliale Dysfunktion Aktuelles Bild - Abb. 7: Endotheliale Dysfunktion Abb. 8: KHK - Sekundärprävention Abb. 9: EUROPA-Studie - Hypothese Abb. 10: EUROPA-Studie - Perindopril Zum letzten Bild
Abbildung 7: Endotheliale Dysfunktion
As the dysfunctional endothelium progresses from early to more mature stages of atherosclerotic lesions, abnormal activity within the blood vessel continues: A fatty streak is formed within the vessel wall (lipid accumulation). Later, smooth muscle cells begin to migrate into the developing plaque. Leukocytes continue to adhere to the endothelium and after penetration move into the vessel wall. Inflammatory response in the atherosclerotic lesion starts. Platelets adhere to the dysfunctional endothelium contributing to the migration and proliferation of smooth muscle cells and monocytes, but also to platelet aggregation. Platelets accumulating on the vessel wall contribute to thrombus formation. As the atherosclerotic plaque progresses to late stages, a fibrous cap forms over the plaque and walls of the lesion from the vessel lumen. This fibrous cap may then become unstable and rupture causing thrombus formation, and often, CV events.
 
Endotheliale Dysfunktion
Vorheriges Bild Nächstes Bild   


Abbildung 7: Endotheliale Dysfunktion
As the dysfunctional endothelium progresses from early to more mature stages of atherosclerotic lesions, abnormal activity within the blood vessel continues: A fatty streak is formed within the vessel wall (lipid accumulation). Later, smooth muscle cells begin to migrate into the developing plaque. Leukocytes continue to adhere to the endothelium and after penetration move into the vessel wall. Inflammatory response in the atherosclerotic lesion starts. Platelets adhere to the dysfunctional endothelium contributing to the migration and proliferation of smooth muscle cells and monocytes, but also to platelet aggregation. Platelets accumulating on the vessel wall contribute to thrombus formation. As the atherosclerotic plaque progresses to late stages, a fibrous cap forms over the plaque and walls of the lesion from the vessel lumen. This fibrous cap may then become unstable and rupture causing thrombus formation, and often, CV events.
 
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