Cholesterol emboli syndrome pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Nasrin Nikravangolsefid, MD-MPH [2]

Cholesterol emboli syndrome (CES) is the result of the rupture and release of cholesterol crystals from atherosclerotic plaques, produced either spontaneously or iatrogenic that lead to mechanical obstruction of arterioles and inflammatory response activation that cause multiple organ damage.

• It is thought that cholesterol emboli syndrome (CES) is the result of the rupture and release of cholesterol crystals from atherosclerotic plaques, produced either spontaneously or as a result of iatrogenesis.^[1][2]
• Cholesterol emboli syndrome (CES) is defined as the occlusion of 100-200 µm arterioles by cholesterol crystals after their dislodgment from atheromatous plaques, which arise from proximal large arteries such as aorta.^[1]
• Embolization of cholesterol crystals lead to several damages including^[1]
  • Endothelial injury
  • Activation of complement system
  • Oxidative stress injury
  • Activation of the renin–angiotensin–aldosterone system (RAAS) due to renal arteries obstruction and hypoperfusion
  • Leukocyte infiltration and release of its enzymes which cause inflammation
• Cholesterol emboli can involve many organs including brain, kidneys, eyes, skin, muscles, and gastrointestinal tract. ^[3]

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