Cholesterol emboli syndrome pathophysiology

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

Pathophysiology

• It is thought that cholesterol emboli syndrome is the result of rupture and release of cholesterol crystals from atherosclerotic plaques, produced either spontaneously or as a result of iatrogenesis, ref name="Ozkok2016">Ozkok, Abdullah (2016). "Cholesterol embolization syndrome: report of two cases". Turk Kardiyoloji Dernegi Arsivi-Archives of the Turkish Society of Cardiology. doi:10.5543/tkda.2015.94587. ISSN 1016-5169.</ref>
• Cholesterol emboli syndrome (CES) is defined as the occlusion of 100-200 µm arterioles by cholesterol crystals after their dislodgment from atheromatous plaques, which arised from proximal large arteries such as aorta.
• embolization of cholesterol crystals lead to several damages including
  • 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.

References

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