ISCHEMIC STROKE / ETIOLOGY AND CLASSIFICATION

Created 13/05/2023, last revision 06/11/2023

• cholesterol embolization occurs when small pieces of cholesterol plaque break off from the arterial walls and block small and medium-sized arteries, which can lead to tissue damage
  • large arteries, especially the aorta and its branches, are the usual source of emboli in elderly patients with advanced atherosclerosis
  • embolization is often associated with intravascular procedures, cardiac surgery, and vascular surgery
• it differs from the more common artery-to-artery thromboembolism, in which thrombi formed on the surface of an atherosclerotic plaque embolize into the peripheral circulation
• symptoms may include skin discoloration, pain, and organ dysfunction

• atherosclerotic plaques in large arteries (aorta, CCA, ICA, pelvic arteries)   → atherosclerotic plaques classification
  • plaque formation is the result of a long-term process of lipid particle deposition in the vessel wall, accompanied by a cellular and inflammatory response
  • complex plaques are characterized by a thickness ≥ 4 mm and an irregular, often exulcerated surface. Blood clots (thrombi) occur on the surface of these lesions to varying degrees and extents ⇒ frequently associated with atheroembolism and thromboembolism
• plaque rupture with the release of atheroma masses and cholesterol crystals (spontaneous, traumatic, iatrogenic) and embolization to peripheral segments
  • iatrogenic – during cardiac catheterization, cardiac surgery, angioplasty
  • with the development of catheterization techniques, the incidence of cholesterol embolization is decreasing
  • the incidence of cholesterol embolization during renal artery catheterization procedures is reported to be as high as 30%. The course is usually asymptomatic, or there is a transient increase in urea and creatinine levels
• embolization in small and medium-sized vessels, resulting in their occlusion
• systemic inflammatory response to cholesterol emboli
  • local endothelial proliferation with intimal fibrosis leading to narrowing or permanent occlusion of the affected artery
• organ damage caused by artery occlusion with hypoperfusion and inflammatory response

• the clinical manifestation of cholesterol embolization syndrome is non-specific and is a combination of end-organ lesions and a systemic inflammatory response
  • cholesterol crystals trigger an inflammatory response (fever, fatigue, anorexia)
  • leukocytosis, anemia, and thrombocytopenia
  • ↑ ESR and CRP
• the syndrome should be considered in elderly patients with documented organ manifestations of advanced atherosclerosis, acute renal injury/hepatitis, hypereosinophilia, and skin manifestations such as livedo reticularis or “blue toe syndrome”. Particularly if they have undergone interventional or surgical procedures on large vessels before clinical presentation
• imaging – enables visualization, quantification, and characterization of atherosclerotic lesions
  • CT+CTA / MRI+MRA
    • assessment of extra- and intracranial arteries (incl. ascending aorta and aortic arch) for plaque burden, ulcerations, thrombus presence, etc. 
      
    • assessment of parenchymal damage
  • neurosonology
    • detection of atherosclerotic changes in extra- and intracranial arteries
      
    • monitoring of spontaneous and provoked embolizations during interventional procedures; the limitation is the inability to distinguish cholesterol microemboli from thrombi
  • TEE (assess aortic arch atherosclerosis)
• direct confirmation of atheroma embolization
  • skin or renal biopsy with evidence of atheroma emboli 
  • Hollenhorst plaques/crystals in the retina