From the Ancient Greek chole- (bile) and stereos (solid) followed by the chemical suffix -ol for an alcohol, is an organic molecule. It is a sterol (or modified steroid), a type of lipid molecule, and is biosynthesized by all animal cells, because it is an essential structural component of all animal cell membranes; essential to maintain both membrane structural integrity and fluidity. Cholesterol enables animal cells to dispense with a cell wall (to protect membrane integrity and cell viability), thereby allowing animal cells to change shape and animals to move (unlike bacteria and plant cells, which are restricted by their cell walls).
In addition to its importance for animal cell structure, cholesterol also serves as a precursor for the biosynthesis of steroid hormones and bile acids.
Cholesterol is the principal sterol synthesized by all animals. In vertebrates, hepatic cells typically produce the greatest amounts. It is absent among prokaryotes (bacteria and archaea), although there are some exceptions, such as Mycoplasma, which require cholesterol for growth.
François Poulletier de la Salle first identified cholesterol in solid form in gallstones in 1769. However, it was not until 1815 that chemist Michel Eugène Chevreul named the compound “cholesterine”.
Maekawa et al., investigated possible associations among the presence of cholesterol crystals in embolic debris, the proportions of debris components, and postoperative cerebral embolism in patients undergoing carotid artery stenting (CAS).
Sixty-seven consecutive procedures were performed for internal carotid artery stenosis with CAS at the hospital between November 2015 and February 2018. Procedures for emergency CAS for stroke in evolution or crescendo transient ischemic attack were excluded (n = 12). The embolic debris from remaining procedures (n = 55) was stained with hematoxylin-eosin and the red blood cells, white blood cells, and fibrin were quantified by color-based segmentation. Cholesterol crystals and calcification were examined histopathologically. Diffusion-weighted imaging (DWI) was performed 1-3 days after CAS, and the images were used to classify procedures according to the presence of new lesions.
Of the 55 CAS procedures, new DWI lesions were identified after 32. One patient had symptomatic cerebral embolism. Higher proportions of patients with cholesterol crystals in embolic debris (17 vs. 78%, p < 0.001) and higher proportion of white blood cells (mean 2.3 [0-9.9] vs. 4.2% [0-29.9%], p < 0.01) were observed in the embolic debris of procedures with and without new DWI lesions.
Cholesterol crystals were common in the embolic debris from patients with postoperative ischemic lesions after CAS. These results suggest that inflammatory destabilization of the intraplaque lipid component is related to postprocedural DWI lesions 1).
Studies report that both high and low total cholesterol (TC) elevates SAH risk. There are few prospective studies on high-density lipoproteins (HDL-C) and low-density lipoproteins (LDL-C), and apparently none concerns apolipoproteins A and B 2).