Aernoud Fiolet

65 Viewing Atherosclerosis through a Crystal Lens hope that it may be possible to reduce the ability of CCs to cause local trauma or incite inflammation. This would be necessary because once formed, flat plate CCs remain lifelong extracellular irritants capable of initiating and perpetuating inflammatory injury due to their high melting point (148–150°C), insolubility in water, and resistance to pH changes. That this approach might someday be possible is suggested by in vitro studies demonstrating that the rate of transition of metastable CCs into flat plate forms is reduced by statins, 79 high-density lipoprotein (HDL), 80 ethanol, 20 aspirin, and colchicine (Abela et al unpublished data). Thus, lipid lowering therapy may alter the size and shape of CCs in atherosclerotic plaque 21 (Fig. 8) and in vitro at least, alcohol, high-density lipoprotein, and β -cyclodextrin are able to solubilize them (Table 1). 81, 82, 83 Figure 8. Cholesterol crystal morphology with and without statins. (A) Scanning electronmicrographs of pure cholesterol crystals in vitro demonstrating pointed tip crystals compared with crystals exposed to (B) pravastatin demonstrating blunted tip and smaller size crystals. (C) Cholesterol crystals in carotid plaque from patient not taking statin demonstrates typical crystal formation, whereas (D) crystals in plaque from patient on statin had crystals that were thinned and appear to be dissolving. 79