Differential contributions of major lipid components of atheroma to outcome of cerebral atheroembolism. A study in an animal model.
Cerebral atheroembolism, in which mainly lipid emboli are released from rupturing atheromatous plaques, may occur without apparent effect, or result in cerebral ischemia and infarction. The reasons behind these unpredictable consequences were sought in the interaction, in vitro and in an animal model, between the main lipid components of advanced plaques. Pure preparations of representative lipids were each harmless when embolized into the cerebral circulation. In contrast, combinations in proportions similar to those in advanced human plaques caused infarction, whether these were synthetic mixtures or extracts from plaques of the entire lipid fraction. The most important physical interaction between the lipids was aggregation of crystals by oils. Between cholesterol and the mainly liquid esters, this created in vitro a range of glutinous aggregates. Triglyceride lowered the melting point of esters, increasing their oiliness, and reduced the cohesiveness of aggregates in the face of operative mechanical forces through a fall in viscosity. Phospholipid, acting principally as an emulsifying agent, promoted dispersion of the oil, secondarily freeing the crystals from its aggregating effect. In the plaque, the balance of these factors will determine the size and number of particles likely to embolize, and, therefore, the clinical outcome should the plaque rupture.
D000818:Animals; D001161:Arteriosclerosis / Q000139:chemically induced*; D002784:Cholesterol / Q000378:metabolism; D002788:Cholesterol Esters / Q000378:metabolism; D002542:Intracranial Embolism and Thrombosis / Q000139:chemically induced*; D050356:Lipid Metabolism; D008055:Lipids / Q000009:adverse effects; D010743:Phospholipids / Q000378:metabolism; D051381:Rats; D014280:Triglycerides / Q000378:metabolism
D002788:Cholesterol Esters; D008055:Lipids; D010743:Phospholipids; D014280:Triglycerides; D002784:Cholesterol