Stroke, Vol 12, 445-453, Copyright © 1981 by American Heart Association
DL Rail, TJ Steiner and FC Rose
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.
ARTICLES
Differential contributions of major lipid components of atheroma to outcome of cerebral atheroembolism. A study in an animal model