ABSTRACT
Treatment of aortic atheromatous disease is controversial, and there have been no random-
ized therapeutic trials to study the effectiveness of various strategies. Anticoagulants have
been posited to aggravate cholesterol crystal embolism (1), but in several patients, aortic
thrombotic masses have disappeared after anticoagulant therapy (2,3). By preventing the
formation of thrombi over ulcerated areas of aortic atheromas, heparin and/or coumadin could theoretically facilitate contact of the atheromatous material with the lumen and
promote cholesterol embolism. Koren et al. (4) followed 78 patients who had protruding
proximal aortic plaques .5 mm thick during an average of 29 weeks while they were being treated with antiplatelet drugs or anticoagulants. Four of the 38 patients taking
heparin or warfarin developed a blue toe syndrome and/or renal insufficiency or an increased frequency of TIAs, although no patient taking antiplatelet drugs developed the
blue toe syndrome (4). The blue toe syndrome was probably caused by cholesterol embo-
lism. Anticoagulation may prevent red thrombus formation on top of atherosclerotic
plaques, allowing the embolization of plaque components.
