ABSTRACT
Although clinicians and pathologists have recognized for more than a century that athero-
sclerotic lesions appear early within the aorta and that aortic atherosclerosis is often
severe, only recently has the relationship between aortic disease and stroke been
studied during life. Studies of patients with stroke and transient ischemic attacks have
now firmly established that the thoracic aorta is a very important source of brain embo-
lism. The first report on this subject was published more than a half a century ago.
Meyer in 1947 described two patients with syphilitic aortic aneurysms that developed
cholesterol crystal embolism considered to have derived from material in the aneurysms
(1). A decade later, Winter described two additional patients with syphilitic aneurysms
of the proximal aorta (2). The ascending aorta of Winter’s first patient was “covered by
innumerable atheromata most of which were eroded and partly calcified. Soft thrombi con-
taining cholesterol crystals were adherent to many” (1). Many brain arteries were blocked
by cholesterol crystal containing thrombi. In another patient who also had multiple brain
cholesterol crystal emboli, the “entire intimal surface of the aorta, but in particular the
aneurysm, was covered by atheromatous plaques, many of which were ulcerated and
covered by soft thrombi” (2).
