NEUROLOGY 1994;44:1231
© 1994 American Academy of Neurology
Atheromatous embolism in the brain
A clinicopathologic analysis of 15 autopsy cases
J. Masuda, MD,
C. Yutani, MD,
J. Ogata, MD,
Y. Kuriyama, MD and
T. Yamaguchi, MD
Research Institute (Drs. Masuda and Ogata), the Department of Pathology (Dr. Yutani), and the Cerebrovascular Division (Drs. Kuriyama and Yamaguchi), National Cardiovascular Center, Osaka, Japan.
We report 15 autopsy cases with cerebral atheromatous embolism (14 men and one woman, 57 to 76 years of age) and analyze their pathologic features. Cardiovascular surgery or catheterization triggered the atheromatous embolism in the brain in six cases (aortocoronary bypass, two; emergency aortocoronary bypass after percutaneous transluminal coronary angioplasty, one; graft implantation for thoracic aortic aneurysm, two; coronary angiography, one). The events that had triggered embolism were not clear in the remaining nine cases. Pathologic examination of the brains revealed that nine cases had single or multiple cortical hemorrhagic infarcts corresponding to the border zones between two main cerebral arterial territories. Many of the leptomeningeal arteries located in the subarachnoid spaces of cortical sulci and surfaces adjacent to the infarcts were occluded by atheromatous emboli composed mostly of cholesterol crystals. The internal diameters of the occluded arteries ranged from 50 to 300 µm. Arterial territorial infarcts were present in six cases, three of which had thromboemboli containing various amounts of cholesterol crystals occluding the major arteries or their large branches supplying the infarcted areas, which were pale in two cases and hemorrhagic in one. The other three cases had hemorrhagic infarcts in which atheromatous emboli were present only in the small leptomeningeal arteries and were composed mostly of cholesterol crystals. Atheromatous embolism in the brain frequently causes border-zone infarcts by occlusion of the terminal cortical branches, and sometimes causes arterial territorial infarcts if the emboli are associated with fibrin and sufficiently large to occlude the larger arteries.
Address correspondence and reprint requests to Dr. Junichi Masuda, National Cardiovascular Center, Research Institute, 5-7-1, Fujishirodai, Suita, Osaka 565, Japan.
Supported by the Research Grant for Cardiovascular Diseases (2A-6) from the Ministry of Health and Welfare of Japan.
Received October 25, 1993. Accepted in final form January 20, 1994.
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