1983 年 11 巻 2 号 p. 251-259
The clinicopathological findings are described in three autopsy cases with cerebral infarcts caused by cholesterol crystal emboli. From the point of views of embolic sources, cause of emboli, location and size of infarcts in the brain, moreover involved organs other than brain, the present studies are investigated. Cholesterol crystal emboli were lodged in small cerebral arteries (cortical and perforating branches arising from main cerebral arteries), though they were not found out in medium-sized cerebral arteries (anterior, middle and posterior cerebral arteries). Infarcts were prone to be seen in case of perforating branch obstruction by cholesterol crystal emboli, on the other hand, infarcts were not produced in cortical branches even if they were completely occlusive. Whether infarcts were produced, is thought to be difference in vessel anastomosis. Vessel anastomosis is in cortical branch better than in perforating branch.
The infarcts occurred in perforating branches area, were characteristically small in size less than 10mm in diameter, but they were not enough to be symptomatic. In predisposing factor, all of three patients have had essential or reno-vascular hypertention and severely ulcerative atherosclerosis of aorta. Two of three cases have had atherosclerotic aneurysms of aortic arch with ulceration. Case 1 and 3 have had hypertention, severe atherosclerosis complicated with atherosclerotic aneurysm of aortic arch and old myocardial infarct of left ventricle of heart. In case 1 and 3, cholesterol crystal emboli may originate from aortic arch atherosclerotic aneurysm due probably to cardiac catheterization.
Multiple infarcts due to cholesterol crystal emboli were found out in kidney, spleen, liver, pancreas, gall bladder, adrenal gland, stomach, small and large intestines except for brain. The kidney, spleen, liver and pancreas were most frequently involved in present three cases. We note that cholesterol crystal emboli in renal artery induce acute renal failure and rend-vascular hypertention, like in case 1 and 2. We emphasize that clinician might be careful not to produce cholesterol crystal emboli on coronary angiography in patient with advanced ulcerative atherosclerosis.