Spectral analysis was used to examine 257 carotid arteries in 227 patients who had undergone carotid endarterectomy at 1, 3, 6, and 12 months after surgery and annually thereafter. Routine intraoperative completion angiography ensured that the operations were technically satisfactory. Postoperative restenoses were identified in 38 patients (15%). In 23 arteries (9%), the restenosis exceeded a 50% diameter reduction while in 15 arteries (6%) the stenosis was less than 50% of the diameter. Restenosis developed in 24/96 women (25%) and 14/161 men (9%). Twenty-nine (70%) stenotic lesions occurred within 12 months. In three patients early lesions regressed. Reoperation with patch angio-plasty was required in six patients. When the 219 carotid arteries that remained widely patent were compared to the 38 that restenosed , no differences were noted for age, diabetes mellitus, hypertension, smoking, or degree of preoperative stenosis. Early stenotic lesions appear to be due to myointimal hyperplasia, which is probably platelet mediated. The predominant female sex distribution may be explained by differences in platelet responsiveness in men and women.
Three-dimensional TOE provides additional information to 2D-TOE in aortic dissection assessment, particularly in entry tear size quantification. Agreement between entry tear area defined by 3D-TOE and CT was excellent. Three-dimensional TOE permits better morphological and dynamic understanding of aortic dissection when the flap is spiroidal.
SUMMARY Cerebral blood flow (CBF) has been measured using a non-invasive Xenon'33 clearance technique in six normal subjects after 2 days pretreatment with oral indomethacin at a dose of 100 mg/day. The results were compared with placebo given in a double blind balanced cross-over design. Indomethacin was found to result in a reduction in resting CBF of about 25% but the reactivity of the cerebrovascular circulation to carbon dioxide was preserved at normal levels. Infusions of epoprostenol (prostacyclin, PGI2) at a dose of 5 ng/kg/min resulted in a reduction of CBF of about 10% after placebo but no significant change in CBF after indomethacin. The results suggest that prostaglandins are involved in the maintenance of cerebrovascular tone but not in the mechanism of cerebral vasodilation accompanying hypercapnia. The combination of indomethacin and PGI2 has been proposed as a treatment of cerebral artery spasm and the findings suggest that the combination therapy would not be accompanied by undesirable intracerebral steal.There is considerable evidence, recently reviewed by Pickard,' which suggests that prostaglandins and particularly prostacyclin (epoprostenol, PGI2) are involved in the control of cerebral blood flow (CBF). The evidence comes from two separate lines, firstly experiments on the effects of indomethacin used as an inhibitor of prostaglandin synthesis, and secondly animal experiments on the direct effects of PGI, both in vitro and in vivo. Pickard and Mackenzie2 first showed that in baboons intraarterial indomethacin reduced resting CBF, and almost abolished the rise in CBF that normally results from hypercapnia. Similar findings were recently reported in humans studied 1 hour after
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