Chondrosarcoma of the aorta: a rare source of bowel and lower extremity emboli.

Malignant aortic tumors occur infrequently. At least 70 cases of primary aortic malignancies have been reported in the literature. Within this group, chondrosarcoma is exceedingly rare, with only 1 case having been reported. An aortic chondrosarcoma developed in our patient and embolized to the small bowel and lower extremities. Although initially thought to arise from the abdominal aorta, this tumor, in fact, originated from the thoracic aorta. This case illustrates the need for complete aortic imaging when unexplained recurrent embolization occurs. In general, the survival rates with chondrosarcoma are diminished, but this patient survived 69 months after he was initially seen.

Endothelial cell adaptation to chronic thrombosis.

BACKGROUND: The autogenous vein graft has proven to be the most durable conduit in lower extremity vascular bypass grafts. Failures due to thrombosis, intimal hyperplasia, and progression of atherosclerotic disease commonly plague the vascular surgeon. Part of the ability of vein grafts to provide a nonthrombogenic surface relies on the capability of the endothelial cell to produce prostacyclin, a potent vasodilator and inhibitor of platelet aggregation. Once a graft fails and thromboses, little is known as to the effects of the thrombus on the function and morphology of endothelial cells. Earlier studies by this laboratory demonstrated the ability of arterialized canine vein grafts to recover function after 5 days of exposure to thrombus. This investigation sought to explore the limits of endothelial cell viability and recovery to extended periods of thrombosis. METHODS: Using a canine model of arterialized vein grafts, prostacyclin production (measured as 6-keto-PGF1a) was assessed in an ex vivo perfusion system from grafts exposed to thrombus for 10 days (group I) and 20 days (group II). Both groups underwent thrombectomy and a recovery period of 30 days. The grafts were perfused with Hanks' balanced salt solution and samples were obtained at 5 and 30 minutes to determine prostacyclin levels. Arachidonic acid was then added to a new perfusate of Hanks' solution and samples were again obtained at 5 and 30 minutes. Results were expressed as PGF/graft area (cm2/min). Representative samples of each graft underwent scanning electron microscopy. RESULTS: Without arachidonic acid, prostacyclin production of group II (20 day) grafts was greater than group I (10 day) grafts at 5 minutes of perfusion (4.31 versus 2.42, P = 0.08) and at 30 minutes (1.86 versus 0.95, P = 0.02). In response to the addition of arachidonic acid both groups increased prostacyclin production (group I, P = 0.004; group II, P = 0.12). A comparison was made between prostacyclin production at baseline and after addition of arachidonic acid. Group I grafts demonstrated a greater percent increase in prostacyclin production compared to group II (385% versus 229%, P = 0.01). Scanning electron microscopy showed no differences in endothelial coverage between the study groups. CONCLUSIONS: These results demonstrate that although endothelial cells are able to recover a basal level of prostacyclin production, the response to substrate stimulation diminishes with increased exposure time to thrombus. This diminished response may be important in understanding the ability of vein grafts to survive after a period of thrombosis.

The effect of thrombus on the vascular endothelium of arterialized vein grafts.

BACKGROUND: It is known that vein grafts can be salvaged by clot removal, but patency rates are diminished. This study was designed to determine the effects of thrombus on vascular endothelium and the ability of the endothelium to recover normal function. METHODS: Thirty external jugular vein grafts were placed as bilateral femoral artery interposition grafts in 15 mongrel dogs and allowed to arterialize for a period of at least 12 weeks. Six control grafts were not exposed to thrombus (C-NT). Six other control grafts were exposed to thrombus for 7 days and removed, ie, allowed no in vivo recovery (C-T). The remaining 18 grafts in 9 canines were exposed to autologous thrombus for 5 days and then flow was restored. The right femoral graft was removed 7 days after thrombectomy and the left removed 30 days after thrombectomy. At the time of removal, the grafts were perfused with a balanced salt solution alone and then with arachidonic acid added to the same volume of the salt solution. Perfusates were collected at 5, 15, and 30 minutes. These perfusates were assayed for the presence of 6-keto-prosglandin F1 alpha (6-keto-PGF1(1 alpha)), a metabolite of prostacyclin (PGI2). Over the 30-day recovery period, the amounts of 6-keto-PGF1(1 alpha) produced with and without arachidonic acid added were compared to assess endothelial response. Electron micrographs of the endothelium of all vein grafts were compared to the assay findings. RESULTS: When arachidonic acid was added to the perfusion system, there was a several fold increase in the production of 6-keto-PGF1(1 alpha) over baseline in all grafts allowed recovery. Grafts (C-T) that were allowed no in vivo recovery had no response to arachidonic acid. Ratios of 6-keto-PGF1(1 alpha) production with arachidonic acid stimulation to 6-keto-PGF1(1 alpha) production without stimulation were calculated to compare endothelial function. The electron micrographs showed the vascular endothelium to be severely injured after contact with thrombus, but recovered by 7 days. CONCLUSIONS: This study suggests that the endothelium of canine vein grafts is injured by contact with thrombus for 5 days but can recover structure and function. This recovery is detectable at 7 days post-thrombectomy.