ABSTRACT
INTRODUCTION: Popliteal artery aneurysms (PAA) are the most prevalent form of peripheral arterial aneurysms. Greater saphenous vein grafts and endoaneurysmorrhaphy remains the mainstay therapy for open repair of PAA. True aneurysmal degeneration of lower extremity infrainguinal autologous vein grafts are relatively rare and its etiology is not completely understood. CASE PRESENTATION: We present a case of a 57-year-old man with recurrent autologous venous graft aneurysmal dilatations following a surgical popliteal artery aneurysm repair. DISCUSSION: The pathogenesis of true aneurysmal graft dilatation remains speculative with possible pathogenesis including progression of underlying atherosclerosis, systemic dilating diathesis, autologous venous graft varicosities, low-grade infections and post-stenotic dilatations. Management of venous graft aneurysms should be subjected to the same criteria as other aneurysms. Diagnosis requires a high index of suspicion. The initial study of choice is duplex ultrasonography as it can diagnose the aneurysm and distinguish it from other popliteal masses, provide accurately measurements and identify thrombus within the aneurysm. Once diagnosed, surgical repair should be performed as soon as possible as graft dilatation tends to occur overtime and is typically followed by a rapid increase in size over a short period of time. CONCLUSION: Aneurysmal degeneration of autologous saphenous venous graft following PAA repairs occur infrequently. Its etiology remains largely speculative. Accurate diagnosis and early surgical intervention can prevent progression of aneurysmal dilatation and minimize the potential of complications.
ABSTRACT
OBJECTIVE: Prenatal exposure to lipopolysaccharide (LPS) or high-fat diet (HFD) results in hippocampal impairment and cognitive deficits in offspring rats. What is not clear is how prenatal exposure to LPS combined with pre- and post-natal HFD would affect the hippocampus in offspring rats. METHODS: 32 pregnant rats were randomly divided into four groups, including control group; LPS group (pregnant rats were injected with LPS 0.4 mg/kg intraperitoneally on the 8th, 10th and 12th day of pregnancy); HFD group (maternal rats had HFD during pregnancy and the lactation period, and their pups also had HFD up to the third month of life); LPS+HFD group (rats were exposed to the identical experimental scheme with LPS group and HFD group). The serum IL-6 and TNF-alpha concentration was measured in three-month-old offspring rats in all groups. Hippocampal morphology and expressions of glial fibrillary acidic protein (GFAP), Tau and synaptophysin (SYP) in offspring rats were measured. RESULTS: Serum IL-6 and TNF-alpha concentration in the HFD group increased significantly compared with the control group, LPS group and LPS+HFD group. Compared with the control group and the LPS+HFD group, cells in the LPS and HFD groups were smaller and arranged in disorder, and cell membrane was not complete, nucleoli and nuclear heterochromatin stained darkly with hematoxylin. GFAP and Tau expression in the hippocampus of the LPS and HFD groups increased significantly compared with the control group and LPS+HFD group. SYP expression in the LPS and HFD groups decreased significantly compared with the control group and HFD group, increased in the LPS+HFD group. CONCLUSION: Prenatal exposure to LPS combined with pre- and post-natal HFD result in a protective effect on the hippocampus in offspring rats, and it might be a benefit from the predictive adaptive response to prenatal inflammation.
