PubMed · 7952789
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T Diamond. Operative viva E.. https://pubmed.ncbi.nlm.nih.gov/7952789/
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Elevated plasma homocysteine is an acknowledged risk factor for arteriosclerotic occlusive disease, but little clinical evidence is available regarding its role in acute arterial thrombosis in the absence of an underlying lesion. A 45-year old man presented with an acute abdomen. A magnetic resonance arteriogram (MRA) showed occlusion of the superior mesenteric artery. At exploration, necrotic ileum was resected and the superior mesenteric artery was thrombectomized, restoring normal mesenteric flow. The plasma homocysteine level was 98.8 mmol/L, more than eight times the normal level. No embolic source was identified and an MRA and contrast arteriogram showed no residual occlusive disease in the superior mesenteric artery. Additional studies documented pernicious anemia, which was treated with cobalamin (vitamin B12) injections. This case provides further evidence of an association between hyperhomocysteinemia and acute arterial thrombosis. Hyperhomocysteinemia can result from easily correctible vitamin B12, B6, or dietary folate deficiencies. Plasma homocysteine levels should be determined in young individuals with acute arterial thrombosis whenever a hypercoagulable state is suspected.
Recently, carotid artery stenting (CAS) has emerged as a treatment option for carotid artery stenosis. Since the procedure is new, management of its complications is not standardized. This case report describes one method of arterial reconstruction after failed CAS. A 64-year-old male underwent CAS of his right internal carotid artery (ICA) for an asymptomatic 65% stenosis. Seven months later the stented area had narrowed to 95%. Arteriography revealed that the common and external carotid arteries (ECA) were free of disease so we elected to perform a transposition of the distal ICA onto the proximal ECA. The ECA and its branches were completely mobilized and the ascending pharyngeal and lingual arteries divided. The ICA was divided distal to the stent. Transection of the occipital artery provided an arteriotomy for an end ICA to side ECA anastamosis, thus preserving ECA flow. Postoperative surveillance after 8 months has revealed no recurrent stenosis. Operative repair of restenosis after CAS may be challenging if standard endarterectomy is not possible. Other options for reconstruction are feasible but if the common and external carotid arteries are disease-free, an ICA to ECA transposition provides a simple all-arterial repair that avoids bypass and prosthetic material.
Although intimal hyperplasia is a major cause limiting the long-term patency of the vein grafts, its precise mechanisms, including the effect of poor runoff, has not yet been well characterized. We thus designed the present study to try to determine the effect of poor runoff arterial flow to the phenotypic alterations of the graft wall by immnohistochemistry using anti-intermediate filaments (alpha-SM actin, desmin, and vimentin) and anti-myosin heavy chain (SM1, SM2, and SMemb) specific antibodies. Vein grafts implanted under the poor runoff hind limb of rabbits showed enhanced intimal hyperplasia, however, no apparent difference in the cytoskeleton expression, including intermediate filaments and MHC, between two groups until 4 weeks. Interestingly, six of eight vein grafts at 2 weeks after implantation in both groups showed the accumulations of perivascular fibroblast-like phenotype (negative for SM1, alpha-SM actin, and desmin) in some parts of the outer neointima, whereas the inner neointima at 2 weeks and the whole neointima at 4 weeks were mainly occupied by a smooth muscle phenotype (positive for these three). Although the cellular origin of these cells is still unknown, these results suggest that the migration of non-muscle mesenchymal cells is involved in the neointima and thus may provide a clue for better understanding vein graft remodeling.