40 research outputs found

    Homocysteine in Myointimal Hyperplasia

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    AbstractIntroduction: homocysteine, a sulphur-containing non-essential amino acid, appears to play a role in the pathophysiology of atherosclerosis. However, its role in myointimal hyperplasia, the cause of almost 30% of failures of interventional therapeutic procedures, is much less clear. Methods: a review of the published scientific data concerning the role of homocysteine in myointimal hyperplasia was performed using MEDLINE and other on-line databases. Evidence was sought from cell culture experiments, animal models and clinical studies. Results: several clinical studies have recently been published linking plasma homocysteine levels to restenosis in coronary and peripheral arterial disease. However, several contradictory studies also exist making the role of homocysteine unclear. There are currently no published randomised trials. Cell culture and animal model experiments have elucidated several potential mechanisms by which may stimulate myointimal hyperplasia. Possible mechanisms include endothelial cell activation with the enhanced release of inflammatory cytokines and growth factors and a direct effect on vascular smooth muscle cell migration and proliferation. Conclusion: further studies are required before the true role of homocysteine in the pathogenesis of myointimal hyperplasia can be clearly evaluated. If evidence does confirm a role, the ease with which homocysteine levels can be normalised makes it an attractive alternative therapeutic target for intervention

    Extended storage of whole blood with 3-deazaadenosine for homocysteine assay

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    Outcome following surgery for thoracic outlet syndrome

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    AbstractIntroduction: the diagnosis of thoracic outlet syndrome (TOS) relies heavily on subjective rather than objective assessment criteria. Subsequently, published results after surgical decompression vary considerably. This study aimed to use a symptom-based patient-directed questionnaire to assess the outcome after decompression for TOS. Methods: sixty patients who underwent decompression procedures were identified from a prospectively maintained vascular database. Patient records were analysed for details regarding initial presentation, investigation, type of procedure used for decompression and management. Outcome questionnaires were sent to all identified patients to give a patient-based outcome measure. Results: eighty-four per cent of patients responded. In 90% of these patients there was an improvement in symptoms post-surgery with a median follow up of 43 months. The results were not influenced by the procedure or approach used. Conclusion: surgery remains an effective tool in the management of TOS. A simple patient-directed questionnaire as used in this study could assist in the standardisation of outcome assessment.Eur J Vasc Endovasc Surg 26, 170-175 (2003
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