The creation of an arteriovenous fistula (AVF) is frequently used to achieve easier access for haemodialysis in patients with chronic renal insufficiency. The most frequent late complication of AVFs is aneurysm formation, which carries the risk of spontaneous rupture. This study reports on 18 patients with giant aneurysms that developed on antebrachial AVFs who were operated on over a period of 6 years. Colour duplex ultrasonographic examination of the upper extremity was performed in all but one patient in the preoperative period. Surgical management included resection of the aneurysm and re-establishment of arterial continuity. There were no complications such as infection, ischaemic extremity loss, neurological sequelae or mortality. Colour duplex ultrasonographic examinations after 6 months were all normal. The mean follow-up period was 29.1 months (range 7-50 months). There were no additional vascular complications observed during follow-up. Early surgical intervention is the recommended treatment of choice for giant aneurysm complicating antebrachial AVF.
Background: Acute myocardial infarction (AMI) remains as one of the most common lethal diseases in the world and therefore it is necessary to understand its effect on molecular basis. Genome-wide microarray analysis provides us to predict potential biomarkers and signaling pathways for this purpose.Objectives: The aim of this study is to understand the molecular basis of the immediate right ventricular cellular response to left ventricular AMI.Material and Methods: A rat model of left anterior descending coronary artery ligation was used to assess the effect of left ventricular AMI on both the right ventricle as a remote zone and the left ventricle as an ischemic/infarct zone. Microarray technology was applied to detect the gene expression. Gene Ontology and KEGG pathways analysis were done to identify effected pathways and related genes.Results: We found that immune response, cell chemotaxis, inflammation, cytoskeleton organization are significantly deregulated in ischemic zone as early response within 30 min. Unexpectedly, there were several affected signaling pathways such as cell chemotaxis, regulation of endothelial cell proliferation, and regulation of caveolea regulation of anti-apoptosis, regulation of cytoskeleton organization and cell adhesion on the remote zone in the right ventricle.Conclusion: This data demonstrates that there is an immediate molecular response in both ventricles after an AMI. Although the ischemia did not histologically involve the right ventricle; there is a clear molecular response to the infarct in the left ventricle. This provides us new insights to understand molecular mechanisms behind AMI and to find more effective drug targets.
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