Infrainguinal occlusive disease: endovascular intervention is the first line therapy.

The preferred treatment of infrainguinal occlusive disease at many centers has undergone a paradigm shift from open bypass to endovascular intervention as the first-line therapeutic modality. Our own experience supports a percutaneous first approach. Though skeptics initially cited lower primary patency rates for angioplasty when compared with bypass, more recent studies have shown favorable secondary patencies nearly challenging that of bypass.

Assessing the effectiveness of endografts: clinical and experimental perspectives.

The increasing use of endografts to treat abdominal aortic aneurysms has prompted the need for improved postoperative imaging and surveillance. Although patients benefit from decreased morbidity with endovascular repair compared with open abdominal aortic aneurysm repair, the long-term outcome of stent repair has yet to be fully determined. The persistence of endoleaks highlights the need for close follow-up, particularly because this may lead to aneurysm rupture, even after endograft repair.

Receptor for advanced-glycation end products: key modulator of myocardial ischemic injury.

Background: The beneficial effects of reperfusion therapies have been limited by the amount of ischemic damage that occurs before reperfusion. To enable development of interventions to reduce cell injury, our research has focused on understanding mechanisms involved in cardiac cell death after ischemia/reperfusion (I/R) injury. In this context, our laboratory has been investigating the role of the receptor for advanced-glycation end products (RAGE) in myocardial I/R injury.

RAGE and its ligands: a lasting memory in diabetic complications?

The complications of diabetes are myriad and represent a rising cause of morbidity and mortality, particularly in the Western world. The update of the Diabetes Control and Clinical Trials Group/Epidemiology of Diabetes Interventions and Complications Research Group (DCCT/EDIC) suggested that previous strict control of hyperglycaemia was associated with reduced carotid atherosclerosis compared to conventional treatment, even after levels of glycosylated haemoglobin between the two treatment groups became indistinguishable. These intriguing findings prompt the key question, why does the blood vessel 'remember'? This review focuses on the hypothesis that the ligand/RAGE axis contributes importantly to glycaemic 'memory'.

RAGE axis: Animal models and novel insights into the vascular complications of diabetes.

Receptor for AGE (RAGE) is a multi-ligand member of the immunoglobulin superfamily of cell surface molecules. Engagement of RAGE by its signal transduction ligands evokes inflammatory cell infiltration and activation in the vessel wall. In diabetes, when fueled by oxidant stress, hyperglycemia, and superimposed stresses such as hyperlipidemia or acute balloon/endothelial denuding arterial injury, the ligand-RAGE axis amplifies vascular stress and accelerates atherosclerosis and neointimal expansion.