Clinical Research

Restenosis after Coronary Artery Angioplasty and Stent Placement:
Cardiovascular disease is the major cause of mortality in the United States. Most of these deaths are due to myocardial infarction caused by coronary artery atherosclerosis. A recent advancement in the treatment of coronary atherosclerosis is percutaneous transluminal coronary angioplasty combined with implantation of a balloon-expandable stent, which acts as a metallic scaffold to maintain patency of the diseased vessel. An adverse consequence of this procedure, which usually occurs within 3-12 months, is a proliferation of cells in the wall of the artery, a process termed neointimal hyperplasia. In many patients, neointimal hyperplasia narrows the lumen of the vessel (i.e. causes restenosis) and results in impaired myocardial blood flow. The porcine in vivo coronary artery injury model most closely resembles the process of restenosis after stent placement in humans and therefore provides the best system for delineating the pathophysiology of neointimal hyperplasia. Oligonucleotide microarray technology provides unprecedented opportunities to understand and treat human disease. The pattern of mRNA abundance can be used to gain insight into the “molecular circuitry” of disease. In collaboration with Dr. Robert Russo at Scripps Clinic , we are using this technology to explore the molecular basis of restenosis. Our preliminary analysis suggests that levels of mRNA for several genes are dramatically changed. Identification of cell receptors and signaling pathways associated with stent-induced vascular injury in this porcine model may guide the design of novel treatments to prevent restenosis in humans.

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