College - Author 1
College of Engineering
Department - Author 1
Biomedical and General Engineering Department
Degree Name - Author 1
BS in Biomedical Engineering
Date
6-2013
Primary Advisor
Trevor Cardinal, Paul (Mack) Consigny
Abstract/Summary
More than 385,000 people die from coronary heart disease (CHD) annually and treatment costs $108.9 billion each year including the cost of health care services, medications, and lost productivity. CHD decreases heart function by limiting oxygen and nutrient transport carried through the coronary arteries. A complete block to the coronary arteries causes a myocardial infarction in response to an elimination of blood supply to cardiomyocytes. Partial occlusion results in insufficient blood supply to cardiomyocytes, producing myocardial ischemia and angina, which are usually treated with intravascular stents deployed percutaneously, before myocardial infarction occurs. Stents are the most common ways to expand occluded vessels to treat CHD, with over 1 million stents placed in coronary arteries each year. Unfortunately restenosis, the narrowing of vessels due to endothelial damage and inflammation, is a common complication found after stenting with rates for bare metal stents reported to be between 16% and 44% or about 160,000 to 440,000 patients. Even with the recent advancement in stent technology and the introduction of drug eluting stents (DES), restenosis has continued to be a significant problem associated with stenting. DES restenosis is estimated to occur in 200,000 patients in the United States. It has recently been found that DES may also put patients at risk for late-stent thrombosis due to the delayed healing effects of the antiproliferative coating. With medicine growing at a rapid pace, new stent designs are researched to address new complications such as late-stent thrombosis. These newer designs need newer animal models to better understand the response of the vascular wall to newer stent technologies. The purpose of this study was to develop a mouse model of neointimal hyperplasia in response to aortic endothelial denudation. This model would allow for examination of the neointimal hyperplasia and endothelialization responses to next generation intravascular technologies, such as polymeric stents.
URL: https://digitalcommons.calpoly.edu/bmedsp/65