Nano Monitors for Identification of Vulnerable Cardio-Vascular Plaque
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0915-R06-27
Nano Monitors for Identification of Vulnerable Cardio-Vascular Plaque Ravikiran Kondama Reddy1, and Shalini Prasad2 1 Electrical and Computer Engineering, Portland State University, 1600 SW Harrison St, Fourth Avenue Building., Suite 25-02, Porltand, Oregon, 97201 2 Electrical and Computer Engineering, Portland State University, 1600 SW Harrison St, Fourth Avenue Building., Suite 25-02, Portland, Oregon, 97201 1. Introduction One hundred thousand patients undergo surgery daily in the United States, 33 million annually, which is 10% of the population. This costs $ 450 billion annually, averaging $ 13,000 per treatment, which is 40% of the healthcare budget. One million patients have adverse events after surgery annually, costing an additional $ 45 billion. Within the next two decades, surgical patients will increase by 25%, costs by 50%, and complications by 100% as our population ages.(1) The present surgical burden may become a surgical crisis. The best chance to allay this crisis is to improve outcomes after surgery. This goal has become possible with the use of particular medicines, which were developed to address perioperative ischemia, currently the best predictor for post operative cardiovascular morbidity and mortality.(2) Perioperative ischemia and infarction are thought to occur from plaque rupture of an unstable or vulnerable plaque in most cases. It is not known what makes a coronary plaque unstable or rupture, but emerging evidence suggests systemic inflammation may contribute to local plaque instability. Inflammation can activate the endothelium, which then expresses multiple cellular adhesion molecules that recruit monocytes and low density lipoproteins (LDL) into the coronary artery intima. LDL is then oxidized and taken up by macrophages which become activated and release cytokines and proteolytic enzymes. These cytokines can induce apoptosis in smooth muscle cells, which make collagen, the structural support for the plaque. The overall effect of inflammation on this balance is to favor plaque degradation and rupture. Furthermore, the unstable plaque temperature is 1oC higher in myocardial infarction, and is directly related to macrophage density and correlates with systemic levels of cellular adhesion molecules, cytokines, and C-reactive protein (CRP).(5) CRP has received much recent attention as a marker of inflammation. A meta-analysis of the inflammatory marker CRP demonstrated the relative risk of coronary heart disease in persons with elevated CRP was 1.7.(6) CRP was also identified as having a strong linear relation to myocardial infarction, ischemic stroke, coronary revascularization or death in a large retrospective cohort study.(7) In addition, CRP has been shown to have the ability to affect the gene expression patterns of human vascular endothelial cells, to inhibit endothelial progenitor cell differentiation and survival, and induce apoptosis in human coronary artery vascular smooth muscle cells.(8) Many secondary prevention drugs for cardiovascular disease are active in thi
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