Document Type

Master's thesis

Date of Degree

2010

Degree Name

MS (Master of Science)

Department

Biomedical Engineering

First Advisor

S. C. Vigmostad

Abstract

Atherosclerosis is a term coined to describe a state in which arterial wall thickens due to the accumulation of fatty materials like cholesterol. Though not completely understood, it is believed to occur due to the accumulation of macrophage white blood cells and promoted by low density lipoprotein. Increase in accumulation of plaque leads to enlargement of arteries as arterial wall tries to remodel itself. But eventually the plaque ruptures, letting out its inner content to blood stream. The ruptured plaque clots and heals and shrinks down as well but leaves behind stenosis - narrowing of cross section. Depending on the degree of stenosis blood supply from the artery to its respective organ could decrease and even get blocked completely. Frequently, as the vulnerable plaques rupture, thrombus formed as such could flow through bloodstream towards smaller vessels and block them, leading to a sudden death of tissues fed by that vessel. If the plaques do not rupture and artery gets enlarged to a great extent then it results in an aneurysm. Such blockage of coronary arteries in heart can lead to myocardial infarction - heart attack, in carotid arteries in brain can lead to what is called a stroke, in peripheral arteries in legs can lead to ulcers, gangrene (death of tissue) and hence loss of leg, in renal arteries can lead to kidney malfunction. The most disturbing fact about atherosclerosis is the inability to detect the disease in preliminary stages. As stated by Miller (2001), most of the times coronary artery disease (CAD) gets diagnosed only after 50-75 percent occlusion of arteries.

Pages

xii, 125

Bibliography

122-125

Comments

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Copyright

Copyright 2010 Liza Shrestha