The blood vessels of the human body are predominantly made up of endothelial cells (EC) and smooth muscle cells (SMC). The remainder of it is composed of extracellular matric (ECM), which includes collagen, elastin, and glycosaminoglycans (Robbins, 2007, pg. 340). The walls of the vessels can be separated into three layers. The innermost layer, or tunica intima is made up of a single layer of endothelial cells overlying extracellular matrix (Robbins, 2007, pg.340) The next layer, or tunica media is separated from the tunica intima by the internal elastic lamina; the tunica media is mainly composed of SMC’s and ECM. Finally, the outermost layer is the tunica adventitia and is separated from the media by the external elastic lamina. The adventitia consists of loose connective tissue with small vessels and nerve fibers. Atherosclerosis mainly affects the elastic arteries, such as the aorta iliac arteries, of the circulatory system and the medium sized muscular arteries, such as the coronary arteries.
The first step in atherosclerotic plaque formation is the appearance of fatty streaks. Fatty streaks begin in childhood, with increased age and fatty diets the number of fatty streaks increases. With fatty streaks present, the SMC’s proliferate in the tunica intima and the amount of ECM deposition increases. The fatty streak also contains inflammatory cells such as macrophages and T-lymphocytes (Zhao, 2012). The increase in ECM stabilizes the plaque, but as more inflammatory cells accumulate in the intima the SMC’s undergo apoptosis, and this leads to an unstable plaque. The outermost part of the plaque is the fibrous cap and is composed of SMC’s and collagen; deeps to the cap is the necrotic core, which consists of lipid – laden macrophages, foam cells, and necrotic debris (Zhao, 2012). Many factors lead to the formation of an atherosclerotic plaque, they include, endothelial dysfunction, dyslipidemia, inflammation, immunological factors, smoking, and certain diseases such as diabetes and hypertension (Zhao, 2012).
Until the growing plaque reaches 70% stenosis, the plaque grows into the lumen of the artery; there are usually no clinical symptoms. Pathological changes of plaque include rupture, erosion or ulceration (Robbins, 2007, pg.351). When this occurs the plaque is exposed to the thrombogenic effects of the circulatory system, and a thrombosis will be formed. If the patient survives the consequences that could result from thrombus formation, for example a heart attack, the thrombus can be incorporated into the growing plaque. Other complications associated with the atherosclerotic plaques include hemorrhage into the plaque, which can either lead to expansion of the plaque or rupture; because the plaque weakens the wall of the artery, aneurysm formation can also occur (Otsuka, Nakano, Kolodgie, & Virmani, 2012).
Location of the atherosclerotic plaque is key to outcome from a plaque rupture. For example if the iliac or popliteal arteries are affected by atherosclerosis, symptoms can range from mild pain of the legs upon exercise (claudication) to ischemia with a resultant need to amputate (Harris & Dryjski, 2012). If the plaque affects the coronary vessels it can lead to myocardial ischemia and myocardial infarction, or if the blockage is so severe it can lead to death (Wilson, Douglas, Alpert, Simons, & Breall, 2013) Complications from a myocardial infarction include, congestive heart failure, due to contractile dysfunction; arrhythmias; myocardial rupture; papillary muscle dysfunction, which can lead to a valve problem; and finally thromboembolism, which can cause a stroke if it goes to the brain (Robbins, 2007, pg.397)
Atherosclerosis has many complications associated with it. Coronary heart disease is the number one killer in America, and is responsible for over one- third of deaths in people over the age of 35 (Wilson & Douglas, 2013). Therefore management of atherosclerosis is of the utmost concern for at risk patients.
Kumar, V., Abbas, A., & Aster, J. Ed. Robbins Basic Pathology. Philadelphia: Elsevier Saunders. 2007. Print
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