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Coronary heart disease happens when plaque accumulates inside the arteries. The plaque or fat deposits can be available in blood through cholesterol and calcium. The plaque solidifies in the narrow artery as time passes and it makes it difficult for the flow of blood. Consequently, coronary arteries carry blood rich in oxygen to the heart for distribution. Thus, the fat deposits limit the flow of blood to the body. (Koo, 2015). Atherosclerosis disease can affect both the large and medium-sized arteries of the heart, brain, legs, and the kidneys. Partial blockage of the heart arteries results in angina (chest pain). In case the blockage persists the heart, muscle dies and leads to heart attack. Total obstruction of an artery caused by the accumulation of plaque will lead to stroke. Therefore, Atherosclerosis condition is risky and may lead to death.
Currently, Atherosclerosis condition is the leading cause of death and illness in most countries. Despite technology improvement and medical advancements, heart attack and stroke caused mostly by Atherosclerosis are responsible for causing more deaths than any other disease. According to statistics, Atherosclerosis causes one in five deaths.
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Atherosclerosis develops from the oxidation of low-density lipoprotein molecules by oxygen radicals. The oxidized lipoprotein molecule encounters artery walls causing a series of reaction. The lipoprotein is composed of cholesterol. This results in artery inflammation and accumulation cholesterol, which results in muscle cell enlargements and formation of hardcover on the arterial walls (Rafieian-Kopaei, Setorki et al., 2014). Finally, the artery narrows and reduces blood flow and pressure.
Pathophysiology of Atherosclerosis
This involves series of continuous and complex processes, which is related to the chronic inflammatory process that results in the development of Atherosclerosis plaque as the final element. The first step is Atheroma, which is the build-up of cells and cellular remains containing calcium, lipids and connective tissues along the smooth muscles and endothelium lining of the artery walls (Koo, 2015). The next step is the Fatty streak, which is the initial visible appearance of Atherosclerosis in the artery inner surface. A small injury to the blood vessel exists due to bacterial or viral infection, exposure to risk factors such as smoking or chemical.
Upon entering the blood vessel, they cause chronic injury that disrupts endothelial permeability and allows entry of lipids thus triggering an inflammatory response. The toxic substance causes a minor lesion in the inner lining, referred to as intima. The accumulation of oxidized cholesterol in the artery enhances inflammation, which damages the endothelium. The injury together with lipids makes the endothelium to express adhesion thus attracting and binding the circulating monocytes on its surface (Insull, 2009). They penetrate the endothelium, accumulate, and differentiate into macrophages, which are in tissue form. The macrophages produce cytokines, which are inflammatory, and potent chemo attractants. The build-up of lipoprotein trapped in the macrophage is referred to FOAM cells. Furthermore, they produce growth factors, support lipid oxidation, release toxic metabolites, and result in plaque buildup. Production of connective tissues in response to chemoattractants and proliferative cells encourages plaque accumulation. The connective tissues contribute to the formation of the fibrous cap on the atheroma surface. The damaged wall produces growth factors while the lymphocytes prepare for an immune response. The smooth lining produces matrix metalloprotein that causes plaque disruption. This plaque is prone to rupture and result in thrombosis.
Atherosclerosis treatment involves a change in lifestyle, medicine, and surgery (medical procedures). Treatment happens because of the development of the blockage and aims at relieving symptoms, reducing blood clotting, prevention of related diseases, stop the build-up of plaques and widening clogged arteries (Koo, 2015).
Once Atherosclerosis develops, the doctor will commend heart-healthy lifestyle changes. This helps in reducing risk factors thus slowing or stopping Atherosclerosis development. Although these lifestyle changes will not remove blockages, they have proven to minimize risks of strokes and heart attacks. These changes include physical activities, managing stress, weight management, quitting smoking and healthy eating.
In most cases, lifestyle changes are not sufficient to manage cholesterol levels. By taking high blood pressure and high cholesterol drug, there may be reduction and stoppage of Atherosclerosis development (Rafieian-Kopaei, Setorki et al., 2014). There is recommendation of Statin medication to reduce and lower cholesterol levels. Satin drugs are prescribed to individuals with diabetes, coronary diseases, and high lipoprotein levels. Other medication aims at lowering blood sugar levels, reduce inflammation, and prevent blood clotting. Complying with the medicine regulations is important.
There is recommendation of surgery and medical procedures for individuals with severe Atherosclerosis. This includes Coronary artery bypass grafting (CABG). This is where unblocked arteries and veins of the body are used for blood flow thus bypassing blocked arteries. These results in improved blood and oxygen flow thus, minimizing heart attack and relieve chest pain.
Carotid endarterectomy surgery is carried to remove plaques accumulation from the arteries located in the neck region. This will restore efficient blood flow to the brain thus preventing stroke.
Percutaneous coronary intervention is a procedure that unblocks and widens blocked coronary arteries of the heart. This will reduce chest pain by improving blood flow to the heart region.
Being free from Atherosclerosis is possible. Prevention of Atherosclerosis involves controlling of risk factors, which in turn limits the development of Atherosclerosis and improve general health. Factors that put you at risk of Atherosclerosis include smoking, family history of atherosclerosis or heart disease, high blood pressure, high cholesterol, diabetes, inactive lifestyle and overweight or obesity (Insull, 2009). These factors are manageable, and experts agree that by reducing them you lower your chances of developing Atherosclerosis.
Some research studies determine control and prevention of Atherosclerosis. The health department has focused on the dissemination of useful information about atherosclerosis. The aim is to create awareness of a healthy lifestyle to help individuals minimize on atherosclerosis risk factors. Current research showed that atherosclerosis is a chronic disease that is characterized by continuous development resulting from systemic risk elements and pro-atherogenic stimuli. The different pathobiological mechanism involved in plaques progression and atherogenesis is evolving leading to the development of effective treatment strategies that led to decrease in atherosclerosis complications and clinical manifestation (Koo, 2015). Through intracoronary imaging, they managed to characterize atherosclerosis plaques, carry an assessment of atherosclerosis changes with time, and assess the response of the disease to atherosclerosis medication. The current evidence indicates the reversal of presumed risk factors and atheroma regression to atherosclerosis medication to be largely elusive. This step-paved interest of achieving pronounced regression of atherosclerosis plaques using atherosclerosis medications that support modifications of plaque anatomy to produce a favorable outcome for patients.
- Insull, W. (2009). The pathology of atherosclerosis: plaque development and plaque responses to medical treatment. The American journal of medicine, 122(1), S3-S14.
- Koo, J. (2015). The Latest information on intracranial atherosclerosis: diagnosis and treatment. Interventional neurology, 4(1-2), 48-50.
- Rafieian-Kopaei, M., Setorki, M., Doudi, M., Baradaran, A., & Nasri, H. (2014). Atherosclerosis: process, indicators, risk factors and new hopes. International journal of preventive medicine, 5(8), 927.