Abstract
Coronary artery disease is part of the public health burdens in most countries in the world. The understanding of the pathophysiology of the disease has undergone some very significant changes. Previously the condition has been viewed as one that is caused by the deposit of cholesterol in the arterial walls of the heart. However, new evidence has been brought up that shows it is an inflammatory disorder (Eitan & Roguin, 2016). These unique views challenge the existing ones onto whether the disease should be segmental or localized. The aim of the treatment of illness should first involve the tackling of the lesion causing the problem. The recurrence of plaques should be significantly minimized.
Pathophysiology of Coronary Artery Disease
Current research shows that coronary artery disease is as a result of a manifestation of inflammation due to injury r disease. In the past years however it was considered to be the result of a deposit of lipids on the linings of the vessel. The risk factors for the disease have always been established as elevated cholesterol levels (Eitan & Roguin, 2016). It is imperative, therefore, that the lowering of cholesterol levels has been the focus of prevention for Coronary artery disease. The major lipid being lowered in most cases is the Low-density Lipoprotein Cholesterol (LDL-C). The complexity of the action of the molecules has only started to be appreciated recently. Evidence brought forward by researchers seems to suggest that the therapy modes which involve lipid-lowering also reduce inflammation. This reduction, in turn, has the ability to reduce the occurrence of heart disease (Eitan & Roguin, 2016). It also involves people whose LDL-C levels occur in the normal range, which is about less than 130mg/Dl.
Delegate your assignment to our experts and they will do the rest.
Progression of Disease
The cause of Coronary Artery Disease is because of the buildup of cholesterol-fatty deposits on the lining of the arteries. It can also be caused by the deposit of plaque in the filling. They are also called atheromatous plaques or atheromas (Boulanger.et.al, 2017). Their deposit on the arterial wall causes it to thicken. The effect is the narrowing of the space in the artery where the blood necessary for powering the heart flows(Boulanger.et.al, 2017). It reduces the oxygen and nutrient amounts that are reaching the center to allow for its proper functioning.
The development of the plaques can be attributed to the damage or injury present in the endothelium. The latter is the inner lining of the artery(Boulanger.et.al, 2017). Once a site is damaged, the deposit of some compounds such as cholesterol, lipid, lipoprotein and some debris happens on it. The accumulation of these substances occurs either in the wall of the artery or its intima (Boulanger.et.al, 2017). To progress into a material that can cause damage, high concentrations of the low-density lipoproteins accumulate. After this occurrence, they manage to bore through the mutilated endothelium, and they proceed on to oxidation. Through the process, their chemical and biological composition are altered. They thus cannot perform as they usually do (Boulanger.et.al, 2017). The altered LDL now acts by attracting white blood cells, also known as leukocytes. They move towards the arterial wall. Some foam cells are now formed after the migration. They are created due to the appearance of the macrophages, which envelope the lipoproteins. The foam cells now form the fatty streak. The latter is considered to be the earliest visible form of an atheromatous lesion.
After the formation of the fatty streak, the attraction of the smooth muscle cells to the site occurs. Once there, an extracellular matrix is formed due to their multiplication. It is composed of collagen and proteoglycan. This matrix that is formed makes up a significant chunk known as atherosclerotic plaque. The latter turns the properties of the fatty streak and makes it a fibrous plaque(Bujak.et.al, 2015). The net effect of the alterations on the lesions is causing it to bulge. The enlargement that occurs in the inner wall of the blood vessel causes the opening to narrow significantly.
The plaque now begins to transform and makes changes to its structure so that it can support itself. Firstly, it goes through the process of angiogenesis. During this process, it develops its blood vessels so that it can obtain nutrients and oxygen. Calcium then deposits on it, causing it to calcify(Bujak.et.al, 2015). The final plaque is formed. Its structure is such that it has a cap of fibrous tissue. The tissue then covers a core whose property is that it is rich in lipids. It also consists of dead cells which are also known as necrotic cells. The cap edge is critical in causing severe coronary disease. That region is sensitive since it tends to rapture most times. The underlying materials of the core, such as lipids and necrotic materials, are left exposed. The chromogenic factors of the blood act on them(Bujak.et.al, 2015). Platelets come into action, and they act across the plaque by clotting. It further narrows the artery causing the constriction even to be more extensive.
The result of the accumulation of these deposits on the arteries narrows down their spaces. Blood flow is extremely restricted. The person suffering from such a condition can thus experience chest pains. The cause of the aches is due to deprivation of oxygen of the muscles of the heart(Bujak.et.al, 2015). These deposits of plaque on the arterial wall will continue to grow in size. As their growth continues, the vessels continue to be narrowed wholly. The result is that the person will experience a heart attack. Some of these attacks are not fatal, and the person may live. However, most people are not as lucky, and they may end up dying after suffering the attack.
The treatment of coronary artery diseases is possible. It is diagnosed in a different number of tests. The first is a blood test where several things are checked, such as the levels of electrolytes and clotting factors. An electrocardiogram (ECG) can also be carried out to record the electrical activity of the heart (Ambrose & Singh, 2017). It reveals whether the heart is receiving any amount of oxygen. An echocardiogram can also be performed. It looks into the heart structure. It helps to determine whether any damage has been caused to the heart muscle. Based on the test results, then a variety of treatment options can be explored and used. The treatment may include the use of medication (Ambrose & Singh, 2017). The types of medicines in such situations include Beta-Blockers. They reduce the heart rate and thus reduces the pressure. Nitrates can also be prescribed. They serve the purpose of dilating the coronary arteries. Once this occurs, they can ensure that blood flows through without much pressure. Surgery is also an option. It involves either a coronary angioplasty or coronary artery bypass surgery.
Conclusion
In conclusion, the cause of coronary artery disease has thus been proven as an injury to the arterial wall of the heart. Without this damage, it would be impossible for the walls of the artery to be clogged by the deposit of lipids, cholesterol, and other debris. Since people should be encouraged to have a healthy diet, it is essential for ways to detect the injuries and inflammations to be sought (Leopold, 2015). High cholesterol levels in the body should also be lowered, and people taught how to live healthy and active lives. However, the focus should remain on the detection of the inflammations and injuries before they progress into serious problems for the patients.
References
Ambrose, J. A., & Singh, M. (2015). Pathophysiology of coronary artery disease leading to acute coronary syndromes. F1000prime reports , 7 .
Boulanger, Chantal M., Xavier Loyer, Pierre-Emmanuel Rautou, and Nicolas Amabile. "Extracellular vesicles in coronary artery disease." Nature Reviews Cardiology 14, no. 5 (2017): 259.
Bujak, K., Wasilewski, J., Osadnik, T., Jonczyk, S., Kołodziejska, A., Gierlotka, M., & Gąsior, M. (2015). The prognostic role of red blood cell distribution width in coronary artery disease: a review of the pathophysiology. Disease markers , 2015 .
Eitan, A., & Roguin, A. (2016). Coronary artery ectasia: new insights into pathophysiology, diagnosis, and treatment. Coronary artery disease , 27 (5), 420-428.
Leopold, J. A. (2015). Antioxidants and coronary artery disease: from pathophysiology to preventive therapy. Coronary artery disease , 26 (2), 176.
