Is A As Effective As Clopidogrel For The Patient With Acute Coronary Syndrome?

Atherosclerosis is the process in which substances known as plaques, which are made up of cholesterol and platelets, adhere to tears in the walls of arteries. Over time these plaques build up to the point where they occlude blood flow in the arteries. When this happens in the coronary arteries, either directly, as the result of buildup in the arteries themselves, indirectly in the form a clot from another part of the body breaking loose and becoming lodged in the coronary arteries, the usual result is a heart attack.3

Cardiac diseases alone have been estimated, direct and indirect costs, for the overall American population are “approximately $165.4 billion for 2009” (CDC, 2013). A survey found that heart disease accounted for 4.2 million of the hospitalizations in 2006. In 62% of these cases were short stay hospitalizations and occurred amount peoples ages 65 and older. These hospitalization rates also vary by gender, racial, and ethnic groups.

Nevertheless, there is an understandable and noticeable link between circulatory related diseases and lifestyle diseases, such as Coronary Heart Disease. Coronary heart disease can occur when fatty acids, such as cholesterol in an inadequate diet, build up in the walls of the coronary artery. These fatty deposits collect minerals and harden to become a plaque. Eventually, this plaque grows and can swells up, forming an aneurism. In some cases, this aneurism may burst leading to instant death. As it continues to grow and swell up, it finally blocks the artery completely and forms blood clots. This is known as coronary thrombosis. A myocardial infarction, or in other words as heart attack, occurs when no oxygen is able to reach the coronary artery and thus it is unable to fulfil its role in providing the heart muscle with a sufficient supply of blood. Heart attacks are very common in the society nowadays, especially occurring in smokers or obesity related diseases (Millar, June 2014)

After some time passes plaques may solidify therefore limiting blood stream or totally obstructing the corridor. The development of plaque is straightforwardly identified with a people way of life, normal danger elements incorporate stoutness, high blood cholesterol and diabetes. At the point when the endothelium is harmed by blood stream, the cholesterol and fats in the blood get stuck shaping plaques. This outcomes in hypertension due the heart endeavoring to supply obliged levels of blood to the body. In the event that the blood stream to the heart muscles is limited or blocked it may prompt further inconveniences, for example, angina, heart assault or heart

The plaque restricts blood flow to the heart and deprive the heart of oxygen it needs to function properly. CAD can be chronic, which is narrowing of the coronary artery and limitation of the blood supply to part of the muscle, or it can be acute, which results from a sudden plaque that ruptures. According to Warnica (2013), rupturing of the plaque “exposes collagen and other thrombogenic material, which activates platelets and the coagulation cascade, resulting in an acute thrombus, which interrupts coronary blood flow and causes some degree of myocardial ischemia.” The major risk factors that can lead to atherosclerosis and coronary artery disease are hypertension, dyslipidemia, tobacco smoking, diabetes mellitus, obesity, sedentary lifestyle, and genetic predisposition. The risk factors present in M.T.’s life are history of angina pectoris, history of uncontrolled hypertension due to non-compliance with treatment, obesity, and stress. M.T. is overweight with 289 pounds. M.T.’s cholesterol level is high at 280mg/dl. M.T.’s stress is related to experiencing the death of his best friend and business partner from cancer. Having three teenage children who are constantly in trouble at school and a wife who recently lost her job can be a stress factor in M.T.’s

A sufficient coronary artery blood flow is essential to supply oxygen for normal cardiac activities (Craft, 2014, p. 599). Atherosclerosis is a common form of CHD. It is an inflammation disease when plasma cholesterol is high. Risk factors such as hypertension, high cholesterol, smoking and diabetes increase the risk of endothelium injuries, contributing to the increase in oxidated lipid-lipoprotein (LDL). Foam cell is produced by the increase in the number of macrophages signalled by oxidated LDL. Next, the accumulation of foam cells will cause the formation of fatty streak lesions on arteries walls. Over time, fatty streak lesions migrate to the site and form fibrous plaque due to the increase in smooth muscles and collagen. The thickening and hardening initiated by an accumulation in calcified fibrous plaque caused the blood vessels to narrow. As a result, a decrease in tissue perfusion contributing to the development of myocardial ischemia (Craft, 2014, p. 599; McCance & Huether, 2014, pp. 1145-1147).

A non-ST elevation acute coronary syndrome (NSTE-ACS) is a very common presentation to emergency departments everywhere, as well as primary care practices. Therefore, it is important that all providers be well informed on the effectivity of certain treatment regimens.

Coronary heart disease (CHD), also known as ischemic heart disease is the most prevalent form of cardiovascular disease in Australia (Australian Institute of Health and Welfare, 2014). While over 20,000 of deaths in 2011 were attributed to CHD. There were estimated 590,000 Australians 18 years old and above diagnosed with CHD in 2011-2012 (AIHW, 2014; Craft, 2014, pg. 596). Myocardial ischaemia is a common form of CHD. A sufficient coronary artery blood flow is essential to supply oxygen for normal cardiac activities. Myocardial ischaemia develops when there is an insufficient supply of blood and oxygen to support the function of myocardial cells (Craft, 2014, pg. 599). A decrease in blood supply can led to the formation of atherosclerotic plaques by narrowing or occluding the arteries. Other conditions such as hypotension, coronary spasm, dysthymias, hypoxemia and anaemia can also decrease the blood and oxygen supply to the myocardial cells (McCance & Huether, 2014, pg. 1153)

After time of accumulation and build up the plaque it becomes hardened plaque, and the hardened plaque makes the coronary arteries narrower, which lead to reduce the blood flow to the heart muscles.

On the other hand, a number of causes are being attributed to the infarct or to the tightening of the arteries and, according to a journal published by Ellis et al., (2015), the most widespread is thrombus formation. It happens when blood clots emerge from the fatty sediments formed in the arterial lining. As plaques mount up inside the coronary arteries, its passageway gets

The development of an atherosclerotic plaque is relatively a very a complicated process where Plaque rupture accounts for about 76% of fatality lead by thrombi. The evolution of atherosclerosis begins with foam cell accumulation where the macrophages accumulate within arterial wall intima, progresses to form fatty streak where further accumulation of intra and extracellular lipids, this is a potentially reversible stage (Greenland p, 2013) further atheroma/fibroatheroma forms where cholesterol and phospholipids accumulate intramurally. This is a vulnerable state as it is predisposed to spontaneous rupture by inflammation and thrombus deposition may occur. Hemodynamic changes during this stage may cause ischemia or silent infarction, if large plaque rupture total occlusion may cause myocardial infarction or sudden cardiac death. Finally a complex lesion can develop where fibro muscular tissue can be seen with repair efforts followed by repeated plaque formation, this may slowly increase in size and produce significant arterial narrowing.

Men older than age 45 can get coronary artery disease and women over the age 55 can get the disease as well because they can have a history of early heart disease. Some risk factors can also be High blood cholesterol levels (low-density lipoprotein cholesterol),High blood pressure, Cigarette smoking, Diabetes mellitus, Obestiy, Lack of physcial activity, Metabolic syndrome, and Mental stress and depression. There are also some non traditional risk factors like C-reactive protein which can cause inflammation and can also casue a heart attack, Lipoprotein, Homocysteine, Small dense LDL-C proteins and Fibrinogen. The coronary aretery disease starts with growth within the walls of the coronary arteries until the blood flow of the heart muscle is limited which is also

It is mainly as a result of one of these three problems: ST elevation myocardial infarction, unstable angina and lastly non ST elevation myocardial infarction with chest pain being the main symptom (Linton, 2012). There are five main pathophysiologic processes that contribute to the development of ACS: thrombus on pre-existing plaque, active obstruction from coronary spasm, progressive mechanical obstruction, infection and unstable angina due to oxygen supply to myocardial (Linton, 2012). ACS is mainly caused by thrombus formation on a pre-existing plaque and it can be demonstrated through angiography or autopsies (Marshall, 2010). A thrombus is formed from plasma coagulation and platelets. There are risk factors that contribute to ACS such as cigarette smoking, diabetes, hypertension and high blood cholesterol (Linton, 2012). Both men and women are at a risk of having a heart attack. However it is more common in men especially when having a family background of heart attack, being overweight and inactive (Scruth, Carter, Cheng, Rolley, & Page, 2012). Modifying and identifying the risk factors is important as it can prevent further heart problems.

Acute coronary syndrome encompasses patients diagnosed with unstable angina, non-ST elevation myocardial infarction, and ST-elevation myocardial infarction (Amsterdam et al., 2014). Per the American College of Cardiology (2014), a rapid evaluation to identify life-threatening cardiac conditions is imperative for patients presenting to emergency departments with symptoms of acute coronary syndrome and an electrocardiogram is an essential tool for diagnosis (Amsterdam et al., 2014). Patients with ST-elevation myocardial infarction have a 7.4% increase in risk of mortality with every half-hour that passes before implementing appropriate reperfusion therapy (Omar, Helal, Mangar,

As blood pressure rises and “the blood moves with enough force, [it] increases the chances of tearing that plaque loose” and rupturing it (Sapolsky, 2004, p. 45). When a rupture occurs, the material that has become loose, a blood clot known as a thrombus, can pose as much more of a threat to a person’s life than the initial build up of plaque. If the thrombus blocks a coronary vessel then the heart muscle is unable to receive blood that is full of needed oxygen and other essential nutrients, this is known as cardiac ischemia (Steffen, Lecture 11). Ischemia can cause angina and discomfort. Another possible result of a blocked coronary artery is a heart attack, which can lead to death, and if a blood vessel in the brain is clogged then a stoke will occur.