Symptoms And Treatment Of 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

Coronary artery disease (CAD) is the commonest heart disease in the United States1. Approximately, 29% of patients with Myocardial Infarction ( MI ) present with ST- elevation Myocardial Infarction ( STEMI )2. STEMI is the result of complete occlusion of a major epicardial coronary artery due to thrombus formation. STEMI from a small coronary artery presenting as substantial EKG abnormalities similar to occlusion of a major artery and hemodynamic instability is a rare entity. The epidemiology, typical clinical presentation, outcomes, and optimal management in this group of patients are not sufficiently known.

Atherosclerosis is associated with the major killer ailments in America, which include strokes, heart attacks, as well as peripheral vascular disease. The condition arises when there are a narrowing and hardening of the arteries. This is usually a gradual process, and it slowly blocks the arteries. When this happens, it will impede smooth blood flow. It is estimated that at least one million Americans lost their lives to a condition associated with atherosclerosis for the past few years.

The pathophysiology of ACS includes the stable plaque forms get converted into unstable plaque forms.2 These unstable plaque forms have numerous thin fibrous cap cells, inflammatory cells, activated macrophages, and smooth muscle cells. Sympathetic activity increases myocardial contractility, pulse rate, blood pressure, and coronary blood flow which leads to plaque rupture or fissure. As the artery ruptures, it causes thrombus formation and ischemia in this particular artery. Depending on the condition, different thrombi could form. The unstable angina forms a small thrombus formation, NSTEMI forms a partial thrombus formation, and STEMI forms a complete and persistent thrombus. The risk factors involved in ACS are age, physical inactivity, and history of hypertension, diabetes, or angina. The signs of acute coronary syndromes are an acute heart failure, tachycardia, bradycardia, or heart blockage, and the symptoms of ACS consist of chest pain, pain in the extremities, nausea, shortness of breath, heavy

Coronary illness is the development of plaque (fat store on the inward dividers of the veins) in the coronary conduits that supply O2 rich blood to the heart muscle, the development of plaque is called atherosclerosis. 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

Atherosclerosis is characterized by the buildup of plaques, or fatty deposits, on the inner walls of arteries, making it more difficult for blood to pass through. Another disease is hypertension, more commonly known as high blood pressure, which leads to an increased risk of a stroke or heart attack. A stroke is when a blood clot forms and blocks up a blood vessel. This means that blood cannot travel to the brain, so brain cells become deprived of oxygen, leading to impaired brain functioning. A heart attack is also caused by a blood clot, in this case, a part of cardiac muscle dies. Depending on how much muscle dies, a heart attack may occur. One interesting fact about this system is that if all of the blood vessels within the adult human body were to be stretched out, they would reach about 60,000 miles. There are about 5 liters of blood in the

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).

If builds hard plaque in the arteries that irrigate the heart, the blood flow decreases or stops. This

2(529) Atherosclerosis is the main pathologic process responsible for the progression of this disease. Initiation of atherosclerosis begins with injury to the endothelial lining of the arterial wall. Platelets adhere to the injury site causing aggregation and growth factors to be released (PDGF). 4(110) An inflammatory response is then activated promoting further adhesion of platelets. Next, blood cells pick up low-density lipoprotein (LDL) turning them into non-functioning cells, or plaque. The build of plaque causes intimal hyperplasia, forming a fibrous cap, which slowly occludes the lumen of the artery. 5

The National Heart Foundation of Australia (2014) estimated that more than 350,000 Australians had experienced heart attack at some point in their lives, and about 54,000 cases are reported annually. In a statistical report circulated by Wong et al., (2013), more men than women who ages 30 to 65 years old, account of encountering this life-threatening disease in the last five years. This had claimed the lives of 8,611 Australian nationals in 2013, or in a mean of 24 people die every day (Wong et al., 2013).

Coronary arteries undergo a compensatory mechanism in relation to the area of the elastic lamina, which is involved with plaque this is known as adaptive or positive remodelling where it preserves the artery until 40% of the lesion is occupied, thus stenosis may not be clinically evident and can be asymptomatic. Positive

The coronary arteries supply oxygenated blood to the heart muscle. Plaque is a substance that can clog these arteries and cause a condition called atherosclerosis. The buildup of plaque can occur over many years which can ultimately lead to coronary heart disease (CHD). Plaque can harden and cause the arteries to become narrowed. This reduces the flow of oxygenated blood. Plaque may also burst and a blood clot may form causing a blockage of blood flow to the heart. In result to the blockage angina or a myocardium infarction can occur.

Coronary artery disease is the most common cause of a myocardial infarction (MI). As a result of CAD, plaque builds up in the arteries, thus narrowing the coronary arteries and preventing adequate blood flow to the heart. This condition is called atherosclerosis. In 2012, Huether, S., & McCance, K. defines Atherosclerosis when it begins to occur when there has been an injury to the coronary vessel wall. When injury occurs on the vessels endothelial layer it triggers a clotting mechanism. That mechanism sends chemotaxsis signals through the body for monocytes/macrophages to come clean the open vessel wall that is leaking LDL into the blood. The macrophages attempt to digest the fatty substance but have a hard time doing so. When the cells cannot digest the LDL, cell proliferation happens and they become static. Static macrophages turn into foam cells that then begin to cover the open vessel wall. Stasis of these foam cells occurs and forms a fatty streak, beginning to slowly occlude the artery. Then with time, build up of collagen occurs on top of the

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.

These aggregates accumulate in the blood vessels especially the brain, causing plaques that replace muscle end elastic fibers that give the vessels their structural properties and making them vulnerable to breakage. This may lead to hemorrhagic stroke, dementia, death, brain damage amongst other things.3