This is a branch of medicine that is concerned with the study of causes and the origin of a disease. Coronary Artery Disease is a kind of blood vessels disorder that is medically categorized as atherosclerosis. It is a Greek word ‘athere’ that means ‘fatty mush’ and skleros that stands for ‘hard’. This combination reveals that atherosclerosis usually begins as a soft fat deposit that hardens with time. Atherosclerosis is usually defined as the hardening of the arteries. Although the condition can take place on any artery in the body, the fatty deposits have a higher preference to the coronary artery. Arteriosclerotic heart disorder and coronary heart disease are common terms used to describe the process of this disease.
Atherosclerosis is an important cause of the disease and is described by a lipids and cholesterol central deposit primarily within the arterial walls. The dawn of this plaque development results from a complex interaction between the blood components and the features that form the vascular walls. Inflammations and endothelial injuries play a very important role in the growth of atherosclerosis.
The standard intact endothelium is just a easy barrier that lies between the walls and the pore of the blood vessel. It is normally non-creative to leukocytes and platelets as well as fibrinolysis, coagulation, and the complement factors. Nonetheless, the endothelial walls can acquire injuries due to use of cigarettes, hyper-lipidaemia, diabetes, hyper-homocysteinemia, and other infections that cause local inflammatory responses (Becker et al., 2008).
C-reactive protein, popularly known as CRP, is a non-specific inflammation marker that increases in many patients with Coronary Artery Disease. Chronic exposition of minor elevation of CRP may trigger the rupture of plaques that promote the oxidation of low density lipoproteins cholesterol that leads to more uptakes by macrophages in the endothelium lining.
Coronary artery disease (CAD) is usually a progressive disease that may take time to mature. When the symptoms start to show, the disease is usually in its advanced stages. The commonly known stages of development are as follows:
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(a) Fatty streak – this is the earliest lesions of atherosclerosis that are characterized by lipid filled smoothness in muscle cells where a yellow tinge appears. Fatty streaks may be observable in the coronary artery by the age of 15 and involve an increase in the surface area with the age of the patient. Professionals and pathologists believe that any treatment directed to lower LDL cholesterol is a good measure in reversing the process.
(b) Fibrous plaque stage – this is the stage when progressive changes in the endothelium of the arterial walls begin. The changes can appear in the coronary artery by the age of 30, but continue increasing with age. Normally, the repairs of endothelium happen immediately, but for people with CAD it may not be easily replaced. This allows the growth factors and the LDLs to stimulate smooth muscle proliferation that thickens the arterial walls. Once the endothelium injuries have taken place, lipoproteins (responsible to transport proteins through the bloodstream) transport cholesterols and other forms of lipids into the intima of the artery.
The fatty streaks are eventually covered by collagen that forms a whitish or yellowish fibrous plaque. These plaques may form on one portion of the arteries or in a round fashion all over the entire lumen. The borders may appear smooth or irregular in shape with jagged rough edges. This results in the narrowing of the vessels’ lumen, thus reducing the blood flow to distal tissues.
(c) Complicated lesion – this is the final stage in the development of atherosclerosis lesion and usually the most dangerous. As the growth of fibrous plaque continues, there is usually more inflammation that may result in plaques instability, rupture, and ulceration. Upon compromising the integrity of the arterial inner walls, platelets accumulate in large numbers resulting in thrombus.
Pathogenesis of Atherosclerosis Plaque
Atherosclerosis is usually the major cause of CAD. This process begins to disrupt the endothelium functions as a result of buildup of lipoprotein particles in the internal walls of the coronary vessels. Watery insoluble lipids are transported in the circulation as attachments to water resolvable lipoproteins. Highly concentrated low density lipoproteins permeate dysfunctional endothelium making it undergo oxidation in diabetic glycation. Modified low density lipoproteins attract leucocytes in the intima, but can be scavenged by macrophages resulting in forming foam cells. The cells eventually duplicate giving rise to the initial pathological lesion known as the fatty streaks.
The recruitment of smooth muscle cells is then followed by their migration to the site of foam-covered cells. The even muscle cells are then multiplied to trigger synthesize of extracellular milieu (proteoglycan and collagen). Larger volumes of plaque are then occupied by extracellular conditions that the smooth muscle cells secrete. Fatty streak is converted to the fibrous plaque, and at this point the lumen becomes encroach by the lesion begins.
Small plasma vessels begin to form in the plates which subsequently calcify. Inflammation is quite important in promoting smooth muscle migration of cells during proliferation. The complicated final lesion consists of a rubbery cap overlying through the lipid enriched core containing the necrotic substance and is extremely thrombogenic.
Coronary arteries have two major branches that result from the aortic root resulting in the left and right coronary artery. Subsequently, the left coronary artery divisions off to the left circumflex artery (LCX) and the left anterior descending (LAD) which supplies the left ventricle with blood together. Just like in any other vascular bed, the flow in the arteries obeys Ohm’s law, meaning that the flow is equal to perfusion pressure divided by the resistance of the given vasculature. However, contrary to other vascular beds, both resistance and the pressure gradients vary all through the cardiac cycle. This is influenced by the contraction during systole and relaxation at diastole.
At systole, the ventricular pressure dramatically increases reducing the gradient of the driving pressure that nearly abolishes all blood flows. At diastole, the ventricular pressure is quite low resulting in a larger pressure gradient and a consequential larger flow. The diastolic flow is the major component responsible for the supply of the working myocardium.
Histology techniques were applied to measure the comprehensive morphology of atherosclerotic lesions and the vasculature. However, following euthanasia, body tissues were fixed in a 4% buffered formaldehyde that was embedded in paraffin for sectioning. Histology was among the most common ways to evaluate changes in pathology as well as detect spatial occurrence in the structure and proteins of laboratory rats’ specimen.
Signs and Symptoms
The commonest signs and symptoms of Coronary Heart Disease most often seen by a clinical practitioner is angina pectoris. Angina pectoris is a clinical term that describes a temporary chest discomfort taking place in a patient’s body. This happens when the heart fails to get enough blood and oxygen. The heart as a muscle receives its blood supplies from the coronary arteries that carry oxygen and nutrients that the heart requires. When the heart muscles fail to get enough blood for its basic function, it no longer functions to its full capacity. Physical exertion, extreme temperatures, strong emotions, or eating may increase the demands of the heart. Someone with angina experiences some provisional pain, fullness, pressure, or some sort of cuddling at the centre of the chest, neck, jaws, shoulders, higher arm, or the upper back. This is usually referred to as angina as it can be relieved by removing the stressor (Boden et al., 2007).
However, the angina episode should not be confused with a heart attack, but having it is an increased risk of a heart attack. A heart attack happens when the blood stream is reduced to some parts of the heart and the muscle dies. Angina can serve as an important sign to prepare the patient in seeking timely medical attention to avoid a heart attack. Prolonged and unattended angina may lead to any form of heart attack and double the risks of having rhythmic heart abnormalities. Either of the above medical conditions can lead to a premature death.
Time is a very important factor concerning angina. The more the heart is deprived of the adequate flow of blood (ischemia), the more the heart muscles are deprived of oxygen and the higher is the risk of heart rhythmic abnormalities and heart attack. The longer a patient experiences angina chest pains, the more the cardiac muscles are in a risk of malfunctioning or dying.
Other symptoms of CAD include:
(i) A common sensation is felt beneath the sternum and radiates to the left shoulder then down to the inner arm, then straight through the back to the throat, teeth and the jaws, and sometimes to the upper abdomen.
(ii) A vague and somehow troublesome ache and a precordial devastating sensation.
(iii) Stress or physical exertion that causes a typical precipitation persists for a few minutes and subsides after rest or introduction of nitro-glycerine.
(iv) Worse exertion after taking a meal.
(v) Worse cold weather on first contact with cold air after a previous contact with a warm room.
(vi) Modest rise in the rate of heart beat.
(vii) Notable elevation of diastolic and systolic blood pressure and some hypertension.
Clinical Manifestation of Coronary Artery Disease
CAD can present itself in different ways. The standard way of demonstration is with chest uneasiness. Chest discomforts result from myocardial ischemia, which is subordinate to coronary artery disease, but it is clinically referred to as angina pectoris or the squeezing of the heart. This discomfort is not localized but radiates through the upper arms as low as to the tummy button and up once again to the lower jaws.
These sensations may be related with dyspnea or quickness of breath and usually result from myocardial ischemia, but this appears as the last manifestation. However, because of myocardium’s overreliance on coronary blood flow for quantity of energy, diastolic and systolic dysfunctions set in within a few beats of the coronary occlusion. After this, the electrocardiogram immediately starts to record abnormalities even before the patient starts to experience the angina pectoris. This theory explains the reason why a patient may describe associated short breath when experiencing the angina. The two symptoms together indicate that the myocardium is fed by a narrow vessel.
More frequent clinical manifestation of the coronary artery disease is as follows. The scenarios may grow from one another and their credit allows for proper supervision so as to prevent any possible harmful consequence (Gamberger, 2010). Acute coronary syndrome is a term used to refer to unstable angina, non ST-segment boost as well as ST-segmented elevation myocardial infarction. A significant proportion of patients with this acute coronary syndrome (ACS) detected with ST-segmented elevation myocardial infarction while the rest are recorded having unstable angina.
Stable angina – this occurs predictably after application and is usually relieved by relaxation. This is usually due to increase in demand of oxygen in the face of inadequate coronary flow. The more severe the narrowing is, the less is the exertion extent required to induce ischemia and angina. As the narrowing severity increases, the amount of exertion needed to precipitous angina also reduces. Some kinds of exertion are standardized to result in angina like climbing stairs and after taking a meal.
There is individual variability in different patients in the amount of efforts required in precipitation of angina and it is usually referred to as variable threshold angina. This is where the vasoconstriction component may assist in lowering the angina threshold.
Treatment of this angina is by use of beta-blockers so as to reduce myocardial O2 requirements. Ca++ channel blockers are used to vasoligate and reduce the preloads or any afterloads. Nitrates are also important in vasoligation and reduction of preload. In case a medical therapy fails, surgical revasculisation or percutaneous interventions with balloon angioplasty may be performed. Of equal importance is the risk factor modification to address dyslipidaemia, smoking, hypertension, and physical inactivity.
Unstable angina – this is usually diagnosed clinically when patients with this medical condition can be presented in one of these three clinical scenarios.
(a) Acceleration of stable angina to one occurring with fewer activities and more intensity, but it lasts longer.
(b) Angina at its state of rest.
(c) A new onset of angina that is usually accompanied by severe discomfort.
While the pathogenesis of ST-segment elevation myocardial infarction is a complete occlusion of coronary vessels, pathogenesis of unstable angina is usually severe, but not a total occlusion of the prime vessels. This condition is usually a result of:
(b) Plaque disruption with the formation of clots and interruption of distal blood vessels,
(d) Mechanical occlusion, and
(e) Increase in myocardial oxygen demand due to extra-cardiac reasons such as anemia and thyrotoxicosis that plays a very important role in a patient’s pathogenesis of unstable angina.
Due to the fact that the formation of thrombus is an integral part of the pathogenesis in unstable angina, such anticoagulants like aspirin, heparin, and recent inhibitors are vital ingredients of therapeutic armamentarium. Oxygen consumption reduction by the use of beta-blockers and nitrates is also an important treatment. Any rise in one of the cardiac serum makers, troponin may have a very bad prognosis and therefore such patients are treated more aggressively with glycoproteins IIB/IIA inhibitors and also the use of early cardiac catheterization.
Diagnostic Studies for Coronary Artery Disease
Various tests can be used to diagnose possible presence of heart diseases. The choice of which and how to perform the test depends on the risk factor of the patient, the history of the heart problems, and the prevailing symptoms. Under normal circumstances, the tests begin with the common ones and more simple ones and then progress to the complicated ones. Routine tests that are used to determine the risk of a heart disease is checking for unhealthy cholesterol levels and presence of high blood pressure among adults. Other specific tests are important is assessing people who may have a high risk factors and symptoms of diabetes. Such tests may include the following:
(I) Electrocardiograms (ECGs)
This instrument measures and records the electrical activities of the heart. Between 20-50% of patients suffering from silent ischemia or angina have normal readings in the ECGs. The ECGs wave measure corresponds to the relaxation and contraction patterns of diverse parts of the heart. The machine is extensively used to diagnose heart diseases ranging from congenital heart cardiac disorders in infants to myocardial infarction in adults.
(II) Exercise stress test
This test is used in the evaluation of the coronary artery and can be performed in some of the following situations:
(a) Patients with possible angina so as to determine the chances of having a coronary artery disease
(b) Patients with a previously stable angina and now having symptoms
(c) Follow-up patients with a historical record of known heart disease and/or after a coronary bypass surgery
(d) Patients with certain forms of heart rhythmic disturbances
(e) After a heart attack before leaving the hospital or soon after it.
This is a non-invasive test that applies ultra sound scan to the heart. It is a more expensive test than the others, but more valuable, especially to determine whether there is a heart muscle damage and the extent of the damage (Lavrac%u030C, 2003). A stress echo-cardiogram can also be performed to evaluate abnormal findings from a bodybuilding treadmill test. Examples include identifying exactly what part of the heart is responsible for quantifying the number of muscles infected.
(IV) Radio-Nuclide imaging
This procedure uses the imaging techniques and computerized analysis to plot and detect the passage of radioactive tracers through the heart region. The tracing is generally given intravenously. This imaging process is important for diagnosing and determining the following:
- The severity of unstable angina when cheaper diagnostic approaches are unreliable or unavailable
- The severity of the coronary artery disease
- The progress of surgery for coronary artery disease
- To detect whether there is any heart attack that occurred
Blood flow imaging test is also referred to as thallium stress test and is typically used together with the exercise test to determine the flow of blood to the heart muscles. This test is usually a reliable measure of severe heart events and can be used to determine the angiography need if the CT scan identifies calcification in the arteries. A minute before the patient stops the exercise; the doctor may administer a radioactive tracer in the intravenous line (Gencer et al., 2010). Then, the patient lies down to have a heart scan. Damages from a prior heart attack always persist when the scan is done repeatedly, but the injuries caused by angina will have been solved by that time.
Psychosocial Ramifications of Coronary Artery Disease
Study shows that CAD is among the leading causes of death in the world, killing more than 8 million patients every year. It was initially thought that this medical condition was one of the lifestyle diseases of the industrialized nations. However, CAD is increasing rapidly in the developing countries as well. As the world population continues to increase, the deaths attributed to CAD are also estimated to increase.
Due to the social, psychological, economic and financial burden the disease imposes on the society and patients, greater interest arise to suggest for methods of reducing its prevalence. Therefore, many researchers are attempting to discover methods of lowering the risk factors. Research shows that some of the risk factors related to particular mechanisms while others are not. Among the best established Coronary Artery Disease risk factors, there are biological, demographic, and character related including older ages, family history, gender, use of abusive drugs like smoking, personal history of the cardiovascular diseases, high blood pressure and blood cholesterol, obesity, physical inactivity, and excessive intake of alcohol (Raab, 1969).
A growing research body has established the negative psychological factors associated with the disease like hostility, depression, and anxiety as major causes of increased cardiovascular events. A person’s psychology figures a lot in the success of any medical intervention that influences the motivation to seek help and abide by the medical regime. The focus of this review counts on the intervention that targets psychological health care and psychological risk factors. Therefore, it reviews in greater details the aspect of smoking cessation, dieting programs, and exercise. Interventions targeting depression reduction have quite a significant impact on the occurrence or non-occurrence of cardiovascular activities among the patients.
In conclusion, psychological treatments appear to be more effective in treating psychosocial symptoms of CAD patients. However, there remains a subgroup of patients who regard medical treatment as the most beneficial to them other than the psychological interventions.
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