Coronary Artery Disease Is Epidemic within Western Cultures - Essay Example

Coronary Artery Disease is Epidemic within Western Cultures Introduction: This is the story of a 60-year-old man diagnosed with severe coronary artery disease, which is the typical picture of older men of the Western world. They live a life of their own style at its full spirit, but eventually develop this disease in the coronary arteries leading to suffering, loss of quality of life, morbidity, and even death. With rapid globalization, in many parts of the world, this is increasingly becoming the typical picture, and this disease is the most prevalent serious disease in elderly individuals of the developed Western nations. Therefore, in this context, it would be worthwhile to examine how this disease develops and how it manifests itself. If there is any link available between the pathological process and the alteration of the normal physiology of the heart, based on evidence of the life styles of these individuals, some directives may be deduced to lessen the risk of development of this disease. Anatomy of an Artery: Coronary artery disease involves these arteries, but to be able to understand what exactly happens there, it is important to understand their microscopic anatomy. The walls of these arteries are made up of three layers, an inner coat of tunica media which mainly is comprised of smooth muscle tissues and an outer coat of tough fibrous tissue, tunica externa or adventitia. The most important layer in terms of pathogenesis of coronary artery disease is tunica intima, which consists of flat endothelial cells (Tortora and Grabowski, 2003, Chap 21). Physiology of Cardiovascular System: The primary function of the heart is to circulate blood through the body. It does this by acting as a mechanical pump. The walls of the heart are composed primarily of cardiac muscle cells and are called myocardium. The inner surfaces of the walls that enclose the cardiac chambers and are in contact with the blood within the cardiac chambers are known as endocardium. The blood being pumped through the heart chambers does not exchange nutrients and metabolic end products with the myocardial cells. They, like the cells of all other organs, receive their blood supply via arteries that branch from the aorta. The arteries supplying the myocardium are the coronary arteries, and the blood flowing through them is termed the coronary blood flow. The coronary circulation must deliver O2 at a rate that keeps pace with cardiac demand. Under resting conditions, blood flow to the heart is about 70 mL/min per 100 g, and it increases five- to six-fold during maximal cardiac work. Myocardial O2 consumption is also very high at rest, which is 20 times the resting value in skeletal muscles, and it increases about fivefold during maximal cardiac work. The relevant important physiology is that blood flow to the heart is governed almost entirely by intrinsic factors. The rate of O2 use by the myocardium is proportional to cardiac work; hence, factors such as systolic pressure or afterload, heart rate, and stroke volume, all influence myocardial O2 consumption. As cardiac work increases due to any reason, the elevated metabolic activity results in dilation of the coronary arterioles, thus increasing blood flow to heart muscle. This phenomenon is known as active hyperemia. Other than this, the coronary vasculature normally exhibits excellent pressure flow autoregulation. Moreover, the average blood flow over the entire cardiac cycle is uniformly distributed across the wall of the left ventricle. Although the intrinsic mechanisms are too slow to keep blood flow constant through the cardiac cycle, they can adjust flow so that the average flow meets the metabolic needs of the myocardium. There is a compensatory mechanism to meet this blood deficit so that the arterioles supplying the inner layers remain more dilated during the systole and these layers receive extra blood during diastole to perfuse them. This compensatory response diminishes the dilatory reserve of the inner muscle layers and, as a result, the subendocardium is always the most vulnerable to ischemia whenever the coronary arteries are obstructed, as occurs in coronary artery disease (Tortora and Grabowski, 2003, Chap 20). Coronary Artery Disease Epidemiology: Coronary artery disease is prevalent in the United Kingdom; it is the most common cause of death and premature death, amounting to 1 in 5 men and 1 in 6 women. According to recent data, about 101,000 people die each year. Thus, this 60-year-old man is at risk of death due to his coronary artery disease. There are certain lifestyle risk factors associated with coronary artery disease and, currently, death rates under the age of 55 have fallen by 46%, although not as much as in other countries. This has been attributed to lifestyle associated risk factor modification, such as a decline in smoking or dietary control. Moreover, other contributory factors are: better understanding of the disease, better available treatment in terms of both drugs and surgery, and secondary prevention. Most commonly these deaths occur in the winter seasons. Moderate to severe coronary artery disease usually leads to myocardial infarction and angina with incidence of 600 per 100,000 men in the age group of 30 to 69 and 200 per 100,000 women with increase in incidence with age. As in this individual, heart attack resulting from coronary artery disease occurs more with increasing age in men, although a larger number of people of both sexes suffer from angina, which results from reversible ischemia of the cardiac muscle. Prevalence of the disease is currently 7.4% in men and 4.5% women, with the highest findings being in Scotland and the lowest in England, with the lower socioeconomic groups showing higher evidence of disease (British Heart Foundation Statistics Database, 2007). Therefore, this individual represents almost an epidemiologic model of patients with coronary artery disease. Currently, the mortality is falling but the morbidity associated with coronary artery disease is increasing. The direct healthcare costs and productivity losses due to this disease is about 7.9 billion. In this man, the other risk factors that might be associated with his coronary artery disease could be looked into. Epidemiologic studies identify them to be increasing age, male gender, social deprivation, low socioeconomic status, smoking, poor nutrition in the form of diet containing high fat, high sodium, low fibres and fruits, and low polyunsaturated fatty acid (PUFA). Moreover, other factors that increase the already heightened risk are infrequent exercise and sedentary habits, stress and anxiety, alcohol, smoking, diabetes, high blood pressure, overweight and obesity, family history, and dyslipidaemia (Guilbert, 2003, 230). Aetiology: Except for age, dyslipidemia is the most important predictive factor for coronary artery disease. Aetiologically, there is a strong, independent, continuous, and graded relationship between total cholesterol (TC) levels, or low-density lipoprotein (LDL)-cholesterol (C) level and the risk of CAD events. Even within a given arterial bed, atherosclerosis tends to occur focally, typically in certain predisposed regions. In the coronary circulation, for example, the proximal left anterior descending coronary artery exhibits a particular predilection for developing atherosclerotic occlusive disease. Atherogenic dyslipidaemia is an integral component of metabolic syndrome and is a major contributor to the cardiovascular risks in these patients. It was demonstrated that addition of dyslipidemia to the presence of diabetes or hypertension results in an increased risk of myocardial infarction by nineteen-fold. It is also important to note that an abnormal lipid profile was found to be a more significant risk factor than either hypertension or diabetes alone. The typical lipid abnormalities defined in patients with metabolic syndrome consist of a three factors: increased triglycerides, decreased high density lipoprotein cholesterol (HDL), and increased concentrations of small, dense, low density lipoprotein-cholesterol (LDL) (Mozaffarian et al., 2006, 1601-1613). Pathogenesis: The basic lesion in the arteries is development of fatty streak. The formation of these early lesions of atherosclerosis most often seems to arise from focal increases in the content of lipoproteins within regions of the intima. This accumulation of lipoprotein particles may not result simply from an increased permeability, or "leakiness," of the overlying endothelium. Rather, these lipoproteins may collect in the intima of arteries because they bind to constituents of the extracellular matrix, increasing the residence time of the lipid-rich particles within the arterial wall. Lipoproteins that accumulate in the extracellular space of the intima of arteries often associate with proteoglycan molecules of the arterial extracellular matrix, an interaction that may promote the retention of lipoprotein particles by binding them and slowing their egress from the intima. In dyslipidaemia, there is an increased influx of free fatty acids into the liver, the consequences of which are an increase in hepatic production and release of very low density lipoproteins (VLDL) and triglycerides associated with decreased clearance of these substances, resulting in increase in VLDL and triglycerides levels. Transportation of cholesterol and triglyceride ester between HDL, LDL, and VLDL leads to formation of triglyceride-rich LDL and HDL particles, which become the preferred substrate for hepatic triglyceride lipase (Levy, 1986, 18-22). Due to the lack of hepatic lipase, there is poor clearance of small, dense particles of LDL-cholesterol, which are more atherogenic and have higher susceptibility to oxidation. Elevated levels of triglyceride-rich lipoproteins lower HDL-cholesterol by inducing cholesterol exchange from HDL to VLDL via cholesteryl-ester transfer protein. A high proportion of small, dense LDL particles have been classified as an LDL subclass B, which gets deposited over time between the media and intima of the arterial wall. Lipoproteins sequestered from plasma antioxidants in the extracellular space of the intima become susceptible to oxidative modification (Kuo, 1994, 519-527). Oxidatively modified low-density lipoprotein (LDL), rather than being a defined homogenous entity, actually comprises a variable and incompletely defined mixture. After the accumulation of extracellular lipid, recruitment of leukocytes occurs as a second step in the formation of the fatty streak. Laminar shear forces, such as those encountered in most regions of normal arteries, can also suppress the expression of leukocyte adhesion molecules. Sites of predilection for forming atherosclerotic lesions often have disturbed laminar flow. Once adherent to the surface of the arterial endothelial cell via interaction with adhesion receptors, the monocytes and lymphocytes penetrate the endothelial layer and take up residence in the intima. Once resident within the intima, the mononuclear phagocytes differentiate into macrophages and transform into lipid-laden foam cells. In addition to locally produced mediators, atherogenic risk factor signals related to blood coagulation and thrombosis likely contribute to atheroma evolution and complication. Current evidence suggests that fatty streak formation begins underneath a morphologically intact endothelium. In advanced fatty streaks, however, microscopic breaches in endothelial integrity may occur. Microthrombi, rich in platelets, can form at such sites of limited endothelial denudation, due to exposure of the highly thrombogenic extracellular matrix of underlying basement membrane. The result clinically may be appreciable by development of acute coronary syndrome in this individual leading to plaque disruption, thrombotic occlusion of the arterial lumen leading to acute reduction of blood supply to the muscles of the heart (Fuster et al., 1992, 242-250). Signs and Symptoms: The typical patient with angina is a man >50 years or a woman >60 years. This man would, in a possible attack, complain of chest discomfort, usually described as heaviness, pressure, squeezing, smothering, or choking and only rarely as frank pain. When the patient is asked to localize the sensation, he or she will typically press on the sternum, sometimes with a clenched fist, to indicate a squeezing, central, substernal discomfort. Angina is usually crescendo-decrescendo in nature, typically lasts 2 to 5 min, and can radiate to the left shoulder and to both arms, especially to the ulnar surfaces of the forearm and hand. It can also arise in or radiate to the back, interscapular region, root of the neck, jaw, teeth, and epigastrium. Angina is rarely localized below the umbilicus or above the mandible. Although episodes of angina are typically caused by exertion such as, exercise, hurrying, or sexual activity or emotion such as, stress, anger, fright, or frustration and are relieved by rest, they may also occur at rest, which is called unstable angina. The patient may be awakened at night distressed by typical chest discomfort and dyspnoea. Nocturnal angina may be due to episodic tachycardia or to the expansion of the intrathoracic blood volume that occurs with recumbency; the latter causes an increase in cardiac size and myocardial oxygen demand that lead to ischemia and transient left ventricular failure. The threshold for the development of angina pectoris may vary by time of day and emotional state. Many patients report a fixed threshold for angina, which occurs predictably at a certain level of activity, such as climbing two flights of stairs at a normal pace. In these patients coronary stenosis and myocardial oxygen supply are fixed and ischemia is precipitated by an increase in myocardial oxygen demand. Angina may also be precipitated by unfamiliar tasks, a heavy meal, exposure to cold, or a combination. Exertional angina is typically relieved by rest in 1 to 5 min and even more rapidly by rest and sublingual nitroglycerin. Examination of the fundi may reveal increased light reflexes and arteriovenous nicking as evidence of hypertension. There may also be signs of anemia, thyroid disease, and nicotine stains on the fingertips from cigarette smoking. Palpation may reveal cardiac enlargement and abnormal contraction of the cardiac impulse. Auscultation can uncover arterial bruits, a third and/or fourth heart sound, and, if acute ischemia or previous infarction has impaired papillary muscle function, an apical systolic murmur due to mitral regurgitation (Bugiardini and Merz, 2005, 477-484). Heart Failure: The principal prognostic indicators in patients known to have CAD are age, the functional state of the left ventricle, the locations and severity of coronary artery narrowing, and the severity or activity of myocardial ischemia. On cardiac catheterization, elevations of left ventricular end-diastolic pressure and ventricular volume and reduced ejection fraction are the most important signs of left ventricular dysfunction and are associated with a poor prognosis. Patients with chest discomfort but normal left ventricular function and normal coronary arteries have an excellent prognosis. In patients with normal left ventricular function and mild angina but with critical stenoses even have low mortalities. Obstructive lesions of the left anterior descending coronary artery proximal to the origin of the first septal artery are associated with a greater risk since it usually perfuses a greater quantity of myocardium (Fox et al., 2001, 228-236). With any degree of obstructive CAD, mortality is greatly increased when left ventricular function is impaired; conversely, at any level of left ventricular function, the prognosis is influenced importantly by the quantity of myocardium perfused by critically obstructed vessels. Therefore, it is useful to collect all the evidence substantiating past myocardial damage leading to left ventricular failure with decreased residual ventricular function. The larger the quantity of established myocardial necrosis, the less the heart is able to withstand additional damage and the poorer the ventricular function and more the heart failure (McMurray and Pfeffer, 2005, 1877-1899). A postmyocardial damage heart failure due to coronary artery disease usually presents with episodes of pulmonary edema, transient third heart sounds, or mitral regurgitation, and echocardiographic or radioisotopic or roentgenographic evidence of cardiac enlargement and reduced ( Read More