Secondary Prevention in Coronary Heart Disease - Essay Example

TOPIC: Secondary Prevention in Coronary Heart Disease (CHD) I. Introduction Coronary heart disease (CHD), otherwise known as the coronary artery disease (CAD), is defined as the narrowing of minute blood vessel supplying the heart with blood and oxygen (Kang, 2010). In Great Britain, CHD is considered to be the second most reported longstanding illness in the year 2006 (British Heart Foundation Statistics Website, 2010). The National Health Service in England (2009) noted that CHD is the leading killer in the UK with mortality ratio of 1:4 in men and 1:6 in women and about 300,000 individuals suffers from heart attack annually. A health survey done in England in 2006 suggests that the prevalence of CHD in men was 6.5 percent and in women was only 4 percent; however, these rates are increasing with age (British Heart Foundation Statistics Website, 2010). In Scotland, the prevalence of CHD is much higher with percentage rate of 4.6 than the 4.3 percent reported cases in Wales and 3.5 percent in England (British Heart Foundation Statistics Website, 2010). From the aforementioned data, it can be observed that the variation of prevalence of CHD is wide within the United Kingdom. On the other hand, the prevalence of CHD in England alone ranges from 2.3 percent in London to 4.9 in North East of England. In Scotland only, the prevalence rate of CHD is higher compared to that in England where 3.9 percent cases were observed in Lothian and Orkney and 8.4 percent in Shetland (British Heart Foundation Statistics Website, 2010). The National Institute for Health and Clinical Excellence (2007) noted that death rate from CHD in the UK is more than 103,000 deaths per year and considered to be one of the highest in Europe, and this rate varies with age, gender, socio – economic status, ethnicity and geographic location in the UK. Scottish Intercollegiate Guidelines Network (2007) and the British Heart Foundation (2008) noted that various types of aetiology with a number of potentially modifiable risk factors are identified with cardiovascular diseases. These are: (1) Sex – male in their forties are more risk of acquiring CHD; however, when women reaches their menopausal stage, they became more at risk in acquiring CHD than men (2) Genes – having history of CHD in the family (3) Diabetes (4) Hypertension (5) Abnormal level of cholesterol Metabolic syndrome (6) Smokers (7) Chronic disease in the kidney (8) Atherosclerosis (9) Alcoholism (10) Stress (11) Lack of exercise Among the aforementioned risk factors of acquiring CHD and peripheral vascular disease, smoking is believed to be the principal risk factor causing it. During the increasing myocardial demand, smoking have shown to be associated with impaired coronary blood flow responses, and in patients having coronary artery diseases, smoking is noted to contribute to myocardial ischemia. II. Pathophysiology of Coronary Heart Disease Libby and Theroux (2005) and Leon 2009 stated that atherogenesis, which is considered to be the most important cause and the underlying foundation of coronary heart disease, is a complex relationship of diverse risk factors involving the arterial wall in addition to blood and molecular message interface. Atherosclerosis, a chronic inflammatory condition, also involves the coronary’s subendothelial layer as well as the large and medium sized arteries (Leon, 2009). Leon added that multiple risk factors have initiated this disease process during the early stage in life. The most popular explanation of CHD development lies on the major role of inflammation in the entire phases of atherogenesis including its participation in the complications of atherogenesis in the local, myocardial, and systemic area (Libby and Theroux, 2005). Leon (2009) noted that endothelial dysfunction and infiltration of lipid are fundamental in the atherosclerotic process’ initiation and progression. Coronary occlusion caused by thrombosis that is initiated by disruption of a vulnerable lipid – laden plaque in a thin, noncalcified fibrosis cap triggers acute coronary syndromes after many asymptomatic decades. Libby and Theroux (2005) explained that during atherogenesis, the arterial endothelium encounters products of bacteria and the glycoxidation products associated with hyperglycemia or excess adipose tissue’s proinflammatory cytokines augmenting adhesion of molecular expression that promotes the blood leukocytes to stick to the arterial wall’s inner surface. The expression of chemoattractant cytokines regulated by signals associated with risk factors of atherosclerosis determines the transmigration of the adherent leukocytes (Libby and Theroux, 2005). Libby and Theroux added that once the mononuclear phagocytes and T lymphocytes are within the intima of the artery, they communicate with arterial walls’ endogenous cells including the endothelial and smooth muscle cells. Atherogenesis depends on the exchange of the major messages of the mediators’ inflammation and immunity. These include the prostanoids, leukotrienes, histamine, and cytokines that regulate classically the vascular tone and increases vascular permeability (Libby and Theroux, 2005). Libby and Theroux (2005) noted that in the early phase of atheroma, the smooth muscle cells migrate from tunica media to intima as a principal consequence of inflammatory turmoil and at the extracellular matrix, they proliferate and elaborate. In response to various oxidative, hemodynamic, inflammatory, and autoimmune signals, the aforementioned cells secrete matrix metalloproteinases in concert with the endothelial cells and monocytes (Libby and Theroux, 2005). Numerous functions of vascular cells are modulated by these metalloproteinases, including the activation, proliferation, migration, and cell death. Certain constituents of the extracellular matrix bind to lipoproteins delaying them at the intima (Libby and Theroux, 2005). This process subsequently renders them susceptible to oxidative modification and glycation, and the products of alteration of lipoprotein sustain and propagate the responses to inflammation (Libby and Theroux, 2005). Calcification occurs as the lesion progresses, and cell death will commonly occur in addition to proliferation in a well established atherosclerotic lesion. The extracellular tissue factor deposition that results from the death of lipid – laden macrophages accumulates in the intima, coalesce, and form the lipid – rich necrotic core (Libby and Theroux, 2005). National Heart Service in England (2009) and Women’s Health Concern, UK (2007) further explains that CHD happens when fatty substances are built up in the coronary arteries resulting to blockage or interruption of the coronary blood supply. During the passage of time, fatty deposits fill up the arterial wall, and the build up of fatty deposits narrows the coronary arteries restricting the blood supply to the heart causing chest pains or angina pectoris (National Heart Service in England, 2009). Subsequently, heart attack or myocardial infarction results from complete blockade of coronary artery. This event can be reduced by making simple changes in our lifestyle (National Heart Service in England, 2009). III. Psychological Impact of Coronary Heart Disease In a variety of patients, having been diagnosed with cardiovascular heart disease can be a terrifying incident, and brings about several outcomes in their psychological well – being and social life (Donders, 2004). For this reason, Donders made a suggestion that it is essential to offer not only medical assistance to these patients, but psychological help as well. Donders further elaborated that having these ill feeling towards these ailment poses the patient to a much greater risk of recurring cardiovascular disease. To help these patients from suffering this outcome, it is essential that people diagnosed with coronary heart disease should also socialise with someone who are in the same type of situation for them to build a strong support group (Leon, et al., 2005). Thirty percent of these patients experience depression. Additionally, a moderate to severe level of anxiety is experienced by approximately 50 percent of patients who just had myocardial infarction. To optimise the patient’s well – being and to provide the context for adherence to medical regimen, the emotional impact of myocardial infarction must be addressed for maximum recovery (Leon, et al., 2005). IV. Secondary Preventions of Coronary Heart Disease To effectively reduce the rate of morbidity and mortality resulting from coronary heart disease, secondary preventive measures such as prophylactic drug therapy, anti – platelet agents, beta – blockers, statins, and ACE inhibitors are necessary (McLeod, Brooks, and Taylor, 2004 and Murchie, 2003). Changes in lifestyle and controlling the risk factors that include cessation in smoking, modification in the diet, and reduction of weight are also necessary to prevent coronary heart disease (McLeod, Brooks, and Taylor, 2004 and Murchie, 2003). The main priority of the National Service Framework is the identification of factors causing coronary heart disease and future provision of healthcare (McLeod, Brooks, and Taylor, 2004 and Murchie, 2003). (1) Lifestyle Management and Changes To achieve potential health gains, lifestyle modification must play an important role and should be achieved by patients (Kromhout, et al., 2002). Lifestyle modification plays a critical role in preventing coronary heart disease (Maruthur, et al., 2009). Hence, the following recommendations on lifestyle modification are formulated in accordance with the European Society of Cardiology on Prevention of Coronary Heart Disease in Clinical Practice task force report, the American Heart Association dietary guidelines, World Health Organisation, and the National Cholesterol Education Program. These include cessation from smoking tobacco, to use alcohol only in moderation, reduction of salt in the diet, and exercise at least 30 minutes a day. Dietary recommendations that are important includes keeping a balanced energy by consuming energy from saturated fat amounting to only Read More