Risk Factors And Treatment Options For CHD Biology Essay

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Coronary heart disease (CHD) was found to be due to plaque build up inside the coronary arteries restricting and or completely obstruct the blood flow to the heart. Some of the clinical manifestations of CHD are myocardial infarction, stroke and angina. Lipid abnormalities, hypertension, obesity, smoking, and family history of cardiovascular disease have been identified as the main risk factors involved in CHD. Statins, ACE inhibitors, aspirin, beta blockers, calcium channel blockers and nitrates are the mainstream pharmacological therapy in CHD. Coronary artery revascularization procedures such as PCI and GABG were used to correct morphological defects due to CHD. However, CABG was more effective and preferred than PCI as it often requires repeat procedures due to recurrent restenosis.

Introduction

Coronary heart disease (CHD), also known as coronary artery disease (CAD), is a disorder of the coronary arteries. These arteries of the heart are the main blood vessels that surround the heart and provide oxygen and nutrients to the heart muscles (Azen, 1996). CHD is almost always due to atheroma (fatty deposit in the blood vessel) and its complications, particularly thrombosis (formation or presence of a blood clot within a blood vessel).

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The aim of this research paper is to briefly discuss various aspects of CHD such as the epidemiology, aetiology, clinical manifestations, risk factors and current pharmacological, surgical and non-pharmacological treatments.

Epidemiology

In Australia CHD is associated with the highest mortality rate when compared to other diseases and in 2006, CHD claimed 22,983 life (this was 17% of all deaths) (Australian institute of health and welfare, 2006). Together with stroke and vascular diseases in a group, CHD kills more Australians than any other disease group. Around 3.6 million Australians are affected by and vascular diseases, and CHD is expected to increase proportionally as more Australian become over weight. Worldwide similar figures are emerging with 13.7 million people in the US States having CHD. In the UK 1.3 million people have angina and an estimated 330 000 people have a heart attack each year due to CHD (Morris et al, 2001).

However there has been a sharp decline in mortality rate from CHD since the 1970s. Age-standardised CHD mortality rates fell by 45% in males and 44% in females between 1996 and 2006. CHD is more common in the elderly, 7.5% of Australians aged 55-64 years have CHD increasing to 20.3% for those aged 75 years or over (Australian institute of health and welfare, 2006).

Etiology

The word atherosclerosis is of Greek origin and literally means focal accumulation of lipid and thickening of arterial intima. The exact pathogenesis of CHD is not clear, and no single theory adequately explains the atherosclerotic process. Two main explanations have been proposed: the lipid hypothesis and the chronic endothelial injury hypothesis. These explanations are interrelated and are certainly not mutually exclusive (Ross & Fuster, 1996).

The lipid hypothesis states that elevation in lipid plasma levels promotes lipid penetration of arterial walls. In general, it is considered that this process is instigated by abnormal lipid metabolism or excessive dietary intake of cholesterol and saturated fats, particularly when coupled with a genetic predisposition (Davies, 1996). Low-density lipoproteins (LDLs) are the primary atherogenic lipid, whereas high-density lipoproteins (HDLs) have a protective effect and probably help mobilize LDLs (Davies, 1996).

When LDLs undergo oxidation in the body, they become harder to mobilize and locally cytotoxic. The development of arterial atherosclerosis may occur when deposits of cholesterol and plaque accumulate at a tear in the inner lining of an artery. As the deposits harden and occlude the arterial lumen, blood flow to distant tissues decreases and a clot may become lodged, completely blocking the artery (Ross, 1999).

The initial step in the formation of atherosclerosis is a weakening of the arterial glycosaminoglycans (GAGs) layer. GAGs protect the internal lining of the artery and promote its repair. The exposed endothelial cells of the artery are subject to free-radical damage, and damage to the endothelial lining makes those sites more permeable to plasma constituents, particularly lipoproteins (Ross, 1999).

In response to cell injury, macrophages migrate from circulation into the cells that line the inside of the artery. Ultimately as this process continues, smooth muscle cells of the intima join connective tissue and intracellular and extracellular lipids to form fibrous plaque (Ross, 1999). Adhesion and aggregation of platelets and release of various growth factors further supplement the fibrotic process, resulting in occlusion of the blood vessel lumen and potential for plaque disruption and thrombus formation.

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Repeated plaque ruptures, not resulting in total lumen closure, combined with the clot patch over the rupture and healing response to stabilize the clot, is the process that produces most stenoses over time (Ross, 1999). The stenotic areas tend to become more stable, despite increased flow velocities at these narrowings. Most major blood-flow-stopping events occur at large plaques, which, prior to their rupture, produced very little if any stenosis (Ross, 1999).

If the fibrous cap separating a soft atheroma from the bloodstream within the artery ruptures, tissue fragments are exposed and released, and blood enters the atheroma within the wall and sometimes results in a sudden expansion of the atheroma size (Ross, 1999). Tissue fragments are very clot-promoting, containing collagen and tissue factor; they activate platelets and activate the coagulation system (Ross, 1999). This result is the formation of a thrombus overlying the atheroma, which obstructs blood flow acutely, resulting in angina or myocardial infarction (Ross, 1999).

Risk factors

Extensive clinical and statistical studies have identified several factors that increase the risk of CHD. There are two categories of risk factors:

1 - Major risk factors are those that research has shown to significantly increase the risk of heart and blood vessel (cardiovascular) disease. This includes increasing in age, gender (males have greater risk or heart attack than women) and heredity (history of parents with CHD) (Pencina, 2009).

2 - Contributing risk factors are associated with increased risk of cardiovascular disease, but their significance and prevalence have not yet been precisely determined. Tobacco smoking increases the mortality rate from CHD by 2â€"3 folds that of nonsmokers (Pencina, 2009). Other contributing factors include: dislipidemia, hypertension, physical inactivity, obesity, diabetes mellitus and to some extent stress and alcohol consumption. These can be can by managed by appropriate pharmacological and non pharmacological treatments (Pencina, 2009), results in significant reduction in severity of CHD.

Treatment options

The treatment goals for patients with coronary artery atherosclerosis are to relieve symptoms and to prevent future cardiac events such as unstable angina, AMI, and death. The mainstays of pharmacologic therapy of angina include nitrates, beta-blockers, statins and calcium channel blockers all of which are discussed below.

The statins are a class of drug used to lower plasma cholesterol level. They lower cholesterol by inhibiting the enzyme HMG-CoA reductase, which is the rate-limiting enzyme of the mevalonate pathway of cholesterol synthesis (Hegele, 2000). Inhibition of this enzyme in the liver results in decreased cholesterol synthesis as well as increased synthesis of LDL receptors, resulting in an increased clearance of low-density lipoprotein (LDL) from the bloodstream (Hegele, 2000). These agents decrease the number of cardiovascular events by slowing the progression of atherosclerosis, stopping new lesion development, stabilizing the existing plaques, and reducing inflammation of coronary plaques.

Early angiographic studies of statin therapy demonstrated reduced progression of coronary disease in proportion to average low-density lipoprotein (LDL) cholesterol levels. Recently Hegele, 2002, researched the effect of Rosuvastatin on Intravascular Ultrasound-Derived Coronary Atheroma Burden (ASTEROID)(Hegele, 2000) evaluated the effect of intensive treatment with rosuvastatin for 24 months on the course of coronary atherosclerosis (Hegele, 2000). The research demonstrated a significant reduction in mean LDL cholesterol and increase in mean HDL cholesterol (Hegele, 2000). Quantitative coronary angiography showed significant net improvement in percent diameter stenosis and minimum lumen diameter of the stenoses, as well as a decrease in atheroma volume (Hegele, 2000).

In a comprehensive meta-analysis of 5 major statin trials totaling more than 30,000 subjects provides indisputable evidence of the effectiveness of statins in a variety of patient subgroups over a 5- to 6-year follow-up period. On average, statin therapy produced a 20% reduction in total cholesterol levels, a 28% reduction in LDL levels, and a 13% reduction in triglyceride levels, along with a 5% rise in HDL levels (Hegele, 2000).

Hegele 2000 suggested that the number of coronary events and coronary deaths was reduced by 31% and 29%, respectively. The total mortality rate was decreased by 21%, and cardiovascular mortality was decreased by 27%. Rate reductions of cardiovascular events were similar between males and females and in persons older than 65 years and those younger than 65 years.

The efficacy of ACE inhibitors on CHD has been examined in blood pressure reduction studies and in studies of subjects with high-risk factors for CHD. In a study carried by the Heart Outcomes Prevention Evaluation (HOPE) (Pitt et al, 2001), which included 9297 subjects with history of CHD, stroke, peripheral vascular disease, or diabetes, along with one other CHD risk factor (eg, hypertension, hypercholesterolemia, hypoalphalipoproteinemia, tobacco abuse, microalbuminuria). Subjects were randomized to placebo or ramipril (10 mg/d). At 5-year follow-up, the cardiac death rate was reduced by 25%, nonfatal myocardial infarction (MI) by 20%, need for bypass surgery by 16%, and all-cause mortality by 16% (Mancini, 1996). The effects were unrelated to the blood pressureâ€"lowering effect.

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Mehta et al 2000, compared the use of aspirin alone to extended dual-antiplatelet therapy with aspirin and clopidogrel for up to 12 months in patients after hospitalization with acute coronary syndrome (ACS). Regardless of the initial treatment strategy (medical therapy, PCI, or CABG), recurrent events reduced 20% at 1 year in the patients treated with both aspirin and clopidogrel. However, in the CHARISMA trial, a strategy of prolonged dual antiplatelet therapy with aspirin and clopidogrel did not significantly reduce recurrent events in patients with stable cardiovascular disease or asymptomatic patients at high-risk for cardiovascular events.

The main goals of treatment in angina pectoris are relief of symptoms, slowing progression of the disease, and reduction of future events, especially heart attacks and, of course, death. Beta blockers (propranolol, atenolol) have a large body of evidence in morbidity and mortality benefits and short-acting nitroglycerin medications have been used since 1879 for symptomatic relief of angina.

Surgical treatments

A coronary artery revascularization procedure is aimed to reduce cardiac workload, improve coronary artery blood flow, and, over the long term, halt and reverse the atherosclerotic process. Coronary blood flow can be improved by percutaneous coronary intervention (PCI) or coronary artery bypass grafting (CABG).

PCI is carried out by the inflation of a balloon within the coronary artery to crush the plaque into the walls of the artery. While balloon angioplasty is still done as a part of nearly all percutaneous coronary interventions, it is rarely the only procedure performed (Boden, 2000). Insertion of a bare-metal stent following angioplasty reduced the rate of restenosis, but many patients still required repeat treatment. Drug-eluting stents, which secrete an antiproliferative drug (eg, sirolimus) over a period of several weeks, have reduced the rate of restenosis to about 10% (Boden, 2000). Now, most PCI is done with stents, and about three fourths of all stents used in the US are drug-eluting stents. Patients with acute stenoses (ie, with unstable angina or acute MI) seem to do better with bare-metal stents. Patients without significant infarct or complication may quickly return to work and usual activities, but strenuous activities should be avoided for 6 weeks (Hlatky et al, 2009).

CABG uses sections of autologous veins (eg, saphenous) or, preferably, arteries (eg, internal mammary, radial) to bypass diseased segments. CABG is typically done during cardiopulmonary bypass with the heart stopped; a bypass machine pumps and oxygenates blood. Risks of the procedure include stroke and MI. For patients with a normal-sized heart, no history of MI, good ventricular function, and no additional risk factors, risk is < 5% for perioperative MI, 2 to 3% for stroke, and ≤ 1% for mortality; risk increases with age and presence of underlying disease. Operative mortality rate is 3 to 5 times higher for a second bypass than for the first; thus, timing of the first bypass should be optimal. Overall risk of PCI is comparable with that for CABG. Mortality rate is 1 to 3%; MI rate is 3 to 5%. In < 3%, initial dissection causes obstruction requiring emergency CABG (Hlatky et al, 2009).

Reversing the modifiable risk factors is usually the first step in prevention of CHD (this is sometimes referred to as therapeutic lifestyle changes (TLC)). This includes smoking cessation and dietary modification. In addition, a Western medical approach may often address the patient's stress management and exercise habits. Treatment is also directed at the coexisting conditions that are associated with increased risk for CHD. These include hypercholesterolemia, hypertension, and hypothyroidism.

Conclusion

CHD is a combination of both lipid and inflammatory processes. Lipid abnormalities, hypertension, obesity, smoking, and family history are all risk factors in CHD. Treatment generally aims to reduce cardiac workload and improve coronary artery blood flow. A combination of both pharmacological and lifestyle changes are necessary to manage and prevent of CHD. Coronary artery revascularization should only be considered if both pharmacological and lifestyle modifications have been tried. The choice of treatment varies from patient to patient depending on their age, comorbidities, preferences and financial status.