Coronary Heart Disease (CHD) is the largest single cause of death in Australia. It is a condition caused by the narrowing of epicardial blood vessels, mainly due to atherosclerosis, leading to ischaemia of cardiac tissue, and subsequently angina, myocardial infarction, or death. CHD may manifest in a number of ways, including stable angina, Prinzmetal's angina, and acute myocardial infarction, and signs include chest pain or discomfort which radiates to the arms, neck, back, jaw and teeth. Pharmacological treatment generally involves the use of Î²-blockers, organic nitrates, Ca2+ receptor blockers, ACE inhibitors, antiplatelet drugs, and statins/fibrates. Non pharmacological treatments include the modification of risk factors and surgical interventions.
CHD is a condition affecting millions of people globally, and which causes an enormous burden on the health care systems of nations around the world.1 It is a condition characterized by the narrowing of the coronary arteries supplying cardiac tissue.2 This impairs the supply of oxygen to these tissues, which may lead to ischaemia, and ultimately to the death of myocardial cells.2 There are a number of therapeutic alternatives available for treatment of the condition, and these drugs work to decrease the workload, and thus oxygen requirements of the heart, improve blood flow and thus oxygen supply to the cardiac tissue, reduce serum cholesterol levels, and also to reduce the levels of platelet aggregation and thus prevent thrombus formation.3 Overall, these medications act to slow the progression of CHD, and reduce the risk of an adverse event occurring. There are also a number of risk factors which may be modified to improve outcomes.
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CHD is a condition caused by the narrowing of epicardial blood vessels leading to ischaemia of cardiac tissue.2 In the most serious of cases, this can lead to an acute MI and ultimately death.2 There are a number of possible causes for the narrowing of the blood vessels, including atherosclerosis, thrombosis, and coronary vasospasm.2
Atherosclerosis of the coronary arteries is by far the most common cause of CHD.2 Atherosclerosis is a complex process involving hypercholesterolaemia and the subsequent accumulation of fatty material into formations known as plaques on the interior endothelial surface of the coronary arteries.2 As these plaques grow in size, they narrow the channel through which blood may flow, reducing the amount of blood and thus oxygen reaching cardiac tissue. Rupturing and embolism of the plaque may lead to the complete occlusion of the coronary blood vessels downstream of the affected area, and thus result in an acute myocardial infarction.4 In addition, rupture of the plaque exposing collagen and other connective tissues precipitates thrombus formation, which may rapidly narrow the blood vessel.4
Although it is not as common as atherosclerosis, thrombosis may also cause CHD. According to Virchow's Triad, a thrombus may form when there is an abnormality in the composition of the blood (hypercoagulability), the quality of the vessel wall (trauma), or the nature of the blood flow (turbulence).6 As with atherosclerosis, thrombus formation in the coronary arteries leads to partial occlusion of the blood vessels supplying cardiac tissue, and embolism may lead to an acute myocardial infarction. Another cause of CHD is coronary vasospasm or stenosis, the abnormal narrowing of a coronary artery due to vasoconstriction, which limits blood flow and oxygen reaching cardiac tissue.2
2.2 Clinical manifestations
The 2 major forms in which CHD may manifest itself include stable angina and acute myocardial infarction. Other manifestations include unstable and Prinzmetal's angina, dyspnoea, collapse on exertion, arrhythmias, acute or chronic heart failure, and sudden death. In some individuals, CHD is asymptomatic.2
Stable angina generally presents as discomfort in the form of tightness, squeezing, or heaviness in the chest, which may radiate to the arms, neck, back, jaws or teeth, with or without associated dyspnoea.2 The feeling of discomfort is sometimes mistaken for indigestion, and usually arises after a period of physical activity, particularly when climbing hills or stairs, and resolves after a few minutes with rest or with administration of glyceryl trinitrate.5
Unstable angina may occur whilst the individual is at rest or with minimal exertion, is generally more severe than stable angina, and also worsens with time.2 Unstable angina generally results from the rupture of an atherosclerotic plaque, resulting in a rapid narrowing of coronary arteries. If the underlying cause of the CHD is vasospasm of the coronary arteries, it may present in the patient as Prinzmetal's angina.2 This form of angina is similar to stable angina, but occurs in cycles and generally whilst the individual is at rest rather than with physical activity.5
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Perhaps the most important tool in the identification of CHD is the electrocardiogram (ECG). Individuals with CHD tend to have abnormal readings in the S-T region of the ECG, most notably ST elevation or depression.4 The presence of an ST elevation on an ECG correlates to an occluded artery, and when associated with the type of chest pain associated with ischaemia, usually indicates that there has been some level of myocardial damage. This diagnosis may be reinforced by the measurement of elevated troponin, cardiac proteins who are a strong marker of myocardial cell damage, levels in the serum.4 If this is the case, the individual has then suffered from a ST elevation MI (STEMI). A MI in which the ST segment is not elevated is also possible, and in this situation, the condition is known as non-ST elevation MI, or NSTEMI.4
In Australia, CHD is the largest single cause of death, with 26 063 deaths occurring in 2002 (19.5% of all deaths). During this year, CHD therefore constituted over half of all deaths from heart, stroke and vascular diseases. According to the national health survey carried out in 2001, 355 600 Australians (1.9% of the population) were suffering from the disease during this year, thus causing a great burden on Australia's health care system.1 It is predicted that by 2020 CHD will become the most widespread health condition in the world.1
The prevalence of CHD was one-third higher amongst males than females, with 2.4% of males suffering from the condition, and 1.6 precent of females.1 Overall, males were twice more likely than females to die from CHD.1 In the Aboriginal and Torres Strait Islander populations, death rates were 2.6 times greater than that in the wider community.1 The prevalence of CHD also increases dramatically with age, with 4.0% of 55-64-year olds, 8.2% of 65-74-year olds, and 13.1% of individuals aged 75 years and over suffering from the condition.1 This equates to almost 2/3 of individuals with CHD falling into the age group of over 65s.1 Overall, the incidence of CHD has been falling in the population over the last few decades, possibly due to better education and improved treatment options.1
2.4 Other factors
There are a number of other factors which may predispose individuals to developing CHD, including modifiable and non-modifiable risk factors. The major modifiable risk factors include serum cholesterol levels, alcohol intake, smoking, hypertension, and physical activity.4
An elevated serum cholesterol levels is a major factor predisposing individuals to develop atherosclerosis, the major cause of CHD.4 Smoking introduces free radicals which may react with LDL, impair myocardial oxygen delivery due to inhaled carbon monoxide, elevate heart rate and blood pressure due to nicotine, and increase platelet aggregation and therefore the formation of thrombi. Smoking therefore also accelerates the risk of MI.4 Non-modifiable risk factors are generally genetic in origin, and results in some individuals being naturally at risk of developing CHD.4
2.5 Treatment options
Î²-blockers, such as atenolol, act to decrease heart rate, contractility, and blood pressure, making the heart pump more efficiently and thus reducing the oxygen demand of cardiac tissue.5 The use of Î²-blockers is extremely useful in individuals who are predisposed to having attacks due to physical activity, as treatment allows for an increase in the amount of exercise an individual may undertake, and ultimately an improvement of cardiovascular performance due to this physical activity.2
As Î²-blockers also act to cause bronchospasm and peripheral vascular spasms, they are contraindicated in patients with asthma and must be used with caution in patients with chronic obstructive airway diseases, peripheral vascular disease, acute heart failure or bradycardia.2 The Î²-blockers most selective for cardiac tissue (atenolol, bisoprolol and metoprolol) are generally used to minimize the incidence of these side effects, but are still considered too non-selective, and remain contraindicated in these conditions.2 It has also been noted that the lipophilic Î²-blockers propanolol and metoprolol are able to readily cross the blood brain barrier, thus causing adverse central nervous system (CNS) effects such as depression, hallucinations and nightmares.2 These medicines are therefore not recommended for individuals with psychiatric disorders, and the use of Î²-blockers with low lipophilicity, such as atenolol, is preferred in these situations.2
Another important point to note is that doses of Î²-blockers should initially start at the lower end of the usual dosing range, and steadily increased according to the response of the individual.2 If treatment with Î²-blockers must be withdrawn, it must not be done abruptly, as this is associated with an increase in the severity and incidence of pain symptoms and MI.2 Therefore, a steady reduction of the therapy over the course of two days is required in this situation.2 Treatment in these ways may minimize the risk of complications associated with this drug class.
b) Organic Nitrates
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The nitrates, such as glyceryl trinitrate, cause vasodilation of veins and arteries, thus decreasing preload and afterload, promote blood flow to the endocardium, relief of vasospasm, and dilation of coronary artery stenosis.5 Due to these effects, nitrate therapy is indicated in the treatment of acute angina, as a preventative measure for exercise or stress related angina, or as long term prophylaxis.5 The major routes of administration are sublingual, buccal, transdermal and intravenous. For acute angina, 0.3-0.4mg of sublingual glyceryl trinitrate has been proven to reduce pain within 3 minutes in 75% of individuals, and is therefore indispensible in these situations.2 For long term preventative treatment, chewable and oral tablets, and transdermal patches are used. Perhaps the most important limitation for the use of nitrates is the development of tolerance due to overuse.2 This may be overcome by administration of the nitrates at a particular time of the day to cover the period in which the individual is most at risk, and adherence to a "nitrate free" period of 8-12 hours, usually during the night.2 The major adverse effects associated with the nitrates include postural hypotension, reflex tachycardia, headaches and flushing. If hypotension becomes too severe, the individual may be at risk of MI or stroke.2
c) Ca2+ Channel Blockers
The effects of the Ca2+ channel blockers include vasodilation of systemic arterioles and coronary arteries leading to a reduction of arterial pressure and coronary vascular resistance, as well as depression of myocardial contractility.2 Ca2+ channel blockers are therefore of particular use in the management of Prinzmetal's angina, which is caused by coronary vasospasm.2 Antiarrythmic effects are also seen in some Ca2+ channel blockers, such as depression of the conduction velocity of the SA and AV nodes.
The dihydropyridine Ca2+ channel blockers, such as nifedipine, are useful solely as arterial dilators, and have no antiarrythmic effects.2 Via the vasodilatory effects of these agents, they cause a decrease in afterload and increase in coronary perfusion, thus increasing the supply of blood and oxygen to the cardiac tissue.2 However, these agents are also known to cause flushing and headaches, as well as reflex tachycardia.2 The dihydropyridine Ca2+ channel blockers are rarely administered alone for the treatment of CHD, but are rather used in concomitant therapy with Î²-blockers, which counteract their effects, particularly reducing the incidence of reflex tachycardia.2 The non-dihydropyridine Ca2+ channel blockers, such as verapamil and diltiazem, however may administered as monotherapy for CHD.2
The non-dihydropyridine Ca2+ channel blockers cause less peripheral vasodilation than the dihydropyridine Ca2+ channel blockers, but greater decreases in AV node conduction.2 They are therefore contraindicated in patients also suffering from ventricular failure. As Î²-blockers have an additive effect on bradycardia and myodepression, caution should be exercised in considering concomitant use with these agents.2 Therefore, the non-dihydropyridine Ca2+ channel blockers are of most use in the treatment of CHD when Î²-blockers are contraindicated in the patient, such as in individuals with asthma.2
d) ACE inhibitors
ACE inhibitors, such as ramipril, have anti-inflammatory, antithrombotic and anti-proliferative properties, and are generally believed to be of benefit in all patients with CHD.2 They also reduce the production of reactive oxygen species, In addition, ACE inhibitors limit progression of heart failure and reduce the recurrence of MI, and are therefore useful in post MI treatment.3
e) Antiplatelet drugs - Aspirin and clopidogrel
The use of the antiplatelet drugs aspirin and clopidogrel prevent the aggregation of platelets, and thus the formation of thrombi.3 As thrombosis is one of the major risk factors associated with CHD, these agents are of great benefit in the treatment and management of CHD, and also to reduce the risk of MI.2 Clopidogrel works in much the same way as aspirin, and is of particular use in patients who are hypersensitive or cannot tolerate aspirin.2 An adverse effect of both drugs is gastrointestinal haemorrhage; however the risk of this may be reduced by administering treatment as a low dose, which is found to be just as effective in regards to antiplatelet effects.3
f) Statins and fibrates
Statins, such as atorvastatin, are the most effective LDL lowering agents, and are therefore used to combat the hypercholesterolaemia associated with CHD.3 They also have antithrombotic, anti-inflammatory and anti-proliferative effects, which are also useful for the treatment of CHD and the prevention of MI, and may therefore be used in individuals with normal cholesterol levels.2 These agents are never solely used for the treatment of CHD, but are indicated to reduce the progression of the disease. If statins are not tolerated, the use of fibrates, which also have LDL lowering properties, may be considered.3
g) Non-pharmacological treatments
Non-pharmacological treatments of CHD include surgical intervention, and modification of the risk factors predisposing individuals to the disease.2 Surgical treatments include angioplasty, stents, coronary artery bypass or heart transplant. All surgery aims to return normal blood flow to the affected cardiac tissue via various methods. Modification of risk factors include reducing plasma cholesterol, reducing alcohol intake, cessation of smoking, treatment of hypertension, and undertaking more physical activity.4 Changes to these modifiable risk factors may significantly reduce the burden of CHD in the individual, and greatly reduce the risk of a MI. Perhaps the most common and important modifiable risk factor is smoking, with active smokers having a risk of CHD increased by a factor of 1.8.4
CHD is the largest single cause of death in Australia.1 In Australia, it results in thousands of deaths each year, and globally is causes an immense burden on health care systems.1 CHD is multifactorial, with factors such as high cholesterol, smoking, alcohol, hypertension, and exercise all playing a part in the manifestation of the disease.4 There are a number of therapeutic alternatives available for treatment of the condition, and they are all designed to normalize these factors. These drugs may work to decrease the workload, and thus oxygen requirements of the heart, improve blood flow and thus oxygen supply to the cardiac tissue, reduce serum cholesterol levels, and also to reduce the levels of platelet aggregation and thus prevent thrombus formation. Overall, these medications act to slow the progression of CHD, and reduce the risk of an adverse event occurring. The ability to detect the signs and symptoms associated with CHD, the correct use of the therapeutic alternatives, knowledge of the potential risk factors and methods which may be used to correct them, all play a part in the effective treatment of this serious condition.