Coronary heart disease (CHD) is the leading cause of mortality and morbidity in the UK. The underlying disease is known as atherosclerosis, which has been described as a focal, inflammatory, fibro-proliferative response to multiple forms of endothelial injury (Ross, 1986). Its clinical consequences lead to myocardial ischaemia, resulting in angina and breathlessness and, if acute, may lead to myocardial infarction.
Grace Lindsay, BSc (Hons), MN, PhD, RN, RM.
Senior Lecturer, Nursing and Midwifery School, University of Glasgow, Glasgow
The incidence of CHD increases with age and in mid-life is more common in men than in women. In 1998 the number of deaths in the UK as a consequence of CHD was 137 153 (British Heart Foundation Health Promotion Research Group, 2000).
The prevalence of angina in the population is not easy to estimate. The percentage of people aged 35-44 years suffering from self-reported angina has been reported as 2%, rising to approximately 20% in people aged over 80 years (Tunstall-Pedoe et al, 1999). However, the problem may be more severe; a large-scale survey of over 11 000 men and women in Scotland aged 45-64 years indicated that the presence of CHD is under-recognised by between 8-10% of the population (Tunstall-Pedoe et al, 1997). While there was an overall reduction of almost a third in rates of myocardial infarction in England and Wales between 1981-82 and 1991-92, during the same period there was a dramatic increase in the prevalence of angina in the population in England and Wales across all adult ages, ranging from 49% to 80% for both men and women.
Angina pectoris is a symptom complex due to reversible myocardial ischaemia. The symptoms are those of chest pain or tightness that can radiate to the arm(s), throat or back. Pain is brought on by effort and emotion and may occur spontaneously and at rest.
Patients with angina pectoris may be divided into clinical subsets according to their symptoms. Those with stable angina have a reproducible pattern in terms of intensity and duration of pain and precipitating factors. Patients with unstable angina include those with recent (less than six months) onset of symptoms or a changing pattern, often involving spontaneous pain at rest, and those with worsening symptoms. One of the most important factors in obtaining a diagnosis is obtaining an accurate clinical history.
This list is not exhaustive and individual patients may experience and describe symptoms in a variety of ways. Time for recovery with rest and/or after sublingual administration of glycerine trinitrate provides an important index of symptom severity and should guide subsequent management and investigation. Frequency, duration, location, severity of pain and/or breathlessness and precipitating factors are all important in clinical assessment. Various classification systems exist that quantify the severity of CHD - the two most widely used are the Canadian cardiovascular classification (Criteria Committee, 1974) and that of the New York Heart Association (Campeau, 1976). Both systems can be used to describe mild, moderate or severe angina based on response to activity or functional limitation as a result of symptoms.
Acute myocardial infarction
Acute myocardial infarction (AMI) develops when myocardial ischaemia occurs for sufficient time to cause necrosis of a localised area of the myocardium. The initial reduction in myocardial blood flow may be secondary to platelet aggregation in the presence of severe atheroma leading to reduced flow and thrombus. Accompanying symptoms may include nausea, weakness, syncope, dyspnoea and sweating.
The pain caused by myocardial infarction is similar to that of angina pectoris, is unlikely to resolve with rest or administration of nitrate therapy and may last for several hours. Many patients, following recovery from the acute event, subsequently experience angina, with AMI being the first clinical manifestation of CHD.
Investigation of angina
Since angina is a symptom complex, objective confirmatory evidence for the diagnosis is necessary. The severity of pain is not a guide to the severity of the disease - minor CHD can be associated with severe chest pain and major CHD can have apparently mild symptoms. Throughout the various dynamic tests that are described below, note should be made of breathlessness and any changes in blood pressure, heart rate and rhythm. If severe changes develop, the test should be discontinued.
The main initial investigation is a 12-lead electrocardiograph (ECG), which provides information on rhythm, presence of heart block, previous myocardial infarction, myocardial hypertrophy and ischaemia. Suggestive ECG changes include ST-segment depression and T-wave inversion with ST/T-wave abnormalities, which correlate with left ventricular dysfunction and left anterior descending artery stenosis, and QRS abnormalities associated with abnormal findings on angiography. However, it should be noted that a normal resting ECG does not exclude the presence of CHD in 50% of those with the condition (Norell et al, 1992).
The exercise stress test provides an objective noninvasive measure of a patient’s cardiovascular capacity. It is the commonest non-invasive cardiological test that can be performed to establish or confirm the diagnosis and prognosis of cardiac disease and is easily repeated. It has low, but not absent, mortality and morbidity (Stuart and Ellested, 1980), but experience and resuscitation equipment is required by people supervising the test.
Exercise testing is recommended for patients suspected of having angina to establish a diagnosis and for those who have had a myocardial infarction to help identify the risk of a further CHD event. Using standard protocols, stress testing by treadmill or bicycle ergometer is important for both making the diagnosis and establishing the degree of disability. There are two main aims of this test. First, to provoke an identifiable clinical response, such as chest pain or dyspnoea, and a change in one or more physiological variables, such as heart rate, blood pressure or the appearance of the ST-segment shift. Second, to determine the workload achieved at the time of the response or at the maximum effort. The most common protocols use a workload that gradually increases with time rather than a fixed one. Short stages and small increases in workload have been shown to be better because they are more easily tolerated by patients, particularly if they are physically unfit. It is important that sufficient exercise levels are attained to stress the myocardium otherwise little information may be gained. In absolute terms workloads are independent of bodyweight and are easy for most people to undertake without specific direction.
A normal exercise test indicates a good prognosis. An exercise test limited by pain or by the development of ischaemic ECG changes or an arrhythmia may identify people at risk who require further investigation, such as coronary angiography. Specific indicators of adverse prognosis are poor maximal exercise capacity and limited systolic blood-pressure response, greater than or equal to 2mm ST depression at any time.
The use of radionuclides enhances the noninvasive detection of CHD. It is initially similar to the exercise tolerance test, with a graded workload, but includes the addition of small amounts of intravenously injected radionuclides (thallium 201). A gamma camera that detects the radioactivity emitted is placed over the patient’s chest and provides an image of the distribution of radioactivity. Thallium 201 is an isotope that is taken up by the myocardium itself. It has a short half-life and is quickly excreted from the body via the kidneys. The rate of uptake reflects myocardial blood supply; the better the blood supply, the higher the uptake of thallium shown in the scan images as ‘hot’ areas.
Images are recorded immediately after exercise testing then again two to four hours later. Ischaemic areas have poor thallium 201 uptake and are detected as ‘cold’ areas on the myocardial image. Such areas may remain ‘cold’ at rest, indicating scar or infarct tissue. Because the scan is performed at two time-points, ‘cold’ areas on initial results may be re-examined to detect if reperfusion has occurred. Reperfusion indicates areas of reversible ischaemia that might benefit from revascularisation. Impaired myocardial perfusion, if present, may be detected without the need for invasive angiography. Estimates of the distribution of isotope throughout the myocardium are recorded at baseline and again two to four hours later. Information on the size of the area of damage, the extent of ischaemia and the artery or arteries involved, for example the left anterior descending coronary artery, may be obtained from this investigation. Furthermore, estimates of ventricular function may be assessed using measurement of the ventricular ejection fractions.
Coronary angiography is an invasive investigation employed to demonstrate the presence or absence of CHD. The procedure allows the generation of images of the coronary arteries and visualisation of the ventricles by transiently introducing a radio-opaque contrast medium. The procedure is undertaken in a dedicated operating theatre/laboratory with emergency resuscitation equipment available. Under local anaesthesia, a sheath is inserted percutaneously into a peripheral artery. A fine, hollow coronary catheter is introduced through the sheath into the coronary ostium under fluoroscopic guidance. Catheters are inserted into either the femoral artery (Judkins’ technique) or brachial artery (Sones technique) and manipulated into the left ventricle. Recording on video or film following the injection of contrast medium provides data on left-ventricular structure and function in terms of contractility.
The image of the coronary lumen allows the presence of coronary stenosis, obstruction or narrowing to be detected. Future management is decided on the basis of clinical symptoms, data from exercise testing and, if available, from radionuclide imaging. However, selective coronary angiography in multiple projections is the principal investigation in selecting patients for coronary angioplasty, coronary stents or coronary artery bypass graft (CABG) surgery. It is the most accurate index available for assessing prognosis for patients with angina pectoris and is of particular value in detecting the origins of obscure chest pain.
Clinical management of patients with angina
Subsequent clinical management of a patient with angina is judged on the basis of the comparative benefits of no treatment, medical treatment relative to coronary artery bypass surgery and percutaneous transluminal angioplasty (Maley, 1986; Califf et al, 1989). The decision is made in conjunction with functional capacity data obtained from either exercise testing alone, or with the additional help of radio-nuclide studies.
For patients with stable angina, percutaneous coronary intervention (PCI) would be the preferred initial treatment choice, with CABG considered as a subsequent treatment. However, the balance between these treatment decisions would be based on the number and nature of diseased vessels. PCI would be indicated in the presence of one or two diseased vessels with discrete lesions. In patients with three diseased vessels and diffuse distribution, CABG would be the preferred option. The use of coronary stents has revolutionised PCI in as much as the procedure is easier to perform, with the instance of re-stenosis greatly reduced, although not eliminated.
Sublingual glycerinetrinitrate (GTN) is an acceptable treatment for short-term symptom control. For longer term prevention of angina symptoms, four classes of cardioactive medications are available: beta-blockers, calcium channel blockers, long-acting nitrates, and potassium channel-opening drugs. The evidence indicates that initial treatment should be with beta-blockers (unless specifically contraindicated) with the addition of other classes as indicated for symptom control (SIGN, 2001). Aspirin should be prescribed as an antiplatelet drug for the secondary prevention of vascular events in patients with angina (Ridker et al, 1991)
CHD risk-factor assessment
CHD risk-factor assessment and interventions are required to address cigarette-smoking status, hyperlipidaemia, hypertension, diabetes mellitus and obesity. National guidelines advise on targets and interventions based on the most recent research findings (SIGN, 2001; DoH, 2000).
This paper has presented a summary of the investigations that are currently available in clinical practice to both confirm a diagnosis of CHD and to document the extent of disease in individuals presenting with chest pain. Although some of the isotope imaging procedures and angiography services are not available at all cardiac centres, the first-line investigation of exercise tolerance testing is universally available in secondary care. Such investigations are particularly important in order to identify those individuals at high risk of future CHD events and to help inform treatment decisions.
The authors would like to thank Dr Ian Hutton, Chairman, Cardiac and Cancer Division, North Glasgow University NHS Trust, and Dr William Martin, Clinical Physicist, for helpful comments during preparation of this paper and for photographs obtained from coronary imaging techniques.
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