Angina ranges from a mild ache to a most severe pain that provokes sweating and fear. It is generally described as ‘heavy’, ‘crushing’ or ‘gripping’, and the patient may indicate the type of pain by clenching the fist or gripping the hands together. Occasionally these symptoms may occur in the arms without any chest pain. There are several types of angina; these are described below.
Classical or exertional angina
Physical exertion, especially after a meal, in cold weather or walking against the wind, provokes this pain. It is also aggravated by anger or excitement. The pain usually fades quickly (in less than 3 min) when the patient ceases exertion. Sometimes the pain will disappear even though exertion continues (‘walking through the pain’); the exertion threshold for the development of pain is very variable. Usually, pain is more easily provoked in the early morning than later in the day. This type of angina can be graded.
This is angina that occurs when the patient lies down. It usually occurs in association with heart failure because of the increased central blood volume and consequent myocardial tensions that develop in the recumbent position. Patients with this symptom usually have severe coronary artery disease.
This is angina that wakes the patient from sleep. It may be provoked by vivid dreams. Patients with this symptom usually have critical coronary artery disease, or the angina may be associated with coronary spasm.
Variant (Prinzmetal’s) angina
A classical attack of variant angina, as described by Prinzmetal, has no obvious provocation. It occurs at rest, especially at night or in the early morning, and is rarely induced by exertion. It occurs more frequently in women and the pain is usually more severe and more prolonged than in classical angina. It produces a characteristic electrocardiographic feature of ST segment elevation developing during the pain. Arrhythmias-both heart block and ventricular tachycardia-are common in the ischaemic episode.
Prinzmetal’s angina is caused by spasm of a coronary artery often in association with an eccentric coronary artery atheromatous lesion. More often, variant angina is not classical Prinzmetal’s angina but is due to variation in coronary arterial tone rather than frank coronary arterial spasm. Such patients have a varying exercise threshold for the provocation of angina.
Unstable angina includes angina of very recent onset, worsening angina or angina at rest. A number of terms, such as crescendo angina, preinfarction angina and intermediate chest pain syndrome, have been used to describe angina that is provoked more easily and persists for a longer duration than ordinary angina or that fails to respond readily to therapy. Whilst the pain is present, myocardial infarction must be considered, but with angina the ECG changes (T wave inversion or ST segment depression) are only transient and cardiac enzyme levels are not elevated. Unless vigorously treated, a large proportion of patients with unstable angina will proceed to develop a myocardial infarction within weeks.
There are usually no abnormal findings in angina, although a fourth heart sound may be heard. Any factor responsible for angina (e.g, thyrotoxicosis) or risk factors may lead to physical signs such as nicotine staining, hypertension or xanthelasma.
The primary diagnosis rests on the description of the chest pain as investigations may be normal.
This is usually normal between attacks, although an old myocardial infarction, left ventricular hypertrophy or other unrelated heart disease may be present. During an attack, transient ST segment depression, symmetrical T wave inversion or tall, pointed, upright T waves may appear.
A normal ECG between attacks or even during an attack cannot definitely exclude angina pectoris. Typical ECG changes during an attack are strong pointers to the diagnosis of angina.
When angina is provoked by exertion, an exercise stress ECG should be performed. ST segment depression greater than or equal to 1 mm suggests myocardial ischaemia, especially if typical chest pain occurs at the same time. The severity of the electrocardiographic changes indicates the extent of the coronary artery disease. Approximately 75% of patients with severe coronary artery disease will give a positive test. Stress testing is less reliable in women and is confused by electrolyte abnormalities, therapy with digoxin, and intraventricular conduction disturbances. A normal stress test does not definitely exclude coronary disease.
UPTAKE OF THALLIUM-201 This is useful:
• When the exercise test is equivocal
• In deciding whether stenotic vessels on angiography are giving rise to ischaemic areas on exercise. A normal perfusion scan after exercise makes significant coronary artery disease unlikely.
This can be used to outline the left ventricle. When part of the left ventricular wall is ischaemic it does not contract normally, producing an abnormal image. This test can be performed at rest and during exertion. The ejection fraction is a good index of ventricular function and is useful in the assessment of patients for coronary artery bypass surgery.
This can be used to assess ventricular wall involvement and ventricular function. An abnormal resting echocardiogram reflects previous ventricular damage. Exercise echocardiography, although technically difficult, may be useful in patients with an equivocal exercise ECG.
This is occasionally useful in patients with chest pain when the cause is unclear. More often, the test is performed to delineate the exact coronary anatomy prior to coronary grafting or coronary angioplasty. Coronary angiography should only be performed when the benefit in terms of diagnosis and potential treatment outweighs the small risk associated with the procedure (a mortality of less than 1 in 1000 cases).
A coronary angiogram may not reveal coronary spasm unless an intracoronary injection of dihydroergotamine has been given. This test is not often performed because the induction of coronary spasm may prove difficult to reverse and its clinical relevance is uncertain.
Management of an acute attack
An acute attack is treated by stopping exercise (exertional angina) or by getting up (decubitus angina) and dissolving a fresh glyceryl trinitrate tablet (0.5 mg) under the tongue. After 2-3 min the angina usually recedes. When the pain is relieved the glyceryl trinitrate tablet is spat out or swallowed to inactivate it. This minimizes the main side-effect, which is a severe pounding headache. Some prefer to use an aerosol formulation of glyceryl trinitrate; this, unlike the tablets, is stable for a long period. If glyceryl trinitrate cannot be tolerated, a capsule of nifedipine may be chewed or sucked. However, this has similar sideeffects to glyceryl trinitrate.
Patients should be reassured that their condition is not uniformly or rapidly fatal. Many have a good prognosis- 30% survive for more than 10 years and spontaneous remission does occur. Any underlying problems such as obesity, thyrotoxicosis, anaemia or aortic stenosis should be treated. Risk factors should be evaluated and steps made to correct them. Smoking must be stopped. Patients must be encouraged not to do things that they know provoke their angina, but this must not lead to a severe restriction of life-style. Regular exercise sufficient to improve the fitness of the patient will tend to increase the threshold to angina. More severe exercise is not recommended unless the cardiovascular response to exertion (treadmill EeG test) has been documented. Emotional crises and overexcitement must be minimized. Medical treatment Patients should be told to suck a tablet of glyceryl trinitrate before exertion rather than waiting for the pain to commence. They must be specifically encouraged to do this, because many prefer to believe that it is better to suffer the pain than to take more tablets. When angina occurs frequently, or with only modest exertion, regular prophylactic therapy should be advised. This consists of nitrates, f3-adrenergic blocking drugs or calcium antagonists.
Nitrates such as glyceryl trinitrate are available in a variety of slow-release formulations, particularly infiltrated skin plasters and buccal pellets. Alternatively, tablets of long-acting nitrate preparations such as isosorbide dinitrate or isosorbide mononitrate may be used. Nitrates are successful in the treatment of angina pectoris because they reduce venous and hence intracardiac diastolic pressures, reduce the impedance to the emptying of the left ventricle, and relax the tone of the coronary arteries.
f3-Adrenergic blocking drugs reduce heart rate (negative chronotropic effect) and the force of ventricular contraction (negative inotropic effect), both of which reduce myocardial oxygen demand, especially on exercise. Sufficient f3-blocker to reduce the resting heart rate to about 60 b.p.m. is usually necessary to achieve relief from angina. Very high doses of f3-blockers are no longer used because of side-effects and the possibility of infarction or arrhythmia on withdrawal, and because many alternative therapies are available. Propranolol 40-80 mg three times daily is the most conventional therapy. Relatively cardioselective f3-blockers (f3,-antagonists) such as atenolol (50-100 mg daily) or metoprolol (50 mg three times daily) are often preferred because they have fewer side-effects.
Calcium channel blockers such as nifedipine, nicardipine, amlodipine, verapamil and diltiazem block calcium flux into the cell and the utilization of calcium within the cell. They relax coronary arteries and other vascular systems and also reduce the force of left ventricular contraction, reducing the oxygen demand and improving angina. Nifedipine 20-30 mg daily is the calcium antagonist most commonly used in angina.
This is a technique of dilating coronary atheromatous obstructions by inflating a balloon against the obstruction. The balloon, which is mounted on the tip of a very thin catheter, is inserted through the obstruction using X-ray fluoroscopy, and it is then inflated with dilute contrast material. Multiple inflations of the balloon using a pressure of several atmospheres will squash and crack the atheroma and relieve the obstruction. This technique is widely applied for the treatment of angina due to isolated, proximal, non-calcified, atheromatous plaques, usually in patients with a relatively short history of coronary ischaemia. Multiple lesions may be treated and repeat procedures can be undertaken. Two complications are acute coronary occlusion (2-4%) and chronic restenosis, which occurs in 30% in the first 6 months after angioplasty.
When angina worsens or persists despite general measures and optimal medical treatment, the option of surgery should be considered. The patient should be assessed using exercise testing and angiography. Symptomatic patients with left main stem obstructions, two- or threevessel involvement and good ventricular function are often treated surgically.
There are three operations currently used for the relief of myocardial ischaemia:
1 Coronary artery vein bypass grafting (CAVBG) involves taking a vein, usually from the leg (saphenous) and bypassing the coronary obstruction by suturing the vein (reversed because of the venous valves) between the aorta and the coronary artery distal to the obstruction.
2 An internal mammary artery may be mobilized and implanted into the left anterior descending coronary artery distal to an obstruction 3 Endarterectomy (removal of an atheromatous obstruction) can sometimes be successful when combined with bypass or internal mammary artery grafting. Surgery provides dramatic relief from angina in about 90% of those operated on. When surgery is performed for left main stem obstruction or for three-vessel disease involvement, an improved life-span and quality of life can be expected. Surgical mortality is well below 1% in patients with normal left ventricular function. Progressive slow occlusion of grafts with atheroma occurs in a significant number of cases (5-10% a year).
Treatment of variant angina
The treatment of variant angina is slightly different. Nitrates and calcium antagonists are useful, but fl-blockers may increase coronary tone and exacerbate the angina, so should not be used. It may be necessary to treat the arrhythmias provoked by the spasm. Surgical relief is rarely necessary or possible.
Treatment of unstable angina
Unstable angina should be managed vigorously. If rest pain persists despite the use of agents such as sublingual glyceryl trinitrate, the patient should be treated with bed rest, mild sedation, intravenous heparin and/or oral aspirin as well as standard medical antianginal therapy. Oxygen may also be beneficial. Calcium antagonists are particularly valuable for the treatment of this condition but usually fl-blockers, nitrates and calcium antagonists are all used in combination. Aspirin decreases both death and myocardial infarction. If medical therapy fails, urgent coronary arteriography is desirable with a view to coronary artery surgery or angioplasty. Fibrinolytic therapy may be of benefit if myocardial infarction is suspected. Alter natively, intra-aortic balloon pumping (see p.553) may help to stabilize the patient.
Irrespective of the immediate success of treatment, early coronary angiography and, depending on the results, urgent referral for surgery are usually advised.