• Left ventricular failure suggests myocardial infarction.

• A raised jugular venous pressure suggests myocardial infarction or pulmonary embolus.

• A pleural friction rub suggests pulmonary embolism or infection.

• A pericardial friction rub suggests pericarditis (Pviral, Psecondary to myocardial infarction) or aortic dissection.

• Aortic regurgitation suggests aortic dissection.

• Unequal pulses or blood pressure in the arms suggests aortic dissection.

• Bony tenderness suggests musculoskeletal pain.

• is predictable

• usually occurs after a constant amount of exercise

• is worse in cold or windy weather

• is induced by emotional stress

• is induced by sexual intercourse

• is relieved by rest, and rapidly relieved by a short-acting nitrate.

• evidence of risk factors (high blood pressure, cholesterol deposits, signs of smoking)

• any signs of cardiac disease (aortic stenosis, an enlarged heart, signs of heart failure)

• anaemia (which will exacerbate myocardial ischaemia)

• signs of peripheral vascular disease (which would suggest that coronary disease is also present).

• An abnormal ECG is usually necessary to make a diagnosis of myocardial infarction before treatment is started.

• An ECG will demonstrate ischaemia in patients with angina provided that the patient has pain at the time the ECG is recorded.

• With pulmonary embolism there may be classical ECG changes, but these are often not present.

• With pericarditis, ECG changes, if present at all, are very nonspecific.

• normal ECG

• ST segment elevation

• development of Q waves

• ST segment returns to the baseline

• T waves become inverted.

INFERIOR INFARCTION

Figures 5.2, 5.3 and 5.4 show traces taken from a patient with a typical history of myocardial infarction: on admission to hospital, 3 h later, and 2 days later. The main changes are in the inferior leads: II, III and VF. Here the ST segments are initially raised, but then Q waves appear and the T waves become inverted. Figure 5.2 includes coronary angiograms showing the effects of an occluded right coronary artery in an inferior STEMI.

ANTERIOR AND LATERAL INFARCTION

The changes of anterior infarction are seen in leads V₂-V₅. Lead V₁ which lies over the right ventricle, is seldom affected (see Fig. 5.5, which includes corresponding coronary angiograms).

When the lateral wall of the left ventricle is damaged by occlusion of the left circumflex coronary artery, leads I, VL and V₆ will show infarction changes. Figure 5.6 shows the record of a patient with an acute lateral STEMI, with the corresponding coronary angiograms. Figure 5.7 shows a record taken 3 days after a lateral infarction, with Q waves and inverted T waves in leads I, VL and V₆.

The ECG in Figure 5.8 shows an acute STEMI affecting both the anerior and lateral parts of the left ventricle.

The ECG in Figure 5.9 was recorded several weeks after an anterolateral myocardial infarction. Although the changes in leads I and VL appear ‘old’, having an isoelectric ST segment, there is still ST segment elevation in leads V₃-V₅. If the patient had just been admitted to hospital with chest pain these changes would be taken to indicate an acute infarction, but this patient had had pain more than a month previously. Persistent ST segment elevation is quite common after an anterior infarction: it sometimes indicates the development of a left ventricular aneurysm, but it is not reliable evidence of this.

An old anterior infarction often causes only what is called ‘poor R wave progression’. Figure 5.10 shows the record from a patient who had had an anterior infarction some years previously. A normal ECG would show a progressive increase in the size of the R wave from lead V₁ to V₅ or V₆. In this case the R wave remains very small in leads V₃ and V₄, but becomes normal-sized in V₅. This loss of ‘progression’ indicates the old infarction.

The time taken for the various ECG changes of infarction to occur is extremely variable, and the ECG is an unreliable way of deciding when an infarction occurred. Serial records showing progressive changes are the only way of timing the infarction from the ECG.

POSTERIOR INFARCTION

It is possible to ‘look at’ the back of the heart by placing the V lead on the back of the left side of the chest, but this is not done routinely because it is inconvenient and the complexes recorded are often small.

An infarction of the posterior wall of the left ventricle can, however, be detected from the ordinary 12-lead ECG because it causes a dominant R wave in lead V₁. Normally the left ventricle, being more muscular than the right, exerts a greater influence on the ECG, so in lead V₁ the QRS complex is predominantly downward. With a posterior infarction, the rearward-moving electrical forces are lost, so lead V₁ ‘sees’ the unopposed forward-moving depolarization of the right ventricle, and records a predominantly upright QRS complex.

Figure 5.11 shows the first record from a patient with acute chest pain. There is a dominant R wave in lead V₁ and ischaemic ST segment depression (see p. 231) in leads V₂-V₄. The chest electrodes were then moved to the V₇-V₉ positions: all in the same horizontal plane as V₅, with V₇ on the posterior axillary line, V₉ at the edge of the spine, and V₈ halfway between, on the midscapular line. The ECG record then showed raised ST segments, with Q waves typical of an acute infarction.

RIGHT VENTRICULAR INFARCTION

Inferior infarction is sometimes associated with infarction of the right ventricle. Clinically, this is suspected in a patient with an inferior infarction when the lungs are clear but the jugular venous pressure is elevated. The ECG will show raised ST segments in leads recorded from the right side of the heart. The positions of the leads correspond to those on the left side as follows: V₁R is in the normal V₂ position; V₂R is in the normal V_i position; V₃R etc. are on the right side, in positions corresponding to V₃ etc. on the left side. Figure 5.12 is from a patient with an acute right ventricular infarct.

MULTIPLE INFARCTIONS

Infarction of more than one part of the left ventricle causes changes in several different ECG territories. This usually implies disease in more than one of the main coronary arteries. The ECG in Figure 5.13 shows an acute inferior myocardial infarction and marked anterior ST segment depression. Later, coronary angiography showed that this patient had a significant stenosis of the left main coronary artery.

Fig. 5.14 is the record from a patient with an acute inferior myocardial infarction. Poor R wave progression in leads V₂-V₄ indicates an old anterior infarction as well.

Figure 5.15 is an ECG showing an acute inferior STEMI and anterior T wave inversion due to an NSTEMI of uncertain age.

Figure 5.16 is an ECG showing an acute anterior myocardial infarction. Deep Q waves in leads III and VF indicate an old inferior infarction.

BUNDLE BRANCH BLOCK AND MYOCARDIAL INFARCTION

ISCHAEMIA WITHOUT MYOCARDIAL INFARCTION

Cardiac ischaemia causes horizontal ST segment depression; to be diagnostic of ischaemia, there must be horizontal or downward-sloping depression of > 0.05 mV in two contiguous leads, and/or T wave inversion of > 0.1 mV in two contiguous leads. Such changes appear and disappear with the pain of stable angina. Persistent pain and ST segment depression ( Fig. 5.24) may not be associated with any rise in troponin level.

If a patient has chest pain that persists long enough for him or her to seek hospital admission, and the ECG shows ST segment depression, the outlook is relatively poor – even when the depression is not marked ( Figs 5.25 and 5.26) and there is no rise in troponin level. These patients usually need further investigation, though on the whole they can be managed as outpatients.

Ischaemia may be precipitated by an arrhythmia, and will be resolved when either the heart rate is controlled or the arrhythmia is corrected. The ECG in Figure 5.27 shows ischaemia during atrial fibrillation with a rapid ventricular rate (this patient had not been treated with digoxin). The ECG in Figure 5.28 shows ischaemic ST segment depression in a patient with an AV nodal re-entry tachycardia and a ventricular rate of > 200/min.

PRINZMETAL’S ‘VARIANT’ ANGINA

Angina can occur at rest due to spasm of the coronary arteries. This is accompanied by elevation rather than depression of the ST segments. The ECG appearance is similar to that of an acute myocardial infarction, but the ST segment returns to normal as the pain settles ( Fig. 5.29). This ECG appearance was first described by Prinzmetal, and it is sometimes called ‘variant’ angina.

AORTIC STENOSIS AND AORTIC DISSECTION

Aortic stenosis is an important cause of angina. The ECG should show left ventricular hypertrophy ( Fig. 5.35). However, the ECG is an unreliable guide to left ventricular hypertrophy and the difficulty of distinguishing it from ischaemia is discussed in Chapter 6.

The presence of left ventricular hypertrophy in the ECG of a patient with chest pain also raises the possibility of aortic dissection.

PRACTICAL ASPECTS OF EXERCISE TESTING

Reproducible exercise testing needs either a bicycle ergometer or a treadmill. In either case, the exercise should begin at a low level that the patient finds easy, and should be made progressively more difficult. On a bicycle, the pedal speed should be kept constant and the workload increased in steps of 25 watts. On a treadmill, both the slope and the speed can be changed and the protocol evolved by Bruce ( Table 5.4) is the one most commonly used.

The workload achieved by a patient on a treadmill is sometimes expressed as metabolic equivalents (METS). The rate at which oxygen is used by an average person at rest is 1 MET, and it equals 3.5 ml/kg/min. However, few people are average, and oxygen consumption is dependent on weight, age and gender, so METS are not particularly useful. Box 5.10 shows the estimated workloads imposed by various activities, and hence how exercise tolerance (as measured on the treadmill) indicates what a patient might be expected to achieve.

A 12-lead ECG, the heart rate and the blood pressure should be recorded at the end of each exercise period. The maximum heart rate and blood pressure are in some ways more important than the maximum workload achieved, because the latter is markedly influenced by physical fitness. However, the ECG recorded during exercise testing is unreliable in cases of:

REASONS FOR DISCONTINUING AN EXERCISE TEST

INTERPRETATION OF ECG CHANGES DURING EXERCISE TESTING

The final report of the test should indicate the duration of exercise, the workload achieved, the maximum heart rate and systolic pressure, the reason for discontinuing the test, and a description of any arrhythmias or ST segment changes.

An exercise test is usually considered ‘positive’ for ischaemia if horizontal or downward-sloping ST segment depression of 2 mm or more develops during exercise, and resolves on resting. By convention, ST segment depression is measured relative to the ECG baseline (between the T and P waves) 60–80 ms after the J point (the point of inflection at the junction of the S wave and the ST segment). A diagnosis of ischaemia becomes almost certain if these changes are accompanied by the appearance and then disappearance of angina. Figures 5.44 and 5.45 show an ECG that was normal when the patient was at rest, but which demonstrated clear ischaemia during exercise. Box 5.11 lists the normal changes in the ECG during exercise, and Box 5.12 lists the changes suggesting a high probability of coronary disease.

There are, however, other ECG changes that may be seen during an exercise test. Figures 5.46 and 5.47 show the records of tests in a patient who had had an anterior myocardial infarction some weeks previously. At rest, some ST segment elevation persisted in the anterior leads. During exercise the ST elevation became more marked. The reasons for this are uncertain. It has been suggested that the change is due to the development of an abnormality of left ventricular contraction, but other evidence suggests that it is simply another ECG manifestation of ischaemia. There is, however, no doubt that this is an abnormal result.

When the resting ECG shows T wave inversion and on exercise the T waves become upright, this is called ‘pseudonormalization’, and it is a sign of ischaemia ( Fig. 5.48).

When the J point and the ST segment become depressed during exercise, but the ST segment slopes upwards, the change is not an indication of ischaemia ( Figs 5.49 and 5.50). Deciding whether ST segment depression slopes upwards or is horizontal can be quite difficult.

False positive changes also occur when exercise testing is performed in patients taking digoxin. Figures 5.51 and 5.52 show the results of an exercise test in a patient being treated with digoxin, whose coronary angiogram was normal.

In a patient suspected of having coronary disease, exercise testing gives the ‘right’ answer in about 75% of patients tested – to be more precise, exercise testing has a sensitivity of 68% and a specificity of 77%. All tests at times give false positive and false negative results, reflecting their specificity and sensitivity, and false positive tests are particularly common in middle-aged women. In an asymptomatic subject in whom the likelihood of coronary disease is low, the chance of a false positive result may be higher than the chance of a true positive. Also, the greater the likelihood that the patient has coronary disease, the more likely it is that a positive test is ‘true’ rather than ‘false’. The statistics (Bayes’ theorem) may seem complex, but the important thing is to remember that exercise testing is not infallible.

Some patients who give a history characteristic of angina, and who have an undoubtedly positive exercise test according to their ECG, have normal coronary arteries. This condition is called ‘Cardiac Syndrome X’. In some cases the patient has structural heart disease (e.g. left ventricular hypertrophy, mitral valve prolapse, myocardial bridging), but most patients have an apparently normal heart and the cause of Cardiac Syndrome X is unknown.

Exercise testing thus has to be used and interpreted with care.

RISKS OF EXERCISE TESTING

Exercise testing involves a risk of about 1 in 5000 of the development of ventricular tachycardia or ventricular fibrillation, and a risk of about 1 in 10000 tests of myocardial infarction or death. There is also a risk of injury if the patient falls, or jumps, off the treadmill. Box 5.13 lists some contraindications of exercise testing.

The ECGs in Figures 5.53, 5.54 and 5.55 are from a patient whose resting ECG was normal, but as the test proceeded he began to develop ventricular extra-systoles and then suddenly developed ventricular fibrillation. This demonstrates the need for full resuscitation facilities to be available at the time of exercise testing.

STEMI

Patients with STEMI require immediate coronary recanalization by means of either percutaneous coronary intervention (PCI) or thrombolysis.

NSTEMI

Patients with NSTEMI should be treated immediately with aspirin, low-molecular-weight heparin, clopidogrel, a beta-blocker (provided there are no contraindications), a statin and nitrates.

Two risk categories of NSTEMI can be identified, which require different subsequent treatments. Patients at high risk have any of:

In addition to the baseline treatment above, these patients require an infusion of a glycoprotein Ilb/IIIa inhibitor followed by coronary angiography before discharge from hospital. Angiography is urgent in unstable patients. Most high-risk patients will need angioplasty or bypass surgery, often as a matter of urgency.

Low-risk patients include those with all of:

Heparin can be discontinued but aspirin, beta-blockers, nitrates, a statin and clopidogrel are continued. As soon as possible, an exercise or another non-invasive test should be performed to assess the probability and severity of coronary disease. On the basis of the test results and the clinical picture, a decision can be made about the need for, and urgency of, coronary angiography.

LONG-TERM TREATMENT AFTER MYOCARDIAL INFARCTION

In all patients it is important to manage risk factors aggressively, with the cessation of smoking, weight control and regular exercise. Aspirin, beta-blockers and statins are needed indefinitely, and clopidogrel for 9 months.

CHRONIC CHEST PAIN

A trial of sublingual glyceryl trinitrate 0.5 mg may help make the diagnosis of angina, and in such cases patients should then be encouraged to use the drug liberally and prophylactically. Beta-blockers are the first-line agents for preventing angina. If the patient is unable to take a beta-blocker (e.g. because of asthma), treatment should start with a calcium-channel blocker such as amlodipine. Nicorandil and ivabradine may also be useful, especially in patients intolerant of other drugs. All these drugs can be combined, or a long-acting nitrate such as isosorbide mononitrate can be substituted for one of these classes of drug. A combination of two of these drug classes is sometimes helpful; the addition of the third seldom provides much further benefit. Secondary prophylactic measures, including aspirin and a statin, are essential.

Otherwise, treatment will depend on the cause of the chest pain. If investigation (see above) reveals that the cause is cardiac, and despite maximum medical therapy the patient remains symptomatic, invasive procedures such as coronary artery bypass grafting or percutaneous transluminal coronary angioplasty may need to be considered.