Introduction

Chest pain is one of the most common presenting complaints in emergency medicine. It is also associated with life-threatening pathology, so it is arguably the most important complaint faced by the emergency physician. It is certainly one of the most challenging. Failure to appropriately diagnose and manage patients with acute chest pain is a frequent cause of avoidable mortality and morbidity, and is a leading cause of malpractice litigation. It is therefore not surprising that physicians often err on the side of caution, but this can also have adverse consequences for the patient and society. Patient anxieties following unnecessary investigation are often unrecognized but may severely affect quality of life, and over-investigation and unnecessary hospital admission for chest pain waste millions of healthcare dollars each year.

Epidemiology

The incidence of acute chest pain presenting to the emergency department (ED) appears to be increasing. Awareness of the importance of early treatment for myocardial infarction has led to public information campaigns that increase ED attendances with chest pain. Meanwhile, general practitioners are increasingly being bypassed in favour of an emergency ambulance response. These changes in health service use have coincided in many developed countries with a reduction in the incidence of coronary heart disease. It therefore seems likely that patients presenting to the ED with acute chest pain have a decreasing prevalence of acute coronary syndrome (ACS) and an increasing prevalence of more benign conditions.

Differential diagnosis

The main differential diagnoses are outlined in Table 5.1.1. The most common causes of acute chest pain are ACS (unstable angina or myocardial infarction), musculoskeletal pain, anxiety, gastro-oesophageal pain and non-specific chest pain. The most serious causes (in terms of threat to life) are ACS, pulmonary embolism and aortic dissection. Because ACS is both common and life-threatening it is inevitably the primary focus of assessment. ACS is discussed in detail in Chapter 5.2, pulmonary embolus in Chapter 5.5 and aortic dissection in Chapter 5.10.

Table 5.1.1 Causes of acute chest pain

Musculoskeletal chest pain may be related to a precipitating episode, such as chest wall injury or physical overexertion. Alternatively, it may be caused by inflammation in chest wall structures. Tietze’s syndrome (costochondritis) is most commonly seen in women and is characterized by tenderness of the costochondral cartilages. Epidemic myalgia (Bornholm disease) is due to inflammation of chest wall muscles and pleura occurring after viral infection, typically with Coxsackie B virus. Herpes zoster produces severe pain along the distribution of a thoracic nerve that may be misdiagnosed as musculoskeletal pain if the patient presents before any rash or vesicles have developed.

Gastro-oesophageal pain occurs when gastric contents reflux into the oesophagus or when the oesophageal muscles spasm. Pneumomediastinum can occur spontaneously after vigorous exercise, vomiting or an asthma attack, or may be associated with barotrauma from diving or inhalation during drug abuse. Pericarditis is most commonly caused by viral infection, but may be associated with systemic illness, such as uraemia or autoimmune disease, or follow myocardial infarction or cardiac surgery (Dressler’s syndrome).

Anxiety-related chest pain is a common and frequently unrecognized cause of acute chest pain. It may also coexist with and be an important factor alongside other causes of chest pain. The patient with coronary heart disease and anxiety-related chest pain presents a particularly difficult diagnostic and management challenge. Anxiety may be related to a specific serious cause of chest pain and can be exacerbated by misguided efforts to provide reassurance through diagnostic testing. In extreme cases this can lead to ‘cardiac neurosis’, in which the patient’s anxieties about cardiac disease cause more severe disruption to their daily activities and quality of life than would be expected from the pathology that worries them.

Pleurisy is typically caused by viral infection and produces pain that is worse on inspiration. It may be differentiated from pulmonary embolus by the presence of systemic features and the absence of breathlessness or risk factors for thromboembolism, although investigation for pulmonary embolism is often required. Pneumonia and pneumothorax can also cause pleuritic pain, but should be evident on chest radiography.

There are a number of serious abdominal complaints that may present as chest pain. These include biliary colic (acute biliary pain), cholecystitis, peptic ulcer disease and pancreatitis. Failure to take a careful history and examine the abdomen may lead to delayed diagnosis.

Finally, a substantial proportion of patients will be labelled entirely appropriately as ‘non-specific chest pain’ after ED evaluation. These patients have pain that simply cannot be categorized into a clear diagnostic group. It is more honest to accept this than to apply an inaccurate diagnostic label.

Clinical features

Clinical assessment is primarily aimed at identifying patients with a significant risk of serious pathology who require further investigation and possibly inpatient care. The most common serious pathology is ACS, so clinical assessment is often focused on associated features; other serious conditions, however, such as pulmonary embolism and aortic dissection, should not be neglected.

ACS is classically associated with chest pain that is crushing, gripping or squeezing in nature and radiates to the left arm, but presenting features in the ED may be much more variable, particularly in patients with no past history of coronary heart disease and a non-diagnostic ECG. Table 5.1.2 shows the likelihood ratios of clinical features that may help to diagnose ACS. It is notable that pain radiating to the right arm or to both arms is a powerful predictor of ACS. Pain described as ‘burning’ or ‘like indigestion’ can be associated with ACS in ED patients, as is pain occurring on exertion. So the diagnoses of gastro-oesophageal reflux or stable angina should be made with great caution. Pain that is sharp or associated with inspiration or movement is less likely to be cardiac, but these findings alone do not exclude ACS. Risk factors for coronary heart disease should be routinely recorded, although they may have surprisingly little diagnostic value. This is perhaps because patients are aware of these risk factors and take them into account when deciding whether or not to seek help for episodes of chest pain. In this respect, social and cultural factors may have an importance influence upon patients’ interpretation of their symptoms and health-seeking behaviour.

Table 5.1.2 Likelihood ratios of clinical features useful for diagnosing acute myocardial infarction

Clinical examination is of limited diagnostic value and aimed mainly at identifying non-cardiac causes of chest pain or complications of ACS, such as arrhythmia, heart failure or cardiogenic shock. Pain that can be reproduced by chest wall palpation is less likely to be cardiac, but this finding does not exclude the possibility of ACS. It is also important to determine specifically that chest wall palpation is reproducing the pain that led to presentation. Simply identifying chest wall tenderness has little value – everyone has a tender chest wall if you press hard enough!

Clinical assessment should not just focus on ACS, but should aim to positively identify other causes. Pulmonary embolism is diagnostically challenging. Suspicion should be raised by chest pain that is clearly pleuritic in nature, haemoptysis, associated breathlessness, features of deep vein thrombosis or risk factors for venous thromboembolism (immobilization, malignancy, recent trauma or surgery, pregnancy, intravenous drug abuse or previous thromboembolism). Clinical examination may reveal tachycardia, tachypnoea or features of deep vein thrombosis (see Chapter 5.5). Aortic dissection is characterized by severe pain radiating to the back with associated diaphoresis. Neurological symptoms or signs, sometimes transient, are common. Clinical examination may reveal a discrepancy between blood pressure in the right and left arms (see Chapter 5.10).

Clinical assessment of chest pain should always include examination of the abdomen to identify tenderness, guarding, rebound tenderness or a positive Murphy’s sign.

Unnecessary investigation can be avoided if non life-threatening pathology can be confidently diagnosed by clinical assessment. Pain that is reproduced by chest wall palpation in a patient at low risk of coronary heart disease and with no significant risk factors for pulmonary embolus can be confidently diagnosed as musculoskeletal. A positive diagnosis is particularly valuable for the patient who is suffering primarily from anxiety-related symptoms. In this case pain is typically described as tightness around the chest and associated with a feeling of restricted breathing. Other features include palpitations (particularly awareness of the heartbeat), sweating, breathlessness, light-headedness, feelings of panic, or paraesthesia of the lips or fingertips.

Clinical investigation

The ECG is the most useful clinical investigation and should be performed on all patients presenting with acute non-traumatic chest pain. Table 5.1.3 shows the value of ECG features for diagnosing myocardial infarction. It is important to recognize that a normal ECG does not rule out myocardial infarction. ST segment elevation or depression, new Q-waves and new conduction defects are specific for acute myocardial infarction and predict adverse outcome. Patients with these features should be managed in a coronary care unit. Other changes associated with myocardial infarction are less helpful. T-wave changes are often non-specific and may be positional, or due to numerous other causes. ECG changes in pulmonary embolism are also non-specific.

Table 5.1.3 Likelihood ratios of ECG features useful for diagnosing acute myocardial infarction

A standard 12-lead ECG may be augmented by serial ECG recording or continuous ST-segment monitoring. These may detect evolving ECG changes or dynamic ST segment changes. However, these techniques may also identify non-specific false-positive changes, such as minor T-wave inversions, especially if they are used inappropriately in patients with a low risk of coronary heart disease. ST-segment monitoring was developed for the high-risk coronary care population. In low-risk ED patients with chest pain it has a very low yield of significant positive findings.

Like clinical examination, the chest radiograph is mainly intended to identify non-cardiac causes for chest pain, such as a pneumothorax or fractured rib, and complications of myocardial infarction, such as left ventricular failure. Although it is often routinely ordered it is also often unhelpful.

Biochemical cardiac markers are key investigations in acute chest pain and are a source of much heated debate. They are also a rapidly developing technology, so this chapter will focus on the principles that should guide their use.

Three key features determine the clinical value of a cardiac marker. The sensitivity tells us how good the marker is at identifying patients with disease, and thus how useful it is for ruling out myocardial ischaemia. The specificity tells us how good the marker is at identifying patients without disease, and thus how useful it is for ruling in myocardial ischaemia (i.e. a specific test that is positive suggests that the patient is very likely to have ischaemia). The prognostic value (often expressed as a relative risk) tells us how good the marker is at predicting future adverse events, such as death, myocardial infarction or life-threatening arrhythmia.

Intuitively, clinicians tend to be most concerned about sensitivity. If a marker lacks sensitivity then it may miss cases of myocardial infarction, leading to potentially catastrophic discharge home without appropriate treatment. However, sensitivity and specificity are often related and may be influenced by the threshold of the marker used to determine a positive test. The lower the threshold used for a positive test the higher the sensitivity and the lower the specificity. Many evaluations of new markers deliberately optimize sensitivity by selecting a low threshold and sacrificing specificity. This may be an acceptable trade-off in a high-risk population, but ED patients with no past history of coronary heart disease and a non-diagnostic ECG typically have a low prevalence of myocardial infarction (<10%). In these circumstances a test with low specificity will generate many false positive results, requiring hospital admission and investigation, as well as unnecessary anxiety for the patient.

The prognostic value of a marker is arguably even more useful than its diagnostic parameters, particularly if the marker can predict high-risk patients who will benefit from treatment. If a prognostically powerful marker is positive then we know the patient needs active intervention; if it is negative then we know that, even if further investigation is required to identify the exact cause of their chest pain, they are unlikely to benefit from hospital admission and treatment.

Prognostic considerations explain recent changes in the definition of myocardial infarction. The original World Health Organization (WHO) definition of myocardial infarction was based on creatinine kinase, a cardiac marker with limited sensitivity and specificity, and only weak evidence of an association with adverse prognosis. The new American Heart Association/European Society of Cardiology definition is based on troponin. Research has shown that the higher the troponin level in ACS the higher the risk of adverse outcome. Furthermore, there appears to be no threshold below which a detectable troponin level carries the same prognosis as no detectable troponin. This makes troponin the optimal cardiac marker for defining myocardial infarction. However, because troponin detects degrees of myocardial damage that are not detected by creatinine kinase, the adoption of troponin in the definition of myocardial infarction has created an apparent increase in the incidence of myocardial infarction. This has led to problems in measuring the sensitivity and specificity of cardiac markers, as these parameters depend on the definition of myocardial infarction used.

Creatinine kinase is released by damaged myocardium, but is also released by muscle and liver, and is measurable in the blood in the absence of pathology. Its MB isoenzyme (CK-MB) is more cardiac specific but shares the same problems. Substantial myocardial damage is required to produce an elevated CK-MB, but CK-MB may also be elevated in the absence of myocardial injury. Its role in diagnosis is becoming increasingly limited, although there is some evidence that measuring the gradient of the CK-MB mass assay may allow early diagnosis of myocardial infarction.

There are two troponin assays, troponin I and troponin T, with little to choose between them in terms of diagnostic or prognostic performance. As mentioned above, any detectable troponin has prognostic significance and suggests pathology. This does not mean that troponin is perfectly specific for ACS. Troponin can be elevated in pulmonary embolus, sepsis, renal failure, congestive cardiac failure and a number of other illnesses. However, in the emergency setting it is reasonable to conclude that any detectable troponin suggests serious pathology that needs inpatient investigation and treatment. This makes troponin an excellent blood test for the ED. It can be used liberally to detect serious pathology with minimal risk of generating false positives.

The only major limitation of troponin is its lack of early sensitivity. It is estimated that troponin takes up to 12 hours after symptom onset to achieve optimal sensitivity. If it is used too early after symptom onset it may produce a false negative result. This has led to the widespread practice of delaying troponin measurement until at least 12 hours after symptom onset to achieve optimal sensitivity. This practice may not be ideal because:

Myoglobin is released early after myocardial damage and may be useful for detecting myocardial infarction during the initial hours after symptom onset. It has very poor specificity, however, so most patients with chest pain and an elevated myoglobin will not have myocardial infarction. This limitation can be addressed to some extent by ignoring the absolute level of myoglobin and basing decision-making on the gradient rise between two measurements.

Markers of myocardial damage, such as troponin and CK-MB, tend to have limited early sensitivity because it takes time for these enzymes to be released from damaged myocardium and achieve detectable levels in the serum. Recent interest has therefore focused on biochemical markers that detect ischaemia, such as ischaemia-modified albumin and heart-type fatty acid-binding protein. These markers may have better early sensitivity than markers of myocardial damage and may identify patients with ischaemia but no infarction. Research is currently under way to define their role.

Many other biomarkers are being developed and emergency physicians can expect to see headline-grabbing publications extolling their virtues. However, they should be wary before indiscriminately using new markers in patients with chest pain. As described earlier, ED patients with chest pain are a heterogeneous population with a relatively low prevalence of ACS compared to the high-risk patients who usually comprise research study populations. Indiscriminate use of markers with limited specificity will lead to many false positive results and consequent patient anxiety, unnecessary investigation and waste of resources.

Provocative cardiac testing, usually using an exercise treadmill, is becoming a practical option in many EDs. Patients typically undergo a short period of observation and cardiac marker testing to rule out myocardial infarction before undergoing an exercise treadmill test. Concerns about the safety of this procedure have been addressed by data from a number of centres: however, it should be recognized that selection of low-risk patients plays a key role in ensuring safety. Performing an exercise test on a patient with ACS can be an alarming experience!

Exercise treadmill testing has limited sensitivity and specificity for coronary heart disease, but is prognostically useful and predicts the risk of adverse events over the months following attendance. It is therefore used to risk-stratify rather than to diagnose. A patient with a negative treadmill test may have coronary heart disease but can be reassured that they are at low risk of an adverse outcome.

The combination of observation and cardiac marker testing to rule out myocardial infarction, followed by provocative cardiac testing to risk-stratify, has been adopted in many hospitals in the form of a chest pain pathway or chest pain unit. These have a number of potential benefits for patients and health services, and some evidence to suggest that they reduce the probability of admission, reduce the risk of discharge with ACS, improve patient satisfaction and quality of life, and reduce health service costs. However, as an organizational intervention, the effect of the chest pain unit will depend heavily on local circumstances and may be influenced by staff attitudes, professional roles and local leadership. Furthermore, the presence of a chest pain unit may attract additional attendances with chest pain. Whether this represents identification of unmet demand or unnecessary work is a matter of opinion.

A variety of other methods of provocative cardiac testing and cardiac imaging may be used to evaluate patients with chest pain. These include echocardiography, radionuclide imaging, stress echocardiography, high-resolution CT scanning and coronary angiography. Their widespread use in the chest pain population is currently limited to the research setting. However, the development of CT as a practical way of providing non-invasive imaging of the coronary arteries raises the exciting possibility of this test being used to simultaneously evaluate for ACS, pulmonary embolism (PE) and aortic dissection. This approach needs careful evaluation, and the caveats mentioned previously about extrapolating data from selected high-risk patients to the general chest pain population will need to be considered. The presence of coronary atheroma does not necessarily confirm that the patient’s chest pain was cardiac.

A number of clinical risk scores have been developed to risk-stratify patients with suspected ACS. The Goldman algorithm and the Acute Cardiac Ischaemia Time Insensitive Predictive Instrument (ACI-TIPI) were developed and validated on large cohorts of patients with chest pain in the 1980s and 1990s. The Goldman algorithm uses a series of questions about the patient’s age, clinical history and ECG findings to categorize patients into a low (<7%) or high (>7%) risk of myocardial infarction, based on the WHO definition used at the time. ACI-TIPI can be incorporated into a computerized ECG. The user enters the patient’s age, gender, and whether chest or left arm pain is the primary symptom. The computer then uses these data and analysis of the ECG to generate a probability of acute cardiac ischaemia.

The Thrombolysis in Myocardial Infarction (TIMI) score has been developed and validated as a predictor of adverse outcome in patients with diagnosed ACS (see Chapter 5.2). Studies have evaluated the TIMI score in ED patients with suspected ACS and shown that higher scores are associated with a higher risk of adverse outcome. This has led to the TIMI score being used to risk-stratify patients with chest pain before a diagnosis of ACS has been confirmed.

Treatment

Treatment of acute chest pain is obviously directed at the specific cause. The treatment of acute coronary syndrome is outlined in Chapter 5.2, pulmonary embolus in Chapter 5.5, and aortic dissection in Chapter 5.10.

Musculoskeletal chest pain, whether due to muscular strain, chest wall injury, Tietze’s syndrome or epidemic myalgia, should be treated with simple analgesia and the patient advised to see their general practitioner if the pain persists beyond a few weeks. It is also worth considering whether anxiety may be exacerbating the symptoms.

Gastro-oesophageal pain can be treated acutely with antacids, although the diagnostic value of observing relief of pain with the so-called ‘GI cocktail’ is debatable. ACS often presents as burning or indigestion-type pain and, pain being typically fluctuant, may ease coincidentally with the administration of an antacid. Gastro-oesophageal pain should be diagnosed with caution and ideally only after ACS has been investigated and ruled out. In these circumstances a course of treatment with a proton pump inhibitor is appropriate. Follow-up will depend on local practice along with the duration and severity of symptoms.

Anxiety-related symptoms range from simple chest wall muscular tension to panic attacks, hyperventilation syndrome and cardiac neurosis. Treatment should therefore be tailored to the patient’s individual needs. In many cases anxiety will be an understandable reaction to concerns about heart disease or other serious pathology. The first step is therefore to provide clear and unequivocal reassurance. If diagnostic uncertainty makes this impossible then it may still be possible to provide reassurance by highlighting the excellent prognosis of patients with chest pain whose tests are negative. Patients with more severe symptoms may benefit from relaxation techniques, cognitive behavioural therapy or treatment with an antidepressant. These are best arranged through the patient’s general practitioner.

Managing anxiety in the ED patient is often complicated by difficulties in satisfactorily ruling out serious physical illness. A diagnosis of anxiety may be considered likely, but until cardiac testing is complete (perhaps even involving coronary angiography) the treating physician may be reluctant to discuss treatment of anxiety with the patient. This is inappropriate. If the patient has significant anxiety-related symptoms then this will adversely affect their quality of life and should be addressed regardless of whether they ultimately also need treatment for cardiac disease.

Non-specific chest pain obviously presents a diagnostic challenge. With no clear diagnosis it is difficult to advise an appropriate treatment. However, patients can be advised that, although no clear diagnosis can be made, about half such patients presenting to the ED have no further episodes of pain over the following month. Those who do suffer further episodes are unlikely to be troubled. Treatment is therefore unlikely to be required.

Finally, an acute episode of chest pain provides an opportunity to identify and manage cardiac risk factors at a time when the patient is likely to be most receptive to lifestyle advice. Smokers should be advised to use the episode as a stimulus to stop smoking, and referral to a smoking cessation service arranged. General dietary and exercise advice may also be helpful. Blood pressure, blood glucose and lipid profile may be requested as part of clinical assessment, although any abnormalities identified should preferably be referred to the patient’s general practitioner, who will be best placed to provide overall cardiovascular risk assessment, intervention and long-term follow-up.

Prognosis

Prognosis will also depend upon the underlying pathology, and the prognoses of various causes of chest pain are discussed in the relevant chapters. Patients with no obvious diagnosis after clinical assessment and ECG have an excellent prognosis, with 6-month mortality less than 1%. There is some evidence that patients who attend the ED with chest pain have a higher risk of adverse cardiac events than the general population, even if cardiac disease is ‘ruled out’ at initial presentation, but this risk is not high enough to warrant active intervention beyond ensuring that any cardiac risk factors identified have been addressed.

Likely developments over the next 5–10 years

Chest pain is responsible for a substantial and growing number of emergency medical admissions in many countries. This is placing a major burden on healthcare systems. The value of hospital admission for ACS and pulmonary embolus is being questioned, and it is likely that there will be increasing efforts to develop outpatient care for people with acute chest pain. These efforts may be successful for younger patients with no comorbidities and a single potentially serious cause for their chest pain, but may be difficult to implement among the growing population of older patients with comorbidities or multiple potentially serious causes for their pain.

A variety of new cardiac markers are being evaluated for the purpose of either identifying ACS at or shortly after attendance, or identifying troponin-negative patients who are at risk of subsequent cardiac events. Current evidence is not sufficient to support the routine use of these markers, but as these biomarkers become commercially available clinicians will have to make careful choices about which to use in their chest pain protocols.

Chest pain management is likely to be influenced by changes in health service policy, which are in turn likely to depend on local social, political and economic factors. These changes will be variable and may be unpredictable. On the one hand, public awareness of the medical significance of chest pain and policies aimed at increasing rapid access to care may lead to increased numbers of patients presenting with chest pain. On the other hand, reorganization of services and attempts to control costs may result in an opposite effect. Specifically, the development of primary angioplasty services may lead to centralization of chest pain services and patients bypassing facilities without primary angioplasty.

Introduction

Acute coronary syndrome (ACS) is the most common life-threatening condition in emergency medicine. Failure to identify and treat it promptly risks avoidable morbidity and mortality.

Aetiology, pathogenesis and pathology

ACS nearly always occurs as a consequence of atheroma in the coronary arteries, commonly known as coronary heart disease (CHD). Many people have coronary atheroma but are asymptomatic because it is not extensive enough to occlude coronary blood flow. Others have a degree of coronary occlusion that does not cause symptoms unless they exert themselves, or if myocardial oxygen demand is increased by some other mechanism, such as anaemia. Cardiac chest pain that only occurs on exertion and is rapidly relieved by rest is known as stable angina and is not classified as ACS.

ACS usually occurs when an atheromatous plaque ruptures or fissures. Haemorrhage may occur into the plaque, or thrombus may accumulate over the fissure. The type of ACS that results from this process depends on the extent of the rupture and degree of haemorrhage or thrombus formation. A gradually progressive occlusion will produce symptoms of unstable angina: progressive symptoms of myocardial ischaemia occurring on less exertion or at rest. A rapidly progressive occlusion may lead to myocardial infarction (MI), with severe pain at rest and the potential for serious complications such as arrhythmia, heart failure, cardiogenic shock or sudden cardiac death.

If coronary occlusion is minor or transient then the consequent myocardial ischaemia will not lead to myocardial damage. If coronary occlusion is severe or prolonged then myocardial necrosis will occur. Traditionally, biochemical cardiac tests (such as creatinine kinase (CK) and troponin) detect markers that are released during myocardial necrosis and are used to define the diagnosis of MI. Recently, alternative cardiac markers (such as ischaemia-modified albumin) have been developed that detect ischaemia without infarction.

Not all coronary artery occlusion is due to coronary atheroma. Prinzmetal angina describes a syndrome in which myocardial ischaemia is associated with coronary artery spasm, and is characterized by transient ST elevation on the ECG. Coronary angiography may show minor atheroma or normal coronary arteries. Uncommonly, coronary artery spasm may be severe enough to cause myocardial necrosis and an associated troponin rise.

Other rare causes of coronary artery occlusion include Kawasaki’s disease, in which occlusion is due to inflammation in the coronary artery and aortic dissection that involves the coronary arteries.

ACS may involve occlusion of one or more of the coronary arteries, and the location of occlusion may determine the clinical presentation, ECG findings and likelihood of complications. Anterior or anteroseptal MI is the most common site and usually results from occlusion of the left anterior descending artery. It has a worse prognosis than other types of MI and complications are more common. Sudden cardiac death may result from total occlusion of the left anterior descending artery, giving a lesion in this location the grim sobriquet of ‘widow-maker’. Lateral infarction is caused by occlusion of the circumflex artery or the diagonal branch of the left anterior descending artery. Inferior MI is caused by occlusion of the right coronary artery or the circumflex artery. It has a better prognosis than anterior infarction and ventricular dysfunction is less likely, although heart block due to involvement of the atrioventricular node is more common. Posterior infarction is usually due to occlusion of the right coronary artery or, less commonly, the circumflex artery in patients with dominance of the left coronary circulation. Posterior or inferior MI may result in right ventricular infarction leading to right ventricular failure.

ACS may be associated with a number of life-threatening complications. Myocardial ischaemia or infarction may lead to arrhythmia, such as atrial fibrillation, ventricular tachycardia and ventricular fibrillation. Supraventricular tachycardias are not usually associated with ACS. Heart block may occur with small infarcts affecting the nodal branch of the right coronary artery or larger septal infarcts. Infarction may lead to myocardial dysfunction, resulting in heart failure or cardiogenic shock. Massive MI may cause papillary muscle dysfunction and mitral regurgitation, ventricular septal defect or cardiac rupture. The probability of any of these complications occurring increases with the severity of myocardial damage incurred.

Epidemiology

Coronary heart disease is the leading cause of death in the world, with 8.1 million deaths in 2002. It is responsible for 6.8% of disability-adjusted life years (DALYs) lost through disease by men and 5.3% of DALYs lost by women. The global burden of CHD is expected to rise from 47 million DALYs in 1990 to 82 million in 2020. Most of this increasing burden will be in developing countries, where currently 60% of the burden of CHD is already felt. However, CHD mortality rates have dramatically decreased in many developed countries since the 1980s. Studies suggest that 50–75% of the falls in cardiac deaths can be attributed to population interventions, particularly those relating to smoking, hypertension and high cholesterol. The remaining 25–50% is due to treatments for patients with CHD, such as thrombolysis, aspirin, angiotensin-converting enzyme inhibitors, statins and coronary artery bypass surgery.

The main risk factors for CHD are well established and include smoking, diabetes, hypertension, hyperlipidaemia and a family history of CHD, while obesity and lack of exercise may play a contributory role. Age and gender are also important. CHD prevalence increases with age, and increases at an earlier age (40 to 50 years) in men than in women (over 60 years). Everyone over the age of 60 is effectively at risk of CHD. Conversely a history of CHD presenting in a relative when they were aged over 60 should not be considered a significant risk factor.

Patients presenting to the emergency department with chest pain in general, and ACS specifically, show a diurnal variation with a peak of attendances during the morning, although many of these attendances relate to symptoms occurring overnight. Presentation is more common on a Monday, when cardiovascular mortality appears to be higher. Cardiovascular mortality also increases during the winter months, particularly in colder climates.

Prevention

Prevention of ACS is achieved principally by preventing underlying CHD, although secondary prevention of ACS in patients with established CHD can be attempted by ensuring appropriate treatment with daily low-dose aspirin, β-blockers and lipid-lowering therapy.

Primary CHD prevention can take place at population or individual patient level by addressing the important coronary risk factors that are amenable to intervention. The most important modifiable risk factors at a population level are smoking, obesity and lack of exercise. These may be tackled by legislation and education, and by economic and social policy. Diabetes, hypertension and hyperlipidaemia can be addressed at an individual level. It is increasingly recognized that the importance of any one risk factor depends on the presence of other risk factors, and so cardiovascular risk is most appropriately assessed by a comprehensive assessment involving all risk factors, along with age and gender. Screening programmes should be based on overall cardiovascular risk assessment, rather than individual risk factors. Similarly, the decision to prescribe treatments for risk factors, particularly lipid-lowering therapy, should be based on overall cardiovascular risk.

This has implications for emergency medicine. It may be tempting to use the patient’s attendance at the ED to undertake opportunistic screening by, for example, measuring blood pressure, blood sugar or lipids, even though they will not influence management of the presenting complaint. This approach is inappropriate because it does not involve overall cardiovascular risk assessment. Furthermore, it may be considered unethical because the patient is effectively being screened (with potential implications for health insurance) without the opportunity to make an informed choice about whether they wish to receive screening. For these reasons, coronary risk assessment for primary prevention is best left to primary care physicians.

Although opportunistic screening in the ED is best avoided, opportunistic patient education about risk factors may be very salient, particularly if the patient has presented with symptoms that could be related to CHD. An episode of chest pain, even if ultimately diagnosed as non-cardiac, may offer an ideal opportunity to promote smoking cessation.

Clinical features

Clinical assessment of suspected ACS is described in detail in Chapter 5.1. Chest pain is suggestive of MI if it radiates to either arm, both arms or shoulders; is described as burning, like indigestion, heavy, pressing or band-like; occurs on exertion; is associated with diaphoresis, nausea or vomiting; or is worse than previous angina or similar to previous MI. Chest pain is less likely to be MI if it is sharp, pleuritic, positional, reproduced by palpation, inframammary in location, or not associated with exertion.

Clinical assessment of cardiac pain is required to determine whether it is due to stable angina or ACS (unstable angina or MI). Stable angina is caused by a fixed narrowing of the coronary artery and is characterized by pain that is predictable, precipitated by exertion, relieved by rest or glyceryl trinitrate (GTN), and is not becoming more frequent or severe. Unstable angina is caused by a dynamic narrowing of the coronary artery and is characterized by pain that may be unpredictable, may occur at rest or minimal exertion, may not be immediately relieved by rest or GTN, or may be increasing in frequency or severity. The latter may also be described as crescendo angina.

Patients with stable angina do not typically present to the ED. They are often used to their symptoms and will not seek medical help unless something unexpected happens. If a patient presents with apparently stable angina the diagnosis should be considered carefully. It should be remembered that pain precipitated by exertion is known to be predictive of MI in ED patients. Stable angina should generally be diagnosed with caution in the ED.

Clinical examination is generally unhelpful in making the diagnosis of ACS, which should be based on clinical history and investigations. However, clinical examination is essential to identify complications of ACS. Heart failure may be identified by poor peripheral circulation, tachycardia, pulmonary crepitations, elevated jugular venous pressure and a third heart sound on cardiac auscultation. The additional finding of hypotension suggests cardiogenic shock. A systolic murmur raises the possibility of papillary muscle rupture or ventricular septal defect secondary to MI, although pre-existing aortic or mitral valve disease are much more common.

Differential diagnosis

Alternative diagnoses and their differentiation from ACS are described in Chapter 5.1. The most potentially serious alternative diagnoses are pulmonary embolus and aortic dissection. These should be considered in any patient with suspected ACS who is diaphoretic, tachycardic, tachypnoeic, hypotensive, or reports associated neurological symptoms but does not have definite ECG features of ACS.

Clinical investigation

The 12-lead ECG is an essential investigation and should be performed as soon as possible after arrival in any patient with the slightest suspicion of ACS. Pre-hospital ECGs can be obtained by some emergency medical services and may be used to prioritize patients and guide triage to high-dependency areas/cardiac catheter laboratories.

The critical decision upon reviewing an initial 12-lead ECG is to determine whether the patient has ACS that may benefit from rapid early reperfusion, i.e. has evidence of ST-elevation MI (STEMI) or MI with new bundle branch block. If there is any doubt about this element of ECG interpretation then senior or specialist advice should be sought immediately. Repeat ECG recording should only be planned if a senior clinician feels there is insufficient certainty to allow for an immediate decision.

Identifying new bundle branch block presents a challenge, especially if previous notes are not immediately available. A number of ECG features seen in association with left bundle branch block, known as the Sgarbossa criteria, suggest an increased likelihood of MI. These are ST-elevation of 1 mm or more that is concordant with (in the same direction as) the QRS complex; ST-depression of 1 mm or more in leads V1, V2, or V3; and ST-segment elevation of 5 mm or more that was discordant with (in the opposite direction to) the QRS complex. These may be used to help identify patients with a new MI, but their absence should not preclude reperfusion in patients who clearly have new bundle branch block or a history that is highly suggestive of an acute MI.

Other ECG changes may be useful in diagnosing AMI and are described in Chapter 5.1 and Table 5.1.3. Q waves typically follow ST elevation, but may appear as early as 4 hours after symptom onset. Their presence does not therefore preclude early reperfusion. Tall, upright T waves (‘hyperacute’ T waves) may be present in the very early stages of infarction. Deep (>3 mm) inverted T waves suggest a subendocardial MI and a troponin rise can be expected. Similarly, patients with significant (>1 mm) ST depression have an increased risk of adverse outcome and are likely to have a troponin rise. Unfortunately, despite suggesting an increased risk of adverse outcome, neither ST depression nor deep T-wave inversion is associated with benefit from thrombolytic therapy.

Other T-wave changes, such as small inversions (<3 mm), flat T waves and biphasic T waves, are common and non-specific. They may suggest ACS, but may also occur in patients with hypertension, patients who are hyperventilating, and in the normal population. If these changes are dynamic (i.e. they develop or resolve on subsequent ECGs) then the suspicion of ACS may be raised, but even quite dramatic T-wave changes can be induced by hyperventilation or changing patient position.

In addition to changes directly suggesting ACS, the ECG should be inspected for any concurrent pathology or evidence of complications. Cardiac rate and rhythm, and P-wave presence and morphology should be evaluated for evidence of arrhythmia or heart block. Tall R waves or S waves suggest ventricular strain or hypertrophy that may contribute to or be a consequence of ACS. A subtle sign that can indicate ischaemia or ventricular dysfunction is poor anterior R-wave progression. Normally R waves progressively increase in size across leads V1 to V4. Small R waves across these leads suggest pathology.

Repeated 12-lead ECG recording or continuous ST-segment monitoring can help to identify transient or dynamic ECG changes. The development of significant (>1 mm) ST deviation provides clear evidence of ischaemia, identifies high-risk patients, and may facilitate rapid identification of patients requiring reperfusion. T-wave changes, by contrast, are non-specific and often arise as a result of hyperventilation or changes in patient position during monitoring. The incidence of significant ST changes decreases and the incidence of false positive T-wave changes increases in patients with a lower likelihood of significant ACS. Therefore, repeated ECG recording and ST-segment monitoring should be reserved for high-risk patients.

A normal or non-diagnostic ECG does not rule out ACS or necessarily stratify the patient to very low risk. In fact, most patients admitted with ACS do not have diagnostic ECG changes. Serial ECG recordings and ST-segment monitoring do not substantially increase the negative predictive value of the ECG or provide very useful prognostic data. Negative ECG recording therefore has limited value.

Biochemical markers are discussed in detail in Chapter 5.1. Their role in emergency medicine is principally diagnostic, in that they are used to identify patients with ACS from among those presenting with chest pain, and to rule out ACS if negative. However, it should be remembered that a negative cardiac marker, even if highly sensitive and performed at an optimal time after the worst symptoms, does not rule out CHD, or even necessarily ACS. Patients with negative markers will still require risk stratification and further cardiac testing if ACS is considered a likely diagnosis.

Biochemical markers (particularly troponin) have a valuable prognostic role. Any patient with an elevated troponin is at increased risk of adverse outcome and has the potential to benefit from hospital admission. If ACS is the likely cause of a troponin elevation then the patient should be admitted under the care of a cardiologist. As a general rule, the higher the troponin level the greater risk of adverse outcome. So patients with minor troponin elevations may be managed conservatively and possibly without ECG monitoring, whereas those with substantial troponin elevations should be managed on a coronary care unit and considered for early percutaneous coronary intervention (PCI), even if they have no significant ECG changes.

Provocative cardiac testing, such as exercise treadmill testing, is also described in Chapter 5.1. Its main role is to risk-stratify patients with chest pain who do not have ECG or biochemical changes suggesting ACS, and thus allow discharge home if negative. Provocative testing can be used to risk-stratify patients presenting with chest pain and known CHD. In these circumstances an early positive test will prompt rapid referral to cardiology for consideration of cardiac catheterization, whereas a late positive or negative test suggests that conservative treatment is appropriate. The use of provocative cardiac testing to risk-stratify patients with troponin-positive ACS is best left to the cardiologists.

As described in Chapter 5.1, radionuclide scanning and CT imaging may be used in some EDs to screen for significant CHD, but their use is not currently widespread and relates mainly to ruling out CHD in low-risk patients rather than risk-stratifying those with ACS.

Criteria for diagnosis

The term ACS covers a spectrum of disorders, including unstable angina, non-ST elevation MI (NSTEMI) and ST-elevation MI (STEMI). The diagnostic definition of MI has been a matter of intense debate in recent years and a consensus is gradually emerging. In contrast, the challenge of defining a diagnosis of ACS per se has been largely overlooked.

The original World Health Organization (WHO) diagnosis of MI is outlined in Table 5.2.1. It required an elevation of creatinine kinase to more than twice the upper limit of the normal range. With the development of troponins it became apparent that this definition failed to include a substantial number of patients with prognostically significant myocardial damage, as evidenced by a troponin rise. Therefore the American Heart Association and European Society of Cardiology (AHA/ESC) developed a new definition of MI, outlined in Table 5.2.2, which required a rise in serum troponin above the 99th percentile of the values for a reference control group.

Table 5.2.1 WHO criteria for definite acute MI (1970)

Table 5.2.2 The AHA/ESC criteria for MI (2000)

The AHA/ESC definition has been widely adopted, despite a number of concerns and criticisms. Patients with ACS who fulfil this definition have a higher risk of adverse outcome than those who do not. However, patients with MI according to the AHA/ESC criteria alone have a lower risk of adverse outcome than those who fulfil both the AHA/ESC and WHO criteria. This has led to problems in maintaining consistent care over time, and some experts have suggested identifying a threshold level for troponin (for example troponin T >1 ng/mL) above which clinically important MI should be diagnosed. This controversy is unlikely to be completely resolved in the near future, particularly if newer and more sensitive biochemical markers are developed. However, the most important issue to recognize is that any detectable troponin is associated with an increased risk of adverse outcome, and the higher the troponin level the higher that risk.

MI can be usefully defined as STEMI or NSTEMI on the basis of the ECG. If there is evidence of significant ST elevation on any ECG (>2 mm in two consecutive chest leads, or > 1mm in two consecutive limb leads) then the patient has STEMI. These patients are likely to benefit from early reperfusion therapy. Patients without these changes but with evidence of myonecrosis based on cardiac markers are defined as having NSTEMI and do not benefit from reperfusion with thrombolytics, although PCI may be beneficial. NSTEMI and ACS without criteria for MI may be categorized together as non-ST elevation ACS. The terms STEMI and NSTEMI have largely replaced the terms Q wave and non-Q wave MI. ST elevation at presentation is usually associated with the subsequent development of Q waves on later ECGs, so the terms may be interchangeable. However, because STEMI and NSTEMI can be differentiated at presentation, when the key clinical decisions have to be made, they have much more practical value than definitions based on the development of Q waves.

The diagnosis of ACS can be made in the absence of a troponin rise if the patient has characteristic ECG changes, such as ST-segment deviation or deep T-wave inversion. However, significant ECG changes are usually associated with a troponin rise. This means that the clinical diagnosis of ACS without MI is usually based on the clinical history, possibly augmented by provocative cardiac testing, myocardial perfusion scanning or coronary artery imaging. As the clinical features are known to be unreliable for ACS (see Chapter 5.1) and many patients with suspected ACS do not receive further cardiac testing, differentiation between ACS and either stable angina or non-coronary pain may be uncertain. This fact is often overlooked when guidelines are developed for ACS. Identifying a patient with ACS or suspected ACS relies on clinical judgement that is often imperfect. This is an important issue because only a minority of patients admitted to hospital with ACS have diagnostic ECG changes.

Treatment

Some treatments are indicated for all ACS, whereas others have specific application to STEMI, NSTEMI and other ACS.

STEMI

Non-STEMI

Antiplatelet therapy

In addition to aspirin, patients should receive clopidogrel 300 mg loading dose and 75 mg/day unless they are likely to undergo emergency coronary bypass surgery or immediate coronary angiography.

Antithrombin therapy

Subcutaneous low molecular weight or unfractionated heparin should be given until angiography or for 48–72 hours. The dose of low molecular weight heparin should be reduced if there is renal impairment. The dose of heparin is as above.

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