An acute myocardial infarction is caused by necrosis of myocardial tissue due to ischaemia, usually due to blockage of a coronary artery by a thrombus. Most myocardial infarctions are anterior or inferior but may affect the posterior wall of the left ventricle to cause a posterior myocardial infarction.

Epidemiology²

• Coronary heart disease (CHD) is the most common cause of death in the UK. CHD is responsible for the deaths of approximately one in five men, and one in six women.
• The average incidence of myocardial infarction for those aged between 30 and 69 years is about 600 per 100,000 for men, and 200 per 100,000 for women.
• Mortality rates from CHD are higher for men than women, people living in deprived areas and in people of South Asian origin. There is evidence of earlier deaths for men than women after an acute myocardial infarction.³
• Pre-menopausal women appear to be protected from atherosclerosis.
• Incidence increases with age and elderly people also tend to have higher rates of morbidity and mortality from their infarcts.
• Incidence rates of myocardial infarction are lower in the South of England compared with the North of England, Scotland and Northern Ireland.

Risk factors

• Non-modifiable risk factors for atherosclerosis include increasing age, male, family history of premature CHD, premature menopause.
• Modifiable risk factors for atherosclerosis include smoking, diabetes mellitus (and impaired glucose tolerance), metabolic syndrome, hypertension, hyperlipidaemia, obesity and physical inactivity.
• Ethnic group: in the UK, the highest recorded rates of coronary artery disease mortality are in people born in India, Pakistan and Bangladesh.⁴

Presentation

• Chest pain (central chest pain may not be the main symptom):
  • Three-quarters of patients present with characteristic central or epigastric chest pain radiating to the arms, shoulders, neck, or jaw.
  • The pain is described as substernal pressure, squeezing, aching, burning, or even sharp pain.
  • Radiation to the left arm or neck is common.
  • Chest pain may be associated with sweating, nausea, vomiting, dyspnoea, fatigue, and/or palpitations.
• Shortness of breath: may be the patient's anginal equivalent or a symptom of heart failure.
• Atypical presentations are common (especially in women, older men, people with diabetes, and people from ethnic minorities), e.g. abdominal discomfort or jaw pain; elderly patients may present with altered mental state.

Signs

Cardiovascular examination findings can vary enormously:

• Low-grade fever, pale and cool, clammy skin.
• Hypotension or hypertension can be observed depending on the extent of the myocardial infarction.
• Dyskinetic cardiac impulse (in anterior wall myocardial infarction) can be palpated occasionally.
• Third and fourth heart sound, systolic murmur if mitral regurgitation or ventricular septal defect develop, pericardial rub.
• There may be signs of congestive heart failure, including pulmonary rales, peripheral oedema, elevated jugular venous pressure.

Assessment for possible acute coronary syndrome¹

• Consider the history of the pain, any cardiovascular risk factors, history of ischaemic heart disease and any previous treatment, and previous investigations for chest pain.
• Symptoms that may indicate acute coronary syndrome include:
  • Pain in the chest and/or other areas (e.g. the arms, back or jaw) lasting longer than 15 minutes.
  • Chest pain with nausea and vomiting, marked sweating and/or breathlessness, or haemodynamic instability.
  • New-onset chest pain, or abrupt deterioration in stable angina, with recurrent pain occurring frequently with little or no exertion and often lasting longer than 15 minutes.
• The response to glyceryl trinitrate (GTN) should not be used to make a diagnosis and symptoms should not be assessed differently in men and women or among different ethnic groups.
• Patients with pre-existing angina should be advised that when an attack of angina occurs, they should:⁵
  • Stop what they are doing and rest.
  • Use GTN spray or tablets as instructed.
  • Take a second dose of GTN after 5 minutes if the pain has not eased.
  • Take a third dose of GTN after a further 5 minutes if the pain has still not eased.
  • Call 999 for an ambulance if the pain has not eased after another 5 minutes (i.e. 15 minutes after onset of pain), or earlier if the pain is intensifying or the person is unwell.

Differential diagnosis

• Cardiovascular: stable angina, another form of acute coronary syndrome (unstable angina or NSTEMI), acute pericarditis, myocarditis, aortic stenosis, aortic dissection, pulmonary embolism
• Respiratory: pneumonia, pneumothorax
• Gastrointestinal: oesophageal spasm, oesophagitis, gastro-oesophageal reflux, acute gastritis, cholecystitis, pancreatitis
• Musculoskeletal chest pain

Consider nonatherosclerotic causes of myocardial infarction in younger patients or if there is no evidence of atherosclerosis: coronary emboli from sources such as an infected cardiac valve, coronary occlusion secondary to vasculitis, coronary artery spasm, cocaine use, congenital coronary anomalies, coronary trauma, increased oxygen requirement (e.g. hyperthyroidism) or decreased oxygen delivery (e.g. severe anaemia).

Investigations

• If diagnosis is suspected, immediately arrange urgent hospital assessment and admission (999 Ambulance).
• ECG:
  • May be helpful pre-hospital setting if the diagnosis is uncertain or in a remote area in the assessment for pre-hospital thrombolysis, but otherwise should not delay getting the patient to hospital.
  • Features may initially be normal but abnormalities include new ST segment elevation; initially peaked T waves and then T wave inversion; new Q waves; new conduction defects.
  • Do not exclude an acute coronary syndrome when people have a normal resting 12-lead ECG.

In hospital

• Full blood count to rule out anaemia; leukocytosis is common; monitor potassium levels (electrolyte disturbances may cause arrhythmias, especially potassium and magnesium); renal function - estimated glomerular filtration rate (eGFR) - should be measured prior to starting an angiotensin-converting enzyme (ACE) inhibitor. Lipid profile needs to be obtained at presentation because levels can change after 12-24 hours of an acute illness. Measure C-reactive protein (CRP) and other markers of inflammation.
• Cardiac enzymes:
  • See separate article Cardiac Enzymes and Markers for Myocardial Infarction.
  • Cardiac troponins T and I are highly sensitive and specific for cardiac damage. The risk of death from an acute coronary syndrome is directly related to troponin level and patients with no detectable troponins have a good short-term prognosis. Serum levels increase within 3-12 hours from the onset of chest pain, peak at 24-48 hours, and return to baseline over 5-14 days. Troponin levels may therefore be normal initially and should be repeated.
  • Myocardial muscle creatine kinase (CK-MB) is found mainly in the heart. CK-MB levels increase within 3-12 hours of onset of chest pain, reach peak values within 24 hours, and return to baseline after 48-72 hours. Sensitivity and specificity are not as high as for troponin levels.
• Serial ECGs and continuous ECG monitoring in coronary care unit (CCU).
• Chest X-ray: to assess the patient's heart size and the presence or absence of heart failure and pulmonary oedema. May also assist in differential diagnosis.
• Pulse oximetry and blood gases: monitor oxygen saturation.
• Cardiac catheterisation and angiography: cardiac angiography defines the patient's coronary anatomy and the extent of the disease.
• Echocardiography can define the extent of the infarction and assess overall ventricular function and can identify complications, such as acute mitral regurgitation, left ventricular rupture or pericardial effusion.
• Myocardial perfusion scintigraphy using single photon emission computed tomography (SPECT): the National Institute for Health and Clinical Excellence (NICE) recommends that myocardial perfusion scintigraphy using SPECT should be the first test used for:⁶
  • People where stress ECG may not give accurate or clear results, e.g. women, people who have certain unusual patterns in the electrical activity of their heart, people with diabetes or people for whom exercise is difficult or impossible.
  • The diagnosis of people who are less likely to have coronary artery disease and who are at lower risk of having heart problems in the future. The likelihood of a person having coronary artery disease can be assessed by considering a number of factors, e.g. age, sex, ethnic background and family history as well as the results of physical examination and investigations.
  • As an investigation in people who still have symptoms following a myocardial infarction or despite having had treatment to improve coronary artery blood flow.

Management

See separate articles Acute Myocardial Infarction Management, Secondary Prevention of Ischaemic Heart Disease and Cardiac Rehabilitation

Complications

See separate article Complications of Acute Myocardial Infarction.

Prognosis

• Mortality rates from coronary heart disease have been falling in the UK since the late 1970s, and have fallen 24% in the last 10 years for people under the age of 75 years.²
• The mortality of acute coronary syndrome with clinical myocardial infarction treated with modern treatments including thrombolysis has been estimated to be 12-15% within 6 months of the acute coronary syndrome.²
• However, up to 50% of people who have an acute myocardial infarction die within 30 days of the event, and over half of these deaths occur before medical assistance arrives or the patient reaches hospital.⁷
• About one third of all deaths occur within the first hour, usually as the result of an acute fatal arrhythmia.⁷
• Prognosis correlates with the degree of myocardial necrosis. Greater degrees of myocardial necrosis are associated with a worse prognosis. The degree of myocardial necrosis can be estimated by various factors - for example:²
  • The rise in serum troponin T
  • Degree and extent of ECG changes
  • Degree of left ventricular dysfunction on echocardiography
• The prognosis also depends on the timing and nature of intervention; the prognosis is improved with successful early reperfusion, preserved left ventricular function and short-term and long-term treatment with betablockers, aspirin, statins and ACE inhibitors.⁸
• Elderly patients with acute myocardial infarction are at increased risk of developing complications and should be treated aggressively.

Prevention

See separate article Primary Prevention of Cardiovascular Disease.

Document references

1. Chest pain of recent onset, NICE Clinical Guideline (March 2010); Assessment and diagnosis of recent onset chest pain or discomfort of suspected cardiac origin
2. Myocardial infarction - secondary prevention, Clinical Knowledge Summaries (January 2008)
3. Rieves D, Wright G, Gupta G, et al; Clinical trial (GUSTO-1 and INJECT) evidence of earlier death for men than women Am J Cardiol. 2000 Jan 15;85(2):147-53. [abstract]
4. Bhopal R, Unwin N, White M, et al; Heterogeneity of coronary heart disease risk factors in Indian, Pakistani, Bangladeshi, and European origin populations: cross sectional study. BMJ. 1999 Jul 24;319(7204):215 [abstract]
5. Angina - stable, Clinical Knowledge Summaries (September 2009)
6. Angina and myocardial infarction - myocardial perfusion scintigraphy, NICE Technology Appraisal (2003); Coronary imaging: Myocardial perfusion scintigraphy for the diagnosis and management of angina and myocardial infarction
7. Myocardial infarction - thrombolysis, NICE Technology Appraisal (2002); The clinical effectiveness and cost effectiveness of drugs for early thrombolysis in the treatment of acute myocardial infarction
8. Garas S et al; Myocardial Infarction, eMedicine, Jan 2010

Internet and further reading

• Coronary heart disease, National service frameworks and strategies, NHS Choices
• ECG Library; © Stephen Gerred (Medical Registrar Auckland, New Zealand) Dean Jenkins (Specialist Registrar, Llandough Hospital, Cardiff, Wales)

Acknowledgements