Acute myocardial infarction

What is acute myocardial infarction?

Myocardial infarction (MI) is one of the most severe presentations of coronary heart disease (CHD).¹

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. Nearly half of potentially salvageable myocardium is lost within one hour of the coronary artery being occluded, and two thirds are lost within three hours.²

Myocardial infarction is now considered part of a spectrum referred to as acute coronary syndrome (ACS). This refers to a spectrum of acute myocardial ischaemia that also includes unstable angina and non-ST-segment elevation myocardial infarction (NSTEMI).³

The new criteria for diagnosing myocardial infarction are detection of rise and/or fall of cardiac biomarkers (preferably troponin) with at least one value above the 99th percentile of the upper reference limit, together with evidence of myocardial ischaemia with at least one of the following:⁴

• Symptoms of ischaemia.

• ECG changes indicative of new ischaemia (new ST-T changes or new left bundle branch block (LBBB).

• Development of pathological Q-wave changes in the ECG.

• Imaging evidence of new loss of viable myocardium or new regional wall motion abnormality.

• Identification of an intracoronary thrombus by angiography or autopsy.

How common is acute myocardial infarction? (Epidemiology)⁵

The British Heart Foundation (BHF) estimates that in the UK:

• CHD is one of the leading causes of death (responsible for around 68,000 deaths each year) and the most common cause of premature death.

• Around 2.3 million people are living with CHD (about 1.5 million men and 830,000 women).

• Around 100,000 hospital admissions each year are due to MIs.

• Around 1.4 million people have survived an MI (about one million men and 380,000 women).

Risk factors

• Non-modifiable risk factors for atherosclerosis include increasing age, being 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.⁶

• Certain ethnic groups have higher risk of CHD. In the UK, the highest recorded rates of coronary artery disease mortality are in people born in India, Pakistan and Bangladesh.⁷ South Asians are thought to have a 40-60% higher risk of CHD-related mortality compared to other populations.

Symptoms of acute myocardial infarction (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 and tend to be seen in women, older men, people with diabetes and people from ethnic minorities. Atypical symptoms include 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 develops, pericardial rub.

• There may be signs of congestive heart failure, including pulmonary rales, peripheral oedema, elevated jugular venous pressure.

Assessment for possible acute coronary syndrome⁸

• Consider the history of the pain, any cardiovascular risk factors, history of CHD and any previous treatment, and previous investigations for chest pain.

• Symptoms that may indicate ACS include:

  • Pain in the chest and/or other areas (eg, the arms, back or jaw) lasting for 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:⁹

  • Stop what they are doing and rest.

  • Use GTN spray or tablets as instructed.

  • Take a second dose of GTN after five minutes if the pain has not eased.

  • Take a third dose of GTN after a further five minutes if the pain has still not eased.

  • Call 999/112/911 for an ambulance if the pain has not eased after another five minutes (ie 15 minutes after onset of pain), or earlier if the pain is intensifying or the person is unwell.

Differential diagnosis

See also the separate Chest pain and Cardiac-type chest pain presenting in primary care articles.

• Cardiovascular: stable angina, another form of ACS (unstable angina or NSTEMI), acute pericarditis, myocarditis, aortic stenosis, aortic dissection, pulmonary embolism.

• Respiratory: pneumonia, pneumothorax.

• Gastrointestinal: oesophageal spasm, gastro-oesophageal reflux disease, acute gastritis, cholecystitis, acute pancreatitis.

• Musculoskeletal chest pain.

Consider non-atherosclerotic 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 (eg, hyperthyroidism) or decreased oxygen delivery (eg, severe anaemia).

Diagnosing acute myocardial infarction (Investigations)

• If diagnosis is suspected, immediately arrange urgent hospital assessment and admission. Call 999/112/911 ambulance.

• ECG:

  • May be helpful in a 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 ACS when people have a normal resting 12-lead ECG.

In hospital

• FBC 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 also separate Cardiac enzymes and markers for myocardial infarction article.

  • Measurement of a biomarker of cardiac cell injury, preferably high-sensitivity cardiac troponin, is recommended in all patients with suspected ACS. In patients with MI, levels of troponin rise rapidly (usually within 1 hour if using high-sensitivity assays) after symptom onset and remain elevated for a variable period of time (usually several days).³

• Serial ECGs and continuous ECG monitoring in a coronary care unit (CCU).

• CXR: to assess the patient's heart size and the presence or absence of heart failure and pulmonary oedema. This may also assist in differential diagnosis.

• Pulse oximetry and blood gases: monitor oxygen saturation.

• Offer 64‑slice (or above) CT coronary angiography if:⁸

  • Clinical assessment indicates typical or atypical angina; or

  • Clinical assessment indicates non-anginal chest pain but 12‑lead resting ECG has been done and indicates ST‑T changes or Q waves.

• If CT coronary angiography is non-diagnostic, offer non-invasive functional imaging - eg:⁸

  • Myocardial perfusion scintigraphy with single photon emission computed tomography (MPS with SPECT); or

  • Stress echocardiography; or

  • First-pass contrast-enhanced magnetic resonance (MR) perfusion; or

  • MR imaging for stress-induced wall motion abnormalities.

• 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.

Acute myocardial infarction management

See the separate Acute myocardial infarction management, Cardiovascular risk assessment and Cardiac rehabilitation articles.

Complications of acute myocardial infarction

See the separate Complications of acute myocardial infarction article.

Prognosis⁵

• The British Heart Foundation reports that in the 1960s, more than 70% of heart attacks in the UK were fatal; today, at least 70% of people survive an MI.

• The overall prognosis depends on the extent of heart muscle damage. A greater degree of myocardial necrosis is associated with a worse prognosis and a higher risk of heart failure.

• Other factors that can adversely affect prognosis include:

  • Delayed reperfusion.

    • Site of the infarction (anterior MI has a less favourable prognosis than inferior MI).

• Choice of treatment (people who undergo revascularisation have better outcomes than those who do not).

  • Comorbidities, eg, hypertension, diabetes, chronic kidney disease, congestive heart failure, and frailty.

    • Complications, eg, heart failure, arrhythmias, bleeding, and depression.

  • Older age.

  • Female sex.

  • Poor compliance with secondary prevention measures.

• A systematic review assessed the prevalence of 30-day readmission following acute MI:¹⁰

• The 30-day readmission rates ranged from 11–14%.

• Acute coronary syndrome, angina, acute ischemic heart disease, and heart failure were the main cardiovascular reasons for 30-day readmission. Non-specific chest pain was the main non-cardiovascular reason for 30-day readmission.

• The other risk factors for readmission included kidney disease, female sex, diabetes mellitus, and chronic obstructive pulmonary disease.

Prevention of acute myocardial infarction

See the separate Prevention of cardiovascular disease article.