Severe left ventricular dysfunction or one of the other mechanical complications of acute myocardial infarction (AMI) cause most of the deaths following AMI. Complications of AMI include:¹

• Ischaemic (including failure of reperfusion): angina, reinfarction, infarct extension
• Mechanical: heart failure, cardiogenic shock, mitral valve dysfunction, aneurysms, cardiac rupture
• Arrhythmic: atrial or ventricular arrhythmias, sinus or atrioventricular (AV) node dysfunction
• Thrombosis and embolic: central nervous system or peripheral embolisation
• Inflammatory: pericarditis
• Psychosocial complications, including depression

Ischaemic complications¹

• Failure of reperfusion is less likely with the availability of primary percutaneous coronary intervention (PCI). Reperfusion should reduce ST elevation to less than 50% within one hour.²
• Patients with infarct extension or postinfarction angina usually have continuous or recurrent chest pain, with protracted elevation in the creatine kinase (CK) level and, occasionally, new electrocardiogram (ECG) changes.
• CK-MB is a more useful marker for tracking ongoing infarction than troponin because of its shorter half-life.
• The diagnosis of infarct expansion, reinfarction, or postinfarction ischaemia can be made with echocardiography or nuclear imaging.
• Medical therapy with aspirin, heparin, nitrates, and betablockers is indicated in patients who have had a myocardial infarction and have ongoing ischaemic symptoms.
• Management is by angiography followed by coronary revascularisation.

Reocclusion of an infarct-related artery

• Occurs in 5% to 30% of patients following fibrinolytic therapy. These patients also tend to have a poorer outcome.
• May occur in up to 40% of patients and can be difficult to diagnose.
• Reinfarction is more common in patients with diabetes mellitus or previous myocardial infarction.

Infarction in a separate territory (recurrent infarction)

• May be difficult to diagnose within the first 24 to 48 hours after the initial event.
• Multivessel coronary artery disease is common in patients with acute myocardial infarction (AMI).

Postinfarction angina

• Angina may occur from a few hours to 30 days after AMI.
• The incidence is highest in patients with non-ST-elevation myocardial infarction (approximately 25%) and those treated with fibrinolytics compared with PCI.

Mechanical complications

Left ventricular dysfunction and heart failure

• Pulmonary oedema is common following a myocardial infarction. Overt cardiac failure following a myocardial infarction is a poor prognostic feature.
• Heart failure is usually due to myocardial damage but may also be caused by an arrhythmia or mechanical complications such as mitral regurgitation or ventricular septal defect.³
• The severity of the heart failure depends on the extent of the infarction and the presence of any other complications, e.g. acute mitral regurgitation.
• Cardiogenic shock occurs in 5-20% of patients following myocardial infarction.
• The Killip classification is one method used to assess the severity of cardiac failure following a myocardial infarction:⁴
  • Cardiogenic I: no crackles and no 3rd heart sound
  • Cardiogenic II: crackles in less than 50% of lung fields or a 3rd heart sound
  • Cardiogenic III: crackles in over 50% of lung fields
  • Cardiogenic IV: cardiogenic shock
• Cardiac failure usually responds well to oxygen, diuretics and angiotensin-converting enzyme (ACE) inhibitors/angiotensin receptor antagonists (and intravenous nitrates if no hypotension).
• Measurement of pulmonary wedge pressure by Swan-Ganz catheterisation in ITU; intravenous positive inotropes may be required.
• Patients who have a left ventricular ejection fraction of 0.4 or less and either diabetes or clinical signs of heart failure should receive eplerenone (an aldosterone antagonist) unless contra-indicated by renal impairment or hyperkalaemia (left ventricular function should be assessed in all patients with acute myocardial infarction (AMI) during the initial hospital admission).⁵
• Spironolactone can be used instead of eplerenone; spironolactone is cheaper but has many more potential adverse effects than eplerenone.
• Oxygen should be administered and pulse oximetry used to monitor oxygen saturation. For patients with severe heart failure, blood gases should be checked regularly, and continuous positive airway pressure or endotracheal intubation with ventilatory support may be required.³
• Percutaneous revascularisation is associated with an improved prognosis. Aggressive treatment with intra-aortic balloon pumping followed by surgical revascularisation may also significantly reduce mortality.
• The mortality rate is over 70% if revascularisation is not possible.

Ventricular septal rupture and free wall rupture

• Risk factors: older age, female gender, nonsmoker, anterior infarction, worse Killip class on admission, increasing heart rate on admission, first myocardial infarction and hypertension.⁶
• The incidence is approximately 0.2% and has dramatically decreased with reperfusion therapy.
• May develop as early as 24 hours after myocardial infarction but often presents 2-7 days afterwards. Mortality rates are greater than 90%.
• Ventricular septal rupture:¹
  • Patients may initially have no clinically significant cardiopulmonary symptoms but rapid recurrence of angina, hypotension, shock or pulmonary oedema develop.
  • Signs of ventricular septal rupture include a new harsh pansystolic murmur best heard at the left lower sternal border, with worsening haemodynamic profile and biventricular failure.
  • Diagnosis is by transoesophageal echocardiography or by showing a step-up in oxygen saturation in the right ventricle on pulmonary artery catheterisation.
  • Urgent surgical repair is the treatment of choice, even if the patient's condition is stable.
• Free wall rupture:
  • Rupture of a free wall causes bleeding into the pericardium, leading to cardiac tamponade, with progressively poorer cardiac function. Death is often immediate.
  • Emergency pericardiocentesis and cardiac surgery are essential for any hope of survival.
• False aneurysm:¹
  • A false aneurysm (pseudoaneurysm) is caused by a contained rupture of the left ventricular free wall.
  • The pseudoaneurysm communicates with the body of the left ventricle through a narrow neck.
  • Pseudoaneurysms may remain clinically silent and be discovered during routine investigations but some patients may have recurrent tachyarrhythmia, systemic embolisation, and heart failure.
  • The diagnosis is confirmed by echocardiography, MRI or CT scan.
  • Spontaneous rupture can occur without warning in approximately one third of patients with a pseudoaneurysm. Therefore, surgical intervention is recommended for all patients.

Acute mitral regurgitation

• Most common with an infero-posterior infarction and may be due to ischaemia, necrosis, or rupture of the papillary muscle.
• Mitral regurgitation following myocardial infarction predicts a poor prognosis but is often transient and asymptomatic.
• Rupture of papillary muscle or chordae tendinae:
  • Causes severe mitral regurgitation within the first week after infarction and is a life-threatening complication. It is most often seen with inferior infarctions.
  • One study found a median time for papillary muscle rupture in patients treated with fibrinolysis to be 13 hours after AMI.¹
  • Papillary muscle rupture is found in 7% of patients in cardiogenic shock and contributes to 5% of the mortality after AMI.
  • Revascularisation decreases the incidence of rupture.¹
• Mitral regurgitation is often accompanied by a pansystolic murmur, but the murmur may be inaudible if left atrial pressure rises sharply.
• Echocardiogram is required to confirm the diagnosis, especially to differentiate from rupture of the interventricular septum, and to assess severity.
• Management:¹
  • Aggressive medical therapy for patients with papillary muscle rupture includes vasodilator therapy. Nitroprusside is useful in the treatment of patients with acute mitral regurgitation.
  • The prognosis is poor for medically treated patients and so patients with papillary muscle rupture should be considered for emergency surgery.
  • Coronary angiography should be performed before surgical repair because revascularisation is associated with improved short-term and long-term mortality.
  • Patients with moderate mitral regurgitation who do not improve with vasodilator therapy are also candidates for surgery.

Left ventricular aneurysm

• Occurs after 2-15% of infarcts. Patients who do not receive reperfusion therapy are at greatest risk (10% to 30%).¹ Five-year survival is 10-25%.
• May be clinically silent or cause recurrent tachyarrhythmias, heart failure or systemic emboli.
• ECG may show persistently raised ST segments and chest X-ray may show cardiomegaly with an abnormal bulge at the left heart border. Diagnosis is made by echocardiography, MRI or CT scan.
• Congestive heart failure with acute aneurysms is managed with intravenous vasodilators, and ACE inhibitors.
• Heart failure with chronic aneurysms can be managed with ACE inhibitors, digoxin, and diuretics.¹
• Anticoagulation with warfarin is indicated for patients with a mural thrombus.
• Refractory heart failure or refractory ventricular arrhythmias in patients with aneurysms is an indication for surgical resection. Revascularisation is beneficial for patients with a large amount of viable myocardium around the aneurysmal segment.¹

Right ventricular failure

• Mild right ventricular dysfunction is common after infero-posterior infarcts but right heart failure only occurs in 10% of these patients.
• May present with hypotension, jugular venous distention with clear lungs and no dyspneoa. Severe right ventricular failure may present with a low cardiac output state, including oliguria and altered mental state.¹
• Diagnosis is made by echocardiography.
• Nitrates, diuretics and any other drugs that reduce preload should be avoided.
• Management is focused on maintaining adequate right and left ventricle filling with fluids (with central venous line insertion and monitoring of cental pressures). Positive inotropes such as dobutamine may also be required.
• Most patients with right ventricular infarction improve after 48 to 72 hours.¹

Left ventricular outflow tract obstruction¹

• Dynamic left ventricular outflow tract obstruction is an uncommon complication of acute anterior myocardial infarction.
• Patients with severe obstruction may appear to be in cardiogenic shock with severe orthopnoea, dyspnoea, and oliguria and may have altered mental state.
• Present with a new systolic ejection murmur heard best at the left upper sternal border, with radiation to the neck, and a new pansystolic murmur at the apex, with radiation to the axilla.
• Echocardiography is the diagnostic test of choice.
• Treatment is based on expanding intravascular volume and increasing afterload. Betablockers should be added slowly.
• Haemodynamic and respiratory status should be monitored closely during treatment. Vasodilators and positive inotropes should be avoided.

Arrhythmias

A life-threatening arrhythmia, e.g. ventricular tachycardia, ventricular fibrillation and total atrioventricular (AV) block, may be the first manifestation of ischaemia. These arrhythmias may cause many of the reported sudden cardiac deaths in patients with acute coronary syndromes. Ventricular fibrillation or sustained ventricular tachycardia has been reported in up to 20% of patients.³

• Arrhythmias may be caused by infarction, reperfusion, toxic metabolites, irritable myocardium, metabolic (especially potassium or magnesium imbalance).
• Some patients exhibit reperfusion arrhythmias (e.g. ventricular ectopics, ventricular tachycardia or idioventricular rhythm) which are usually benign and do not require therapy. However, ventricular fibrillation may also occur.
• Persistent tachycardias may lead to further ischaemia.
• Antiarrhythmic agents are negatively inotropic and may encourage arrhythmias in acute coronary ischaemia. Minor arrhythmias should not be treated.
• Cardiopulmonary resuscitation should be performed in accordance with the Resuscitation Council Guidelines.⁷
• Asystole:
  • Patients with cardiac arrest secondary to asystole or pulseless electrical activity should receive intravenous adrenaline.⁵
  • Patients with pulseless electrical activity should also receive atropine.
• Ventricular arrhythmias:⁵
  • Defibrillation should be administered for patients with ventricular fibrillation or pulseless ventricular tachycardia.
  • Intravenous adrenaline or epinephrine should be used for patients with refractory ventricular tachycardia or ventricular fibrillation.
  • Intravenous amiodarone should be given for refractory ventricular tachycardia or ventricular fibrillation.
  • Intravenous amiodarone, or betablockers may be used for patients with haemodynamically stable ventricular tachycardia.
  • Patients with polymorphic ventricular tachycardia should be treated with intravenous magnesium (consider giving magnesium for all patients with arrhythmias following myocardial infarction).
  • Patients who have monomorphic ventricular tachycardia following an acute myocardial infarction (AMI) or ventricular fibrillation more than 48 hours after infarction are at increased risk and should be considered for urgent revascularisation and insertion of a implantable cardioverter defibrillator.⁵
• Bradycardia, sinoatrial dysfunction or heart block:
  • Sinus bradycardia may be due to drugs, ischaemia or a vagal response.
  • Atropine should be used for patients with symptomatic bradycardia.
  • Temporary transcutaneous pacing should be initiated for patients not responding to atropine. Temporary transcutaneous pacing is only an interim measure until a more permanent method can be employed.
  • Temporary transcutaneous pacing is very painful and may need to use benzodiazepines to sedate the patient.
  • If temporary transcutaneous pacing and atropine are ineffective, consider adrenaline (but adrenaline may worsen ischaemia), dopamine or isoprenaline infusions.
  • Transcutaneous pacing should be followed by a transvenous pacing if bradycardia persists.
  • Heart block and conduction abnormalities occur more commonly with an inferior infarction and are more ominous when they occur after anterior infarction. Heart block is often transient but should be treated with temporary pacing when cardiac output is compromised.
• Sinus tachycardia may be due to pain, anxiety, or drugs.
• Atrial fibrillation and other supraventricular tachycardias may also occur. Atrial fibrillation complicates 10-20% of AMIs but other supraventricular tachycardias are rare and usually self-limited.³

Thrombosis and embolic complications³

• Deep vein thrombosis and pulmonary embolism are now relatively uncommon after infarction, except in patients kept in bed because of heart failure.
• Prophylactic doses of a low molecular weight heparin and compression stockings should be used for prevention.
• Treatment should be with therapeutic doses of a low molecular weight heparin, followed by oral anticoagulation for 3-6 months.

Mural thrombosis and systemic embolism

• Echocardiography may reveal intraventricular thrombi. Left ventricular thrombus occurs in 20% post infarction but in up to 60% of those after a large anterior infarction.
• The thrombus may be large and is associated with embolisation in 15-20% of cases.
• Treatment is anticoagulation with unfractionated heparin or low molecular weight heparin followed by oral anticoagulants for at least 3-6 months, along with thrombolysis and/or surgical repair.⁸

Pericarditis

• Pericarditis is most common following an anterior infarction. The incidence of early pericarditis after acute myocardial infarction (AMI) is approximately 10%. Pericarditis usually develops between 24 and 96 hours after AMI.¹
• The frequency is reduced with early reperfusion in the acute management of infarction.
• Frequently occurs within a few days of the myocardial infarction and presents with a low-grade fever, pericardial friction rub and pleuritic chest pain.
• ECG may show ST elevation in all leads without reciprocal ST depression. Chest X-ray may show globular cardiac enlargement and a small pericardial effusion may be detected using echocardiography.
• Treatment of pericarditis is with anti-inflammatory drugs and analgesia, and a repeat echocardiogram if an effusion was initially present.

Dressler's syndrome

• Dressler's syndrome presents as pericarditis 1 to 8 weeks after AMI, often accompanied by pleural and pericardial effusions. The incidence is between 1% and 3%.¹
• Dressler's syndrome typically presents 2–4 weeks after a myocardial infarction with a self-limiting febrile illness accompanied by pericardial or pleural pain.⁹
• The cause of Dressler's syndrome is unknown, but an autoimmune mechanism has been suggested.¹
• The frequency is reduced with early reperfusion in the acute management of infarction.
• Initial treatment is with non-steroidal anti-inflammatory drugs.
• Steroids are indicated if symptoms are severe or when repeated drainage of a pericardial effusion is necessary.

Depression

• Significant depression occurs in about 20% of patients following myocardial infarction.⁹
• It has been found to more than treble the risk of mortality in the first six months following myocardial infarction.

Document references

1. Cleveland Clinic Center for Continuing Education; Complications of Acute Myocardial Infarction.
2. Van de Werf F, Ardissino D, Betriu A, et al; Management of acute myocardial infarction in patients presenting with ST-segment elevation. The Task Force on the Management of Acute Myocardial Infarction of the European Society of Cardiology. Eur Heart J. 2003 Jan;24(1):28-66.
3. Management of acute myocardial infarction in patients presenting with persistant ST-segment elevation, European Society of Cardiology (November 2008)
4. Khot UN, Jia G, Moliterno DJ, et al; Prognostic importance of physical examination for heart failure in non-ST-elevation acute coronary syndromes: the enduring value of Killip classification. JAMA. 2003 Oct 22;290(16):2174-81. [abstract]
5. Scottish Intercollegiate Guidelines Network (SIGN); Cardiac arrhythmias in coronary heart disease. February 2007.
6. Wehrens XH, Doevendans PA; Cardiac rupture complicating myocardial infarction. Int J Cardiol. 2004 Jun;95(2-3):285-92. [abstract]
7. Resuscitation Council; Resuscitation Guidelines (2005).
8. Keeley EC, Hillis LD; Left ventricular mural thrombus after acute myocardial infarction. Clin Cardiol. 1996 Feb;19(2):83-6. [abstract]
9. Myocardial infarction - secondary prevention, Clinical Knowledge Summaries (January 2008)

Internet and further reading

• Kondur AK; Complications of Myocardial Infarction, eMedicine, Aug 2009.
• Secondary prevention in primary and secondary care for patients following a myocardial infarction, NICE Clinical Guideline (2007)
• Scottish Intercollegiate Guidelines Network (SIGN); Cardiac arrhythmias in coronary heart disease. February 2007.
• Cardiac rehabilitation, SIGN Guideline (2002)
• ECG Library; © Stephen Gerred (Medical Registrar Auckland, New Zealand) Dean Jenkins (Specialist Registrar, Llandough Hospital, Cardiff, Wales)

Acknowledgements