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Complications of acute myocardial infarction

Medical Professionals

Professional Reference articles are designed for health professionals to use. They are written by UK doctors and based on research evidence, UK and European Guidelines. You may find the Heart attack article more useful, or one of our other health articles.

Severe left ventricular dysfunction or one of the other mechanical complications of acute myocardial infarction (AMI) causes most of the deaths following AMI. See also the separate Acute Myocardial Infarction article.

Complications of AMI include12:

  • Ischaemic (including failure of reperfusion): angina, re-infarction, 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).

Continue reading below

Ischaemic complications2

  • Failure of reperfusion is less likely with the availability of primary percutaneous coronary intervention (PCI). One study found that ST-elevation myocardial infarction (STEMI) patients with signs of ongoing ischaemia, treated with primary PCI 12 to 72 hours after symptom onset, had less myocardial salvage and developed larger infarcts than those who presented earlier. However, a large proportion achieved substantial myocardial salvage, indicating a benefit from primary PCI in late-presenting patients3.

  • 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 ECG changes.

  • Myocardial muscle creatine kinase (CK-MB) is elevated in MI. CK-MB levels rise within 3-12 hours of onset of chest pain, achieve peak values within 24 hours and return to baseline after 48-72 hours. However, sensitivity and specificity are not as high as for troponin levels.

  • CK-MB is a more useful marker than troponin for tracking ongoing infarction because of its shorter half-life.

  • The diagnosis of infarct expansion, re-infarction, or postinfarction ischaemia can be made with echocardiography or nuclear imaging.

  • Medical therapy with aspirin, heparin, nitrates, and beta-blockers 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 a minority but significant number of patients following fibrinolytic therapy. These patients also tend to have a poorer outcome.

  • Can be difficult to diagnose.

  • Re-infarction 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 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 (NSTEMI) 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 by mechanical complications such as mitral regurgitation or ventricular septal defect (VSD).

  • The severity of the heart failure depends on the extent of the infarction and the presence of any other complications - eg, acute mitral regurgitation.

  • Cardiogenic shock occurs in 5-20% of patients following myocardial infarction.

  • Killip's classification is one method used to assess the severity of cardiac failure following a myocardial infarction4:

    • Cardiogenic I: no crackles and no third heart sound.

    • Cardiogenic II: crackles in fewer than 50% of lung fields or a third 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 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.

  • 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, non-smoker, anterior infarction, worse Killip class on admission, increasing heart rate on admission, first myocardial infarction and hypertension6.

  • Postinfarction VSD is relatively infrequent but life-threatening7. The incidence 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 rupture2:

    • 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.

    • Postinfarction ventricular septal defects require urgent surgical closure8.

  • 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.

  • Pseudoaneurysm (false aneurysm)2:

    • A 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 scan 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 AMI2.

    • Papillary muscle rupture following AMI usually requires mitral valve replacement. This is being increasingly performed using minimally invasive techniques9.

    • Revascularisation decreases the incidence of rupture2.

    • However, mitral regurgitation is associated with a worse prognosis after myocardial infarction and subsequent revascularisation10.

  • 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.

  • Management2:

    • 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

  • The vulnerable myocardium following an AMI is susceptible to wall stress, resulting in infarct expansion. Subacute cardiac rupture is an extreme form of infarct expansion, whereas ventricular aneurysm is its chronic form11.

  • Occurs after 2-15% of infarcts. Patients who do not receive reperfusion therapy are at greatest risk (10% to 30%)2. 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 CXR may show cardiomegaly with an abnormal bulge at the left heart border. Diagnosis is made by echocardiography, MRI scan or CT scan.

  • Congestive heart failure with acute aneurysms is managed with intravenous vasodilators and with ACE inhibitors.

  • Heart failure with chronic aneurysms can be managed with ACE inhibitors, digoxin, and diuretics2.

  • 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. Successful left ventricular aneurysmectomy with repair using a bovine pericardial patch has been reported12.

  • Revascularisation is beneficial for patients with a large amount of viable myocardium around the aneurysmal segment2.

Right ventricular failure

  • Right ventricle myocardial infarctions accompany inferior wall ischaemia in up to one half of cases13. Mild right ventricular dysfunction is common after infero-posterior infarcts but right heart failure only occurs in a minority of these patients.

  • May present with hypotension, jugular venous distention with clear lungs and no dyspnoea. Severe right ventricular failure may present with a low cardiac output state, including oliguria and altered mental state2.

  • 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 48-72 hours2.

Left ventricular outflow tract obstruction2

  • Dynamic left ventricular outflow tract obstruction can independently result from various causes such as left ventricular hypertrophy, reduced left ventricular chamber size (dehydration, bleeding, or diuresis), mitral valve abnormalities, and hypercontractility (stress, anxiety, or inotropic agents such as dobutamine)14.

  • 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. Beta-blockers should be added slowly.

  • Haemodynamic and respiratory status should be monitored closely during treatment. Vasodilators and positive inotropes should be avoided.

Continue reading below


A life-threatening arrhythmia (eg, ventricular tachycardia, ventricular fibrillation and total 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. The risk of arrhythmic death in survivors of AMI is highest in the first six months after myocardial infarction and remains high for the subsequent two years15.

  • Arrhythmias may be caused by infarction, reperfusion, toxic metabolites, irritable myocardium, and metabolism (especially potassium or magnesium imbalance).

  • Some patients exhibit reperfusion arrhythmias (eg, 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.

  • Asystole:

    • Patients with cardiac arrest secondary to asystole or pulseless electrical activity should receive intravenous adrenaline (epinephrine)5.

    • Patients with pulseless electrical activity should also receive atropine.

  • Ventricular arrhythmias5:

    • Defibrillation should be administered for patients with ventricular fibrillation or pulseless ventricular tachycardia.

    • Intravenous adrenaline (epinephrine) should be used (as a last resort) for patients with refractory ventricular tachycardia or ventricular fibrillation.

    • Intravenous amiodarone should be given for refractory ventricular tachycardia or ventricular fibrillation.

    • Intravenous amiodarone, or beta-blockers 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 AMI or ventricular fibrillation more than 48 hours after infarction are at increased risk and should be considered for urgent revascularisation and insertion of an implantable cardioverter defibrillator5.

  • 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 it may be necessary to use benzodiazepines to sedate the patient.

    • If temporary transcutaneous pacing and atropine are ineffective, consider adrenaline (epinephrine) - but adrenaline may worsen ischaemia; also consider 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.

Thrombosis and embolic complications

  • 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 (LMWH) and compression stockings should be used for prevention.

  • Treatment should be with therapeutic doses of LMWH, followed by oral anticoagulation for 3-6 months.

Mural thrombosis and systemic embolism

  • Echocardiography may reveal intraventricular thrombi. Left ventricular thrombus occurs in 20% after infarction but in up to 60% of those after a large anterior infarction.

  • The thrombus may be large and may be associated with embolisation.

  • The rate of thrombus formation is similar for patients treated with primary percutaneous coronary intervention when compared with patients currently treated conservatively or with thrombolysis16.

  • Left ventricular mural thrombus has not been shown to be related to increased intermediate-term mortality when patients are treated with warfarin17.

Continue reading below


  • Pericarditis is most common following an anterior infarction. The incidence of early pericarditis after AMI is approximately 10%. Pericarditis usually develops between 24 and 96 hours after AMI2.

  • 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. CXR 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 2-5 weeks after AMI, often accompanied by pleural and pericardial effusions. The incidence is between 1% and 3%2.

  • Dressler's syndrome typically presents 2-5 weeks after a myocardial infarction with a self-limiting febrile illness accompanied by pericardial or pleural pain.

  • The cause of Dressler's syndrome is unknown but an autoimmune mechanism has been suggested2.

  • 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.


  • Significant depression occurs in about 20% of patients following myocardial infarction.

  • Myocardial infarction increases the risk of suicide; depression following myocardial infarction impairs the overall prognosis.

Further reading and references

  1. Mullasari AS, Balaji P, Khando T; Managing complications in acute myocardial infarction. J Assoc Physicians India. 2011 Dec;59 Suppl:43-8.
  2. Adam W Grasso, Sorin J Brener; Complications of Acute Myocardial Infarction, Center for Continuing Education, Cleveland Clinic
  3. Nepper-Christensen L, Lonborg J, Hofsten DE, et al; Benefit From Reperfusion With Primary Percutaneous Coronary Intervention Beyond 12 Hours of Symptom Duration in Patients With ST-Segment-Elevation Myocardial Infarction. Circ Cardiovasc Interv. 2018 Sep;11(9):e006842. doi: 10.1161/CIRCINTERVENTIONS.118.006842.
  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.
  5. Cardiac arrhythmias in coronary heart disease; Scottish Intercollegiate Guidelines Network - SIGN (2018)
  6. Wehrens XH, Doevendans PA; Cardiac rupture complicating myocardial infarction. Int J Cardiol. 2004 Jun;95(2-3):285-92.
  7. Isoda S, Osako M, Kimura T, et al; Surgical repair of postinfarction ventricular septal defects-2013 update. Ann Thorac Cardiovasc Surg. 2013 Apr 19;19(2):95-102. Epub 2013 Apr 11.
  8. Yam N, Au TW, Cheng LC; Post-infarction ventricular septal defect: surgical outcomes in the last decade. Asian Cardiovasc Thorac Ann. 2013 Oct;21(5):539-45. doi: 10.1177/0218492312462041. Epub 2013 Jul 9.
  9. Kriechbaum SD, Boeder NF, Gaede L, et al; Mitral valve leaflet repair with the new PASCAL system: early real-world data from a German multicentre experience. Clin Res Cardiol. 2020 May;109(5):549-559. doi: 10.1007/s00392-019-01538-3. Epub 2019 Aug 26.
  10. Boyd JH; Ischemic mitral regurgitation. Circ J. 2013;77(8):1952-6. Epub 2013 Jul 19.
  11. Anzai T; Post-infarction inflammation and left ventricular remodeling: a double-edged sword. Circ J. 2013;77(3):580-7. Epub 2013 Jan 29.
  12. Khanna S, Bhat A, Mardini M, et al; Left ventricular aneurysm: a rare complication of an acute myocardial infarction in the modern era. Oxf Med Case Reports. 2020 Sep 22;2020(9):omaa080. doi: 10.1093/omcr/omaa080. eCollection 2020 Sep.
  13. Ondrus T, Kanovsky J, Novotny T, et al; Right ventricular myocardial infarction: From pathophysiology to prognosis. Exp Clin Cardiol. 2013 Winter;18(1):27-30.
  14. Chockalingam A, Tejwani L, Aggarwal K, et al; Dynamic left ventricular outflow tract obstruction in acute myocardial infarction with shock: cause, effect, and coincidence. Circulation. 2007 Jul 31;116(5):e110-3.
  15. Arsenos P, Gatzoulis K, Dilaveris P, et al; Arrhythmic sudden cardiac death: substrate, mechanisms and current risk stratification strategies for the post-myocardial infarction patient. Hellenic J Cardiol. 2013 Jul-Aug;54(4):301-15.
  16. Osherov AB, Borovik-Raz M, Aronson D, et al; Incidence of early left ventricular thrombus after acute anterior wall myocardial infarction in the primary coronary intervention era. Am Heart J. 2009 Jun;157(6):1074-80. doi: 10.1016/j.ahj.2009.03.020.
  17. Porter A, Kandalker H, Iakobishvili Z, et al; Left ventricular mural thrombus after anterior ST-segment-elevation acute myocardial infarction in the era of aggressive reperfusion therapy--still a frequent complication. Coron Artery Dis. 2005 Aug;16(5):275-9.
  18. Larsen KK; Depression following myocardial infarction--an overseen complication with prognostic importance. Dan Med J. 2013 Aug;60(8):B4689.

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