Complications of Acute MyocardialInfarctionSevere left ventricular dysfunction or one of the other mechanical complications of acute myocardial infarction(AMI) causes most of the deaths following AMI. Complications of AMI include: [1] [2]

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).

Ischaemic complications [2]

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. [3]

Patients with infarct extension or postinfarction angina usually have continuous or recurrent chestpain, with protracted elevation in the creatine kinase (CK) level and, occasionally, newelectrocardiogram (ECG) changes.CK-MB is a more useful marker than troponin for tracking ongoing infarction because of its shorterhalf-life.The diagnosis of infarct expansion, re-infarction, or postinfarction ischaemia can be made withechocardiography or nuclear imaging.Medical therapy with aspirin, heparin, nitrates, and beta-blockers is indicated in patients who have hada myocardial infarction and have ongoing ischaemic symptoms.Management is by angiography followed by coronary revascularisation.

Reocclusion of an infarct-related arteryOccurs in a minority but significant number of patients following fibrinolytic therapy. These patientsalso 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 anginaAngina may occur from a few hours to 30 days after AMI.The incidence is highest in patients with non-ST-elevation myocardial infarction and those treated withfibrinolytics compared with PCI.

Mechanical complicationsLeft ventricular dysfunction and heart failure

Pulmonary oedema is common following a myocardial infarction. Overt cardiac failure following amyocardial infarction is a poor prognostic feature.Heart failure is usually due to myocardial damage but may also be caused by an arrhythmia ormechanical 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 othercomplications - eg, acute mitral regurgitation.

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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 amyocardial infarction: [4]

Cardiogenic I: no crackles and no third heart soundCardiogenic II: crackles in fewer than 50% of lung fields or a third heart soundCardiogenic III: crackles in over 50% of lung fieldsCardiogenic 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; intravenouspositive inotropes may be required.Patients who have a left ventricular ejection fraction of 0.4 or less and either diabetes or clinical signsof heart failure should receive eplerenone (an aldosterone antagonist) unless contra-indicated by renalimpairment or hyperkalaemia (left ventricular function should be assessed in all patients with AMIduring the initial hospital admission). [5]

Spironolactone can be used instead of eplerenone; spironolactone is cheaper but has many morepotential adverse effects than eplerenone.Oxygen should be administered and pulse oximetry used to monitor oxygen saturation. For patientswith severe heart failure, blood gases should be checked regularly, and continuous positive airwaypressure or endotracheal intubation with ventilatory support may be required.Percutaneous revascularisation is associated with an improved prognosis. Aggressive treatment withintra-aortic balloon pumping followed by surgical revascularisation may also significantly reducemortality.The mortality rate is over 70% if revascularisation is not possible.

Ventricular septal rupture and free wall ruptureRisk factors: older age, female gender, non-smoker, anterior infarction, worse Killip class onadmission, increasing heart rate on admission, first myocardial infarction and hypertension. [6]

Postinfarction VSD is relatively infrequent but life-threatening. [7] The incidence has dramaticallydecreased 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: [2]

Patients may initially have no clinically significant cardiopulmonary symptoms but rapidrecurrence of angina, hypotension, shock or pulmonary oedema develop.Signs of ventricular septal rupture include a new harsh pansystolic murmur best heard atthe left lower sternal border, with worsening haemodynamic profile and biventricular failure.Diagnosis is by transoesophageal echocardiography or by showing a step-up in oxygensaturation in the right ventricle on pulmonary artery catheterisation.Postinfarction ventricular septal defects require urgent surgical closure. [8]

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 narrowneck.Pseudoaneurysms may remain clinically silent and be discovered during routineinvestigations but some patients may have recurrent tachyarrhythmia, systemicembolisation, 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 witha pseudoaneurysm. Therefore, surgical intervention is recommended for all patients.

Acute mitral regurgitationMost common with an infero-posterior infarction and may be due to ischaemia, necrosis, or rupture ofthe papillary muscle.

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Mitral regurgitation following myocardial infarction predicts a poor prognosis but is often transient andasymptomatic.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 withfibrinolysis to be 13 hours after AMI. [2]

Papillary muscle rupture following AMI usually requires mitral valve replacement. [9] Revascularisation decreases the incidence of rupture. [2]

However, mitral regurgitation is associated with a worse prognosis after myocardialinfarction and subsequent revascularisation. [10]

Mitral regurgitation is often accompanied by a pansystolic murmur, but the murmur may be inaudible ifleft atrial pressure rises sharply.Echocardiogram is required to confirm the diagnosis, especially to differentiate from rupture of theinterventricular septum, and to assess severity.Management: [2]

Aggressive medical therapy for patients with papillary muscle rupture includes vasodilatortherapy. 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 musclerupture should be considered for emergency surgery.Coronary angiography should be performed before surgical repair becauserevascularisation is associated with improved short-term and long-term mortality.Patients with moderate mitral regurgitation who do not improve with vasodilator therapy arealso candidates for surgery.

Left ventricular aneurysmThe vulnerable myocardium following an AMI is susceptible to wall stress, resulting in infarctexpansion. Subacute cardiac rupture is an extreme form of infarct expansion, whereas ventricularaneurysm is its chronic form. [11] 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 abnormalbulge 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 ACEinhibitors.Heart failure with chronic aneurysms can be managed with ACE inhibitors, digoxin, and diuretics. [2]

Anticoagulation with warfarin is indicated for patients with a mural thrombus.Refractory heart failure or refractory ventricular arrhythmias in patients with aneurysms is an indicationfor surgical resection. The most appropriate surgical approach for patients with post-infarction leftventricular aneurysm remains unclear. [12] Revascularisation is beneficial for patients with a large amount of viable myocardium around theaneurysmal segment. [2]

Right ventricular failureRight ventricle myocardial infarctions accompany inferior wall ischaemia in up to one half ofcases. [13] Mild right ventricular dysfunction is common after infero-posterior infarcts but right heartfailure only occurs in a minority of these patients.May present with hypotension, jugular venous distention with clear lungs and no dyspnoea. Severeright ventricular failure may present with a low cardiac output state, including oliguria and alteredmental state. [2]

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 centralvenous line insertion and monitoring of cental pressures). Positive inotropes such as dobutamine mayalso be required.Most patients with right ventricular infarction improve after 48 to 72 hours. [2]

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Left ventricular outflow tract obstruction [2]

Dynamic left ventricular outflow tract obstruction can independently result from various causes suchas left ventricular hypertrophy, reduced left ventricular chamber size (dehydration, bleeding, ordiuresis), mitral valve abnormalities, and hypercontractility (stress, anxiety, or inotropic agents such asdobutamine). [14] Dynamic left ventricular outflow tract obstruction is an uncommon complication of acute anteriormyocardial 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 radiationto 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 shouldbe added slowly.Haemodynamic and respiratory status should be monitored closely during treatment. Vasodilators andpositive inotropes should be avoided.

ArrhythmiasA life-threatening arrhythmia (eg, ventricular tachycardia, ventricular fibrillation and total AV block) may be the firstmanifestation of ischaemia. These arrhythmias may cause many of the reported sudden cardiac deaths inpatients with acute coronary syndromes. Ventricular fibrillation or sustained ventricular tachycardia has beenreported in up to 20% of patients. The risk of arrhythmic death in survivors of acute myocardial infarction ishighest in the first six months after myocardial infarction and remains high for the subsequent two years. [15]

Arrhythmias may be caused by infarction, reperfusion, toxic metabolites, irritable myocardium, andmetabolism (especially potassium or magnesium imbalance).Some patients exhibit reperfusion arrhythmias (eg, ventricular ectopics, ventricular tachycardia oridioventricular rhythm) which are usually benign and do not require therapy. However, ventricularfibrillation may also occur.Persistent tachycardias may lead to further ischaemia.Antiarrhythmic agents are negatively inotropic and may encourage arrhythmias in acute coronaryischaemia. Minor arrhythmias should not be treated.Cardiopulmonary resuscitation should be performed in accordance with the Resuscitation CouncilGuidelines.Asystole:

Patients with cardiac arrest secondary to asystole or pulseless electrical activity shouldreceive intravenous adrenaline (epinephrine). [5]

Patients with pulseless electrical activity should also receive atropine.

Ventricular arrhythmias: [5]

Defibrillation should be administered for patients with ventricular fibrillation or pulselessventricular tachycardia.Intravenous adrenaline (epinephrine) should be used (as a last resort) for patients withrefractory ventricular tachycardia or ventricular fibrillation.Intravenous amiodarone should be given for refractory ventricular tachycardia or ventricularfibrillation.Intravenous amiodarone, or beta-blockers may be used for patients with haemodynamicallystable ventricular tachycardia.Patients with polymorphic ventricular tachycardia should be treated with intravenousmagnesium (consider giving magnesium for all patients with arrhythmias followingmyocardial infarction).Patients who have monomorphic ventricular tachycardia following an AMI or ventricularfibrillation more than 48 hours after infarction are at increased risk and should beconsidered for urgent revascularisation and insertion of an implantable cardioverterdefibrillator. [5]

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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 toatropine. Temporary transcutaneous pacing is only an interim measure until a morepermanent method can be employed.Temporary transcutaneous pacing is very painful and it may be necessary to usebenzodiazepines to sedate the patient.If temporary transcutaneous pacing and atropine are ineffective, consider adrenaline(epinephrine) - but adrenaline may worsen ischaemia; also consider dopamine orisoprenaline infusions.Transcutaneous pacing should be followed by a transvenous pacing if bradycardia persists.Heart block and conduction abnormalities occur more commonly with an inferior infarctionand are more ominous when they occur after anterior infarction. Heart block is oftentransient 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 complicates10-20% of AMIs but other supraventricular tachycardias are rare and usually self-limited.

Thrombosis and embolic complicationsDeep vein thrombosis and pulmonary embolism are now relatively uncommon after infarction, exceptin patients kept in bed because of heart failure.Prophylactic doses of a low molecular weight heparin (LMWH) and compression stockings should beused for prevention.Treatment should be with therapeutic doses of LMWH, followed by oral anticoagulation for 3-6 months.

Mural thrombosis and systemic embolismEchocardiography may reveal intraventricular thrombi. Left ventricular thrombus occurs in 20% afterinfarction 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 coronaryintervention when compared with patients currently treated conservatively or with thrombolysis. [16] Left ventricular mural thrombus has not been shown to be related to increased intermediate-termmortality when patients are treated with warfarin. [17]

PericarditisPericarditis is most common following an anterior infarction. The incidence of early pericarditis afterAMI is approximately 10%. Pericarditis usually develops between 24 and 96 hours after AMI. [2]

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 globularcardiac enlargement and a small pericardial effusion may be detected using echocardiography.Treatment of pericarditis is with anti-inflammatory drugs and analgesia, and a repeat echocardiogramif an effusion was initially present.

Dressler's syndromeDressler's syndrome presents as pericarditis 2-5 weeks after AMI, often accompanied by pleural andpericardial effusions. The incidence is between 1% and 3%. [2]

Dressler's syndrome typically presents 2-5 weeks after a myocardial infarction with a self-limitingfebrile illness accompanied by pericardial or pleural pain.The cause of Dressler's syndrome is unknown, but an autoimmune mechanism has beensuggested. [2]

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 isnecessary.

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Depression [18] Significant depression occurs in about 20% of patients following myocardial infarction.Myocardial infarction increases the risk of suicide, and depression following myocardial infarctionimpairs the overall prognosis.

Further reading & referencesECG LibraryMI – secondary prevention: Secondary prevention in primary and secondary care for patients following a myocardialinfarction, NICE Clinical Guideline (Nov 2013)

1. Mullasari AS, Balaji P, Khando T; Managing complications in acute myocardial infarction. J Assoc Physicians India. 2011Dec;59 Suppl:43-8.

2. Adam W Grasso, Sorin J Brener; Complications of Acute Myocardial Infarction, Center for Continuing Education, ClevelandClinic

3. 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 ofCardiology. Eur Heart J. 2003 Jan;24(1):28-66.

4. Khot UN, Jia G, Moliterno DJ, et al; Prognostic importance of physical examination for heart failure in non-ST-elevationacute 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 (2007)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. Madesis A, Tsakiridis K, Zarogoulidis P, et al; Review of mitral valve insufficiency: repair or replacement. J Thorac Dis. 2014

Mar;6(Suppl 1):S39-S51.10. 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. Chen X, Qiu ZB, Xu M, et al; Surgery for left ventricular aneurysm after myocardial infarction: techniques selection and

results assessment. Chin Med J (Engl). 2012 Dec;125(24):4373-9.13. 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. 2005Aug;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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Original Author:Dr Colin Tidy

Current Version:Dr Colin Tidy

Peer Reviewer:Dr Hannah Gronow

Last Checked:20/06/2014

Document ID:2454 (v23)

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