Professional Documents
Culture Documents
Complications of Acute Myocardial Infarction
Complications of Acute Myocardial Infarction
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 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 (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.
Page 2 of 7
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 infarction: [4]
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.
Page 3 of 7
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 lifethreatening 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. [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 myocardial
infarction and subsequent revascularisation. [10]
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: [2]
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.
Page 4 of 7
obstruction [2]
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.
Arrhythmias
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 acute myocardial infarction is
highest 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, 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 arrhythmias: [5]
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
defibrillator. [5]
Page 5 of 7
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.
Pericarditis
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 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 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
suggested. [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 is
necessary.
Page 6 of 7
Depression [18]
Significant depression occurs in about 20% of patients following myocardial infarction.
Myocardial infarction increases the risk of suicide, and depression following myocardial infarction
impairs the overall prognosis.
Disclaimer: This article is for information only and should not be used for the diagnosis or treatment of medical
conditions. EMIS has used all reasonable care in compiling the information but make no warranty as to its
accuracy. Consult a doctor or other health care professional for diagnosis and treatment of medical conditions.
For details see our conditions.
Original Author:
Dr Colin Tidy
Current Version:
Dr Colin Tidy
Peer Reviewer:
Dr Hannah Gronow
Document ID:
2454 (v23)
Last Checked:
20/06/2014
Next Review:
19/06/2019
Page 7 of 7
E M I S. E M I S is a trading name of Egton Medical Information Systems Limited.