Complications of Acute Myocardial Infarction

Most deaths following acute myocardial infarction are due to circulatory failure either due to severe left ventricular dysfunction (e.g. arrhythmias) or one of the mechanical complications (e.g. ventricular rupture, papillary muscle rupture).

Failure of reperfusion¹

• Failure of reperfusion is less likely with the availability of primary PCI (percutaneous coronary intervention) centres.
• Reperfusion should reduce ST elevation to less than 50% within one hour.
• Persisting ischaemia is increasingly regarded as an indication for percutaneous angioplasty.
• Reinfarction occurs in 5-30% of patients after fibrinolytic therapy. It is more common in patients with diabetes or history of previous myocardial infarction.
• Recurrent infarction (infarction in a different artery) within 48 hours may occur in up to 40% of patients and can be difficult to diagnose.
• Myocardial creatine kinase (CK-MB) is more useful than troponins for tracking infarct extension or reinfarction because of its shorter half life. Some laboratories do not perform CK-MB assays so need to check with local laboratory. Diagnosis can be made by echocardiography or nuclear imaging. Management is by angiography followed by coronary revascularisation.

Arrhythmias

• 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.
• Anti-arrhythmic 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.²
• Asystole:
  • Patients with cardiac arrest secondary to asystole or pulseless electrical activity should receive intravenous adrenaline.³
  • Patients with pulseless electrical activity should also receive atropine.
• Ventricular arrhythmias:³
  • 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 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 acute myocardial infarction 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.³
• 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 atrial tachycardias may also occur.

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.
• 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 ACE inhibitors (intravenous GTN if left ventricular failure).
• 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 contraindicated by renal impairment or hyperkalaemia (left ventricular function should be assessed in all patients with acute myocardial infarction during the initial hospital admission).³
• Spironolactone can be used instead of eplerenone; spironolactone is cheaper but has many more potential adverse effects than eplerenone.
• 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.
• Treatment with ACE inhibitors (or angiotensin receptor antagonists) and beta-blockers improves both short-term and long-term prognosis.

Cardiogenic shock

• Occurs in 5-20% of patients following myocardial infarction.
• Initial treatment is with a combination of inotropes, vasoconstrictors, and loop diuretics. Percutaneous revascularisation is associated with an improved prognosis. Aggressive treatment with intra-aortic balloon pumping followed by surgical revascularization may also significantly reduce mortality.
• The mortality rate is over 70% if revascularisation is not possible.

Pericarditis

• Pericarditis is most common following an anterior infarction.
• 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-inflammatories and analgesia, and a repeat echocardiogram if an effusion was seen.

Ventricular rupture and ventricular septal defect

• Ventricular rupture occurs in the interventricular septum or the wall of the left ventricle. Both have mortality rates greater than 90%. Rupture usually occurs 3-5 days (but may be up to 3 weeks) after an infarction.
• Risk factors associated with cardiac rupture include female gender, old age, hypertension, and first MI.⁵
• Rupture of a free wall causes bleeding into the pericardium, leading to cardiac tamponade, with progressively poorer cardiac function. Rupture is usually within several days after infarction but may be up to two weeks after. Death is usually immediate. Emergency pericardiocentesis and cardiac surgery are essential for any hope of survival. Occasionally, partial rupture of the free wall may cause a false aneurysm.
• Interventricular septum rupture occurs in approximately 2% of myocardial infarctions. The defect causes a new pan-systolic murmur and increased pulmonary congestion due to a left-to-right shunt.
• Diagnosis is by transoesophageal echocardiography or by showing a step-up in oxygen saturation in the right ventricle on pulmonary artery catheterisation.
• The rupture requires urgent surgical correction or there is very little chance of survival.

Acute mitral regurgitation

• Most common with an infero-posterior infarction and may be due to ischaemia, necrosis, or rupture of the papillary muscle.
• Most mitral regurgitation following infarction is transient and asymptomatic.
• Rupture of papillary muscle or chordae tendinae causes severe mitral regurgitation within the first week after infarction. It is most often seen with inferior infarctions. Fibrinolytic agents decrease the incidence of rupture.
• It 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.
• The management is acute surgical repair with or without revascularisation.

Right ventricular failure

• Mild right ventricular dysfunction is common after infero-posterior infarcts but right heart failure only occurs in 10% of these patients.
• 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. May require central venous line insertion and monitoring of cental pressures. Positive inotropes such as dobutamine may also be required.

Deep vein thrombosis

See separate article on deep vein thrombosis.

Pulmonary embolism

See separate article on pulmonary embolism.

Mural thrombosis and systemic embolism

• 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 risks of embolisation in 15-20% of cases.
• Treatment is anticoagulation with heparin followed by warfarin, along with thrombolysis and/or surgical repair.⁶

Left ventricular aneurysm

• Occur after 2-15% of infarcts. 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.
• Treatment is with anticoagulation. Refractory heart failure and ventricular arrhythmias are indications for surgery.

Dressler's syndrome

• Dressler's syndrome presents as pericarditis, often accompanied by pleural and pericardial effusions, developing between 2 weeks and 3 months after acute infarction or heart surgery.
• Dressler's syndrome typically present 2–4 weeks after an MI with a self-limiting febrile illness accompanied by pericardial or pleural pain.⁷
• Is thought to have an autoimmune mechanism.
• 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.
• It has been found to more than treble the risk of mortality in the first six months following myocardial infarction.