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Patients are at risk of a number of immediate, early and late complications following a myocardial infarction (MI).

''Cardiac arrest''
This most commonly occurs due to patients developing ventricular fibrillation and is the most common cause of death following a MI. Patients are managed as per the ALS protocol with defibrillation.

''Cardiogenic shock''
If a large part of the ventricular myocardium is damaged in the infarction the ejection fraction of the heart may decrease to the point that the patient develops cardiogenic shock. This is difficult to treat. Other causes of cardiogenic shock include the 'mechanical' complications such as left ventricular free wall rupture as listed below. Patients may require inotropic support and/or an intra-aortic balloon pump.

''Chronic heart failure''
As described above, if the patient survives the acute phase their ventricular myocardium may be dysfunctional resulting in chronic heart failure. Loop diuretics such as furosemide will decrease fluid overload. Both ACE-inhibitors and beta-blockers have been shown to improve the long-term prognosis of patients with chronic heart failure.

''Tachyarrhythmias''
Ventricular fibrillation, as mentioned above, is the most common cause of death following a MI. Other common arrhythmias including ventricular tachycardia.

''Bradyarrhythmias''
Atrioventricular block is more common following inferior myocardial infarctions.

''Pericarditis''
Pericarditis in the first 48 hours following a transmural MI is common (c. 10% of patients). The pain is typical for pericarditis (worse on lying flat etc), a pericardial rub may be heard and a pericardial effusion may be demonstrated with an echocardiogram.

''Dressler's syndrome'' tends to occur around 2-6 weeks following a MI. The underlying pathophysiology is thought to be an autoimmune reaction against antigenic proteins formed as the myocardium recovers. It is characterised by a combination of fever, pleuritic pain, pericardial effusion and a raised ESR. It is treated with NSAIDs.

''Left ventricular aneurysm''
The ischaemic damage sustained may weaken the myocardium resulting in aneurysm formation. This is typically associated with persistent ST elevation and left ventricular failure. Thrombus may form within the aneurysm increasing the risk of stroke. Patients are therefore anticoagulated.

''Left ventricular free wall rupture''
This is seen in around 3% of MIs and occurs around 1-2 weeks afterwards. Patients present with acute heart failure secondary to cardiac tamponade (raised JVP, pulsus paradoxus, diminished heart sounds). Urgent pericardiocentesis and thoracotomy are required.

''Ventricular septal defect''
Rupture of the interventricular septum usually occurs in the first week and is seen in around 1-2% of patients. Features: acute heart failure associated with a pan-systolic murmur. An echocardiogram is diagnostic and will exclude acute mitral regurgitation which presents in a similar fashion. Urgent surgical correction is needed.

''Acute mitral regurgitation''
More common with infero-posterior infarction and may be due to ischaemia or rupture of the papillary muscle. An early-to-mid systolic murmur is typically heard. Patients are treated with vasodilator therapy but often require emergency surgical repair.