THE CONTEXT
Myocardial infarction can be recognised retrospectively from electrical, imaging or anatomical evidence. Acute MI subtypes differ in their mechanism and clinical setting.
Recognising a previously unrecognised infarction
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Abnormal Q waves support the diagnosis with or without symptoms when non-ischaemic causes are absent.
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Imaging may demonstrate loss of viable myocardium in a pattern consistent with an ischaemic cause.
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Patho-anatomical findings of a prior myocardial infarction also support the diagnosis.
Type 1 myocardial infarction
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An occlusive thrombus forms at the site of rupture or erosion of an atheromatous plaque; this is atherothrombosis.
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The thrombus may undergo spontaneous lysis over the following days, although irreversible myocardial damage will already have occurred.
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Without treatment, the responsible artery remains permanently occluded in 20%–30% of patients.
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Infarction progresses over several hours, so most patients present while myocardial salvage and improved outcomes remain possible.
Type 2 myocardial infarction and myocardial injury
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Type 2 myocardial infarction results from an imbalance between myocardial blood supply and metabolic demand.
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Examples include sepsis in a patient with three-vessel coronary artery disease or an excessively fast primary arrhythmia despite unobstructed coronary arteries.
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Type 2 myocardial infarction requires clinical evidence of ischaemia, such as ECG changes or chest pain.
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Elevated cardiac troponin without evidence of myocardial ischaemia represents myocardial injury, as can occur in myocarditis. Myocardial injury may be acute or chronic.
Other MI subtypes
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Type 3 myocardial infarction describes sudden death presumed to be due to myocardial infarction.
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Type 4 and type 5 myocardial infarction occur during or following percutaneous coronary intervention and coronary artery bypass grafting, respectively.
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In the procedural setting, clinical evidence of ischaemia distinguishes myocardial infarction from procedure-related myocardial injury.