Inflammatory, mechanical and embolic complications after myocardial infarction
THE CONTEXT
After myocardial infarction, delayed inflammation, structural rupture, ventricular remodelling and thrombus formation produce distinct clinical complications.
Dressler syndrome
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Dressler syndrome is characterised by persistent fever, pericarditis and pleurisy and is probably autoimmune.
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Symptoms tend to appear weeks or months after myocardial infarction and often subside within a few days.
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Prolonged or severe symptoms may require high-dose aspirin, non-steroidal anti-inflammatory drugs or glucocorticoids.
Papillary muscle rupture
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Papillary muscle rupture produces sudden severe mitral regurgitation, typically presenting with acute pulmonary oedema and shock.
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A pansystolic murmur and third heart sound are usual findings, but the murmur may be quiet or absent despite severe regurgitation.
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Echocardiography confirms the diagnosis, and emergency valve replacement may be necessary.
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Lesser mitral regurgitation from papillary muscle dysfunction is common and may be transient.
Ventricular septal rupture
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Ventricular septal rupture usually causes sudden haemodynamic deterioration with a new loud pansystolic murmur radiating to the right sternal border.
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The murmur may be difficult to distinguish from that of acute mitral regurgitation.
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Left-to-right shunting through the resulting ventricular septal defect tends to cause acute right heart failure rather than pulmonary oedema.
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Doppler echocardiography and right heart catheterisation confirm the diagnosis. Emergency surgical repair is required; without it, the condition is usually fatal.
Ventricular expansion and rupture
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Full-thickness infarction causes thinning and stretching of the infarcted segment, termed infarct expansion. Increased wall stress then promotes progressive dilatation and hypertrophy of the remaining ventricle.
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Ventricular rupture may cause cardiac tamponade and is usually fatal, although temporary support until emergency surgery is occasionally possible.
Embolic complications
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Thrombus on the endocardial surface of freshly infarcted myocardium may cause systemic embolism, including stroke or an ischaemic limb.
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Venous thrombosis and pulmonary embolism may also occur, but have become less common with prophylactic anticoagulation and early mobilisation.