Complications
Arrhythmias (e.g., ventricular ectopy, atrial fibrillation, brady- or tachyarrhythmias, ventricular fibrillation [VF], or ventricular tachycardia [VT]) occur from injury to the cardiac conduction system. They may cause sudden death or induce cardiogenic shock.[134] Bradycardia is often seen in right-sided or posterior infarction.
The incidence of VF is <2%. The majority of VT/VF occurs within the first 48 hours after admission.[135]
Electrolyte abnormalities should be monitored and corrected. Cardioversion or anti-arrhythmic therapy may be needed. In patients with heart block or symptomatic bradycardia, transcutaneous or transvenous pacing may be required.
Heart failure in the acute setting develops in about 8% of patients. It is most often secondary to compromised left ventricular function from a large ischaemic event. Pump failure often results in pulmonary oedema, hypotension, and oliguria.
Heart failure requires prompt diagnosis and aggressive stabilisation to prevent progression to shock. Therapy includes diuresis, vasodilators, and staged pharmacotherapy (e.g., ACE inhibitors).
Develops in 4.5% of acute myocardial infarction.[131] NSTEMI accounts for approximately 20% of cardiogenic shock complicating myocardial infarction.[1] Typically, it occurs after a massive myocardial infarction or repeated ischaemic events, and it is predominantly caused by left ventricular failure.[132] Risk increases in time without treatment. Associated mortality is 70% to 80%, with an in-hospital mortality of 59% to 60%.[1][132][133]
Cardiogenic shock requires urgent percutaneous coronary intervention (PCI) or coronary artery bypass grafting (CABG) surgery if not already carried out.[1][61] The patient needs intensive care and pressor support and may need intra-aortic balloon pump counterpulsation or other circulatory assist devices as a bridge towards definitive therapy.
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Most often secondary to papillary muscle rupture or acute left ventricle dilation. Acute mitral regurgitation predominantly occurs after inferior infarction.
Complete papillary muscle ruptures need emergency surgical correction. Moderate to severe mitral regurgitation in association with left ventricular dysfunction is acutely managed as acute heart failure.
Dressler syndrome is mediated by inflammatory byproducts and the formation of ischaemic myocardium. Inflammation involves the pericardium and is treated with non-steroidal anti-inflammatory drugs (NSAIDs) or colchicine (preferably colchicine as it may reduce the risk of recurrence). If haemodynamic compromise is present, pericardiocentesis or surgical intervention is required.
Myocardial infarction has been associated with an increased risk of VTE, particularly for pulmonary embolism.[140]
Depression is a risk factor for cardiovascular disease and for adverse outcomes following acute coronary syndrome (ACS).[49] ACS can also precipitate depression in people without prior psychiatric conditions.[49][136][137] Patients should routinely be screened for depression following a myocardial infarction.[136] Data suggest that a combined psychosocial approach to the treatment of depression improves outcome in patients. Exercise combined with pharmacotherapy may be the most efficacious approach.[48] Pharmacotherapy may be associated with excess risk in patients with residual cardiac dysfunction; cognitive behavioural therapy or exercise therapy may be more appropriate in this patient group.[138]
Often precipitated by cessation of dual antiplatelet therapy. Occurs more frequently with drug-eluting stents.[139]
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