We searched MEDLINE between Jan 1, 2002, and Dec 31, 2015, with the following search terms: “ST segment elevation myocardial infarction”, “non-ST segment myocardial infarction”, “acute coronary syndrome”, “myocardial infarction”, “fibrinolysis”, “thrombolysis”, “angioplasty”, “stent”, “cardiogenic shock”, “anti-platelet therapy”, “anti-thrombotic therapy”, “clinical guidelines”, “quality of care”, and “survival”. Additionally, we reviewed the reference lists of manuscripts identified by this
SeminarAcute myocardial infarction
Section snippets
Epidemiology
Acute myocardial infarction is the most severe manifestation of coronary artery disease, which causes more than 2·4 million deaths in the USA, more than 4 million deaths in Europe and northern Asia,1 and more than a third of deaths in developed nations annually.2 Increased use of evidence-based therapies and lifestyle changes have spurred considerable reductions in mortality from coronary heart disease in recent decades.1 However, myocardial infarction retains a substantial footprint on global
Pathophysiology
Acute myocardial infarction is divided into STEMI and NSTEMI.5 Unstable angina is also considered an acute coronary syndrome (ACS), because it is an imminent precursor to myocardial infarction. Unstable angina has a similar pathophysiology to NSTEMI, and they are together referred to as non-ST-segment elevation ACS (NSTE-ACS). They have traditionally been grouped together for management decisions. In most cases, myocardial infarction is due to disruption of a vulnerable atherosclerotic plaque
Diagnosis
A combined task force of major professional societies revised the definition of myocardial infarction in 2012 to reflect any event leading to myocardial ischaemia causing cardiac myocyte cell death, and suggested myocardial infarction be classified by its pathological cause into five types (appendix p 5).5 In each case, the diagnosis of myocardial infarction relies on biomarker evidence of myocyte necrosis, and either electrocardiographic (ECG) criteria of ischaemia or infarction, or ischaemic
Risk assessment
Early risk stratification of patients with myocardial infarction allows for prognostication and triage via initiation of one of several vital treatment pathways. Several clinical prediction scores estimate short-term and long-term risks of recurrent ischaemic events and death after myocardial infarction. The TIMI risk score is easiest to use, whereas GRACE is more accurate, comprehensive, and applicable to both NSTEMI and STEMI (appendix p 2).11 Dedicated STEMI risk scores also exist, but they
General principles
In NSTEMI, antithrombotic therapy is thought to stabilise the vulnerable plaque and allow endogenous fibrinolysis to restore patency.12 Percutaneous coronary intervention (PCI) is usually pursued to improve blood flow and prevent recurrent ischaemia. PCI should be done within 24 h of NSTEMI if possible, but some studies suggest that PCI could be done in low-risk patients up to 48–72 h without clinical consequence.13 However, doing PCI after 24 h has been associated with longer hospitalisation,14
Aspirin
Randomised trials have shown a reduction in death or myocardial infarction of greater than 50% with aspirin compared with placebo in patients with ACS.68, 69 Guidelines recommend a loading dose of aspirin (162–325 mg) as soon as possible following myocardial infarction, whereas indefinite low-dose aspirin (75–100 mg) is advised for secondary prevention, because it is as effective as higher doses at preventing ischaemic events but causes less bleeding.4, 15, 17
P2Y12 inhibitors
Clopidogrel is a second generation
Complications from acute myocardial infarction
Knowledge of the cardinal features and timing of the complications of myocardial infarction is essential to recognise and properly treat these potentially fatal events (figure 3).
New antithrombotic therapies
When added to DAPT, both rivaroxaban and vorapaxar improve the secondary prevention of cardiovascular events, at the expense of increased bleeding.130, 131 Either therapy could be useful in high-risk patients following myocardial infarction or with established coronary artery disease and low bleeding risk (appendix p 10).
Lipid-lowering therapy
Aggressive control of LDL cholesterol with high-intensity statin therapy (eg, atorvastatin 80 mg) is advised in all patients after myocardial infarction on the basis of results
Future directions
Continued progress in improving outcomes following acute myocardial infarction will be made only with a commitment to research targeted at improving the systems in which care is delivered. The largest gains might be from research into increasing adherence to guideline-directed medical therapies and spreading established systems-based advances to developing countries. Additionally, it is hopeful that emerging technologies and translational science (including novel applications of gene and
Search strategy and selection criteria
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Meta-analysis of ten trials on the effectiveness of the radial versus the femoral approach in primary percutaneous coronary intervention
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