Management of acute myocardial infarction in patients presenting with ST-segment elevation

Abstract

Introduction The definition of acute myocardial infarction The pathogenesis of acute myocardialinfarction The natural history of acute myocardial infarction Aims of management Emergency care Initial diagnosis and early risk stratification Relief of pain, breathlessness and anxiety Cardiac arrest Basic life support Advanced life support Pre-hospital or early in-hospital care Restoring coronary flow and myocardial tissue reperfusion Fibrinolytic treatment Fibrinolytic regimens Percutaneous coronary interventions (PCI) Primary PCI PCI combined with fibrinolysis ‘Rescue’ PCI Assessing myocardial salvage by fibrinolysis or PCI GP IIb/IIIa antagonists and early PCI Coronary artery bypass surgery Pump failure and shock Heart failure Mild and moderately severe heart failure Severe heart failure and shock Mechanical complications: cardiac rupture and mitral regurgitation Free wall rupture Ventricular septal rupture Mitral regurgitation Arrhythmias and conduction disturbances Ventricular arrhythmias Supraventricular arrhythmias Sinus bradycardia and heart block Routine prophylactic therapies in the acute phase Management of specific types of infarction Right ventricular infarction Myocardial infarction in diabetic patients Management of the later in-hospital course Ambulation Management of specific in-hospital complications Deep vein thrombosis and pulmonary embolism Intraventricular thrombus and systemic emboli Pericarditis Late ventricular arrhythmias Post-infarction angina and ischaemia Risk assessment, rehabilitation and secondary prevention Risk assessment Timing Clinical assessment and further investigations Assessment of myocardial viability, stunning and hibernation Evaluation of risk of arrhythmia Rehabilitation Secondary prevention Logistics of care Pre-hospital care The coronary (cardiac) care unit (CCU) The current use of therapies tested by clinical trials Recommendations References The management of acute myocardial infarction continues to undergo major changes. Good practice should be based on sound evidence derived from well-conducted clinical trials. Because of the great number of trials on new treatments performed in recent years and because of new diagnostic tests, the European Society of Cardiology decided that it was opportune to upgrade the 1996 guidelines and appointed a Task Force. It must be recognized, that even when excellent clinical trials have been undertaken, their results are open to interpretation and that treatment options may be limited by resources. Indeed, cost-effectiveness is becoming an increasingly important issue when deciding upon therapeutic strategies. In setting out these new guidelines, the Task Force has attempted to classify the usefulness or efficacy of the recommended routine treatments and the level of evidence on which these recommendations are based. The usefulness or efficacy of a recommended treatment will be presented as: class I=evidence and/or general agreement that a given treatment is beneficial, useful and effective; class II=conflicting evidence and/or a divergence of opinion about the usefulness/efficacy of the treatment; IIa: weight of evidence/opinion is in favour of usefulness/efficacy; IIb: usefulness/efficacy is less well established by evidence/opinion; class III=evidence or general agreement that the treatment is not useful/effective and in some cases may be harmful. The strength of evidence will be ranked according to three levels: level A, data derived from at least two randomized clinical trials; level B, data derived from a single randomized clinical trial and/or meta-analysis or from non-randomized studies; level C, consensus opinion of the experts based on trialsand clinical experience. As always with guidelines, they are not prescriptive. Patients vary so much from one another that individual care is paramount and there is still an important place for clinical judgment, experience and common sense. Myocardial infarction can be defined from a number of different perspectives related to clinical, electrocardiographic (ECG), biochemical and pathologic characteristics.1 It is accepted that the term myocardial infarction reflects death of cardiac myocytes caused by prolonged ischaemia. The ECG may show signs of myocardial ischaemia, specifically ST and T changes, as well as signs of myocardial necrosis, specifically changes in the QRS pattern. A working definition for acute evolving myocardial infarction in the presence of clinically appropriate symptoms has been established as (1) patients with ST-segment elevation, i.e. new ST-segment elevation at the J point with the cut-off points ≥0.2mV in V1through V3and ≥0.1mV in other leads, or (2) patients without ST-segment elevation, i.e. ST-segment depression or T wave abnormalities. Clinically established myocardial infarction may be defined by any Q wave in leads V1through V3, or Q wave ≥0.03s in leads I, II, aVL, aVF, V4, V5or V6. Myocardial infarction can be recognized when blood levels of biomar