Prognosis and risk stratification after myocardial infarction.

Abstract

In order to assess prognosis after myocardial infarction, various methods have been used: estimation of ejection fraction, Holter monitoring, detection of ventricular late potentials using signal-averaging techniques, programmed ventricular stimulation of the heart to test the inducibility of ventricular tachyarrhythmias, and parameters that assess heart rate variability. Left ventricular dysfunction is the major determinant for prognosis after myocardial infarction, but left ventricular end-systolic volume may be better than overall ejection fraction. The presence of an 'arrhythmogenic substrate' may be detected by recording low-amplitude, fractionated activity or by artificially introducing premature ventricular extrasystoles using programmed ventricular stimulation. The signal-averaged ECG represents an independent tool for risk assessment. In some studies, signal-averaging and programmed ventricular stimulation proved to be more sensitive for the prediction of sustained ventricular tachycardia than for sudden death. The risk of an arrhythmic event in patients with an abnormal signal-averaged ECG or an abnormal result of programmed ventricular stimulation is increased, although the majority of these patients still do not experience a fatal or life-threatening arrhythmia. This high number of false-positive results limits the practical applicability of the signal-averaged ECG but also of other techniques such as long-term ECG recording. Recent interest has focussed on heart rate variability, which is considered an index of sympatho-vagal interaction after acute myocardial infarction. Patients with decreased heart rate variability have a poorer prognosis than those with normal parameters. Patency of the infarct-related artery is a major factor that governs the potentially beneficial effects of thrombolytic therapy. Many, but not all, studies have shown a reduced prevalence of late potentials after successful thrombolysis or in the presence of an open infarct-related artery. Effective thrombolytic therapy may prevent the development of an abnormal electrophysiological milieu after myocardial infarction. Finally, neurological factors such as depression have been shown to be independent risk factors for mortality after acute myocardial infarction. The role of psycho-social factors and their mechanisms of action need further attention since they open the door for behavioural modification. In conclusion, there are several promising new techniques for identification of patients at risk of ventricular tachyarrhythmias. These techniques seem to be superior to more conventional methods such as long-term ECG monitoring as well as exercise testing. Methods which determine the arrhythmogenic substrate might be combined with a parameter of left ventricular ejection fraction because of the paramount importance of left ventricular pump function. However, due to the large proportion of false-positive results obtained with any of these methods, it seems unlikely that they will clearly surpass the others and be sufficiently accurate for risk assessment in the individual patient.