Sudden Cardiac Death After Myocardial Infarction

Summary

Recent advances in the understanding of the mechanisms of sudden cardiac death have been paralleled by technical advances in diagnosis and treatment, involving ambulatory Holter monitoring and the use of implantable defibrillators. Risk factors predisposing toward sudden cardiac death in the postmyocardial infarction setting and in patients with congestive heart failure include the presence of ventricular ectopy [> 10 premature ventricular contractions (PVC) per hour], frequent episodes of ventricular pairs and nonsustained ventricular tachycardia on 24-hour Holter monitoring, and a depressed left ventricular ejection fraction. Additional risk factors for sudden cardiac death in coronary artery disease include arterial stenosis in coronary vessels supplying intact myocardium remote from the infarction site, the presence of late potentials on the signal averaged ECG, and attenuation of the normal variation in heart rate. The ability to induce sustained ventricular tachycardia (SVT) on electrophysiological testing is highly predictive of sudden cardiac death after myocardial infarction. Conversely, the ease of suppression of the induced tachycardia with antiarrhythmic agents is correlated with the risk of subsequent lethal ventricular arrhythmia. The detrimental effect of frequent ventricular ectopy (> 10 PVC/h) on survival in coronary artery disease is particularly pronounced in patients with moderately well preserved left ventricular function [ejection fraction (EF) > 30%], thereby suggesting that these patients may be better served by antiarrhythmic therapy than those with severely depressed left ventricular function.

In light of the findings from the Cardiac Arrhythmia Suppression Trial (CAST), that indicated an increased mortality rate associated with the use of the Class Ic antiarrhythmics encainide and flecainide in postmyocardial infarction patients, it is feasible that the use of Class III antiarrhythmics (which prolong cardiac repolarisation rather than conduction) may be more appropriate in this setting. A number of clinical studies are currently addressing the question of whether amiodarone reduces the incidence of sudden cardiac death in coronary artery disease and congestive heart failure.