Background: Ventricular ectopy early after an acute myocardial infarction (AMI) has previously been demonstrated to predict mortality. Less information is available about the prognostic implications of ventricular ectopy occurring late after an AMI, and no information is available about the prognostic implication of the development of ventricular ectopy during the first year after an AMI. Hypothesis: The purpose of the present prospectively conducted trial, a part of the Danish Verapamil Infarction Trial II (DAVIT II), was to evaluate the prognostic implication of (1) ventricular premature complexes (VPCs) recorded by 24-h Holter monitoring 1 week, 1 month, and 16 months after an AMI; and (2) development of > 10 VPCs/h or of any complex ventricular ectopy, that is, pairs, more than two types of VPCs, ventricular tachycardia, or> 10 VPCs/h during follow-up after an AMI. Methods: Patients were monitored 1 week (n = 250), 1 month (n = 210), and 16 months (n = 201) after AMI. Results: Multivariate analyses based on history, clinical findings, and ventricular ectopy showed the following results: After 1 week, > 10 VPCs/h (p = 0.0006) and heart failure (p < 0.007); after 1 month, > 10 VPCs/h (p= 0.003) and resting heart rate (p < 0.02); and after 16 months, ventricular tachycardia (p = 0.002) independently predicted long-term mortality. Mortality was significantly predicted by the development of > 10 VPCs/h from 1 week to 1 month (p= 0.003) and 16 months (p = 0.03), and from 1 to 16 months (p = 0.007) after AMI, as well as by the development of any complex ventricular ectopy from 1 week to 1 month (p = 0.02) and 16 months (p = 0.01), and from 1 to 16 months (p = 0.04) after AMI. Conclusion: The present study demonstrated that 1 week and 1 month after an AMI the quantity of VPCs, that is, >10 VPCs/h, predicted mortality, whereas 16 months after an AMI the quality of VPCs, that is; ventricular tachycardia, predicted mortality.