[Diagnosis of acute myocardial infarction in Denmark]. / Diagnostik af akut myokardieinfarkt i Danmark.

The introduction of new biochemical markers for myocardial damage in the recent years and different application of these methods in different centres may have an impact on the diagnostic criteria for acute myocardial infarction (AMI). By means of a questionnaire we studied the diagnostic criteria for AMI in relation to the use of different biochemical markers among 78 Danish hospitals. There were large variations with regard to the choice of cardiac markers and diagnostic values for different markers. CK-B is the cardiac marker mostly used followed by CK-MB. Troponin-T test was used by about 20% of the centres. Many centres are planning to use CK-MB and Troponin-T test. A common national and international policy for diagnosis of AMI in relation to different cardiac markers should reduce these improper differences.

Prognostic implications of ventricular ectopy one week, one month, and sixteen months after an acute myocardial infarction. Danish Study Group on Verapamil in Myocardial Infarction.

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.

Effect of verapamil on arrhythmias and heart rate during 16 months following an acute myocardial infarction. The Danish Study Group on Verapamil in Myocardial Infarction.

The present study was a prospectively planned subset of the postinfarction, double blind, randomized, multicenter, placebo controlled trial of verapamil, DAVIT II. Patients had 24 hours of Holter monitoring before randomization, i.e., second week after infarction (placebo, n = 122; verapamil, n = 128), after 1 month (placebo, n = 108; verapamil, n = 94) and after 16 months (placebo, n = 75; verapamil, n = 63) of treatment. The purpose was to evaluate the effect of verapamil on the prevalence and changes over time of arrhythmias and heart rate. In patients monitored twice, a significant increase of average ventricular premature complexes (VPC) per hour from before to 1 month (p = 0.0007) and 16 months (p = 0.02) after was demonstrated in the placebo group, and from before to 1 months (p = 0.01) after in the verapamil group. Average VPC/hr did not change from 1 to 16 months of treatment. A significant increment of > 10 VPC/hr was found after 1 (p = 0.03) and 16 months (p = 0.05) compared to prerandomization in the placebo, but not in the verapamil group. A significant increase of supraventricular arrhythmias after 1 month compared with prerandomization was found in the placebo group (p = 0.003) but not in the verapamil group. The prevalence of VPC and supraventricular tachycardia was significantly lower in the verapamil compared with the placebo group after 1 month of treatment. At 16 months no significant difference was found between the two groups. The 24 hour mean heart rate was significantly lower, 3 beats/min, in the verapamil compared with placebo after 1 and 16 months of treatment.(ABSTRACT TRUNCATED AT 250 WORDS)