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Biomedical subjects

O Pedersen-Bjergaard

Publications and source records attributed to O Pedersen-Bjergaard.

At least 19 recordsLinked to original sources
PubMed1998

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.

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PubMed1997

Cardiac event rates after acute myocardial infarction in patients treated with verapamil and trandolapril versus trandolapril alone. Danish Verapamil Infarction Trial (DAVIT) Study Group.

Angiotensin-converting enzyme (ACE) inhibitors improve survival in patients with congestive heart failure (CHF) after an acute myocardial infarction (AMI), but mortality may be as high as 10% to 15% after 1 year. Verapamil prevents cardiac events after an AMI in patients without CHF. We hypothesized that in postinfarct patients with CHF already prescribed diuretics and an ACE inhibitor, additional treatment with verapamil may reduce cardiac event rate. In this multicenter, double-blind study, patients with CHF receiving diuretic treatment were consecutively randomized to treatment with trandolapril 1 mg/day for 1 month and 2 mg/day the following 2 months (n = 49), or to trandolapril as mentioned plus verapamil 240 mg/day for 1 month and 360 mg/day for 2 months (n = 51). Trial medication started 3 to 10 days after AMI. All patients were followed for 3 months. End points in the trandolapril/trandolapril-verapamil groups were death 1/1, reinfarction 7/1, unstable angina 9/3, and readmission for CHF 6/2. The 3-month first cardiac event rate was 35% in trandolapril-treated patients and 14% in trandolapril-verapamil-treated patients (hazard ratio 0.35, 95% confidence interval 0.15 to 0.85, p = 0.015). These data suggest that verapamil reduces cardiac event rates in post-AMI patients with CHF when added to an ACE inhibitor and a diuretic.

Aged↗
PubMed1997

Treatment with verapamil and trandolapril in patients with congestive heart failure and myocardial infarction. The Danish Verapamil Infarction Trial (DAVIT Study Group).

UNLABELLED: EFFECTS OF VERAPAMIL AND TRANDOLAPRIL: Progression of heart failure, sudden death and death from re-infarction are the major cause of the increased mortality in postinfarct patients with congestive heart failure. Angiotensin converting enzyme (ACE) inhibitors such as trandolapril can prevent the progression of heart failure and thus improve survival. The calcium antagonist verapamil has been shown to prevent sudden death and re-infarction in postinfarct patients without congestive heart failure. HYPOTHESIS: The Danish Verapamil Infarction Trial (DAVIT) study group hypothesized the combined treatment with trandolapril and verapamil might prevent cardiac events in postinfarct patients with coronary heart disease. The first double-blind randomized trial included 100 patients and supported this hypothesis, as the cardiac event rate was significantly lower after 3 months in patients treated with the combination than in those treated with trandolapril alone (14 versus 35%, respectively; P = 0.01, hazard ratio 0.35, 95% confidence interval 0.15-0.85).

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1994

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)

Aged↗
PubMed1981

Limitation of myocardial infarct size in patients less than 66 years treated with alprenolol.

Two hundred and eighty-two patients less than 66 years of age admitted with suspected or definite myocardial infarction were allocated in a random fashion to treatment with alprenolol or placebo. Treatment was started immediately upon admission with 5-10 mg alprenolol or placebo intravenously, followed by 200 mg alprenolol or placebo orally twice a day for one year. In 178 patients a definite myocardial infarction was diagnosed. Myocardial infarct size could be estimated from serial determinations of serum total creatine kinase in 42 patients treated with alprenolol and 43 patients receiving placebos. Median infarct size was 20.6 CK g Eq/m2 body surface in the alprenolol group, the corresponding figure in the placebo group being 34.4 CK g Eq/m2 body surface. Median rate of release of creatine kinase from the ischaemic myocardium was 27.7 U/1 per hour and 48.0 U/1 per hour after alprenolol and placebo, respectively. Alprenolol limited infarct size significantly provided the treatment was started within 12 hours of the onset of symptoms.

Aged↗
PubMed1979

Effect of alprenolol on mortality among patients with definite or suspected acute myocardial infarction. Preliminary results.

A double-blind study of alprenolol versus placebo was done in patients with definite or suspected myocardial infarction to show the effect of the drug on mortality-rate after a year of treatment in patients aged less than or equal to 65 and to study the tolerance of the drug by patients greater than 65 years of age. The dose given was 5--10 mg intravenously, followed by 200 mg twice a day, orally. Patients in whom beta-blockade was contraindicated were excluded. All deaths, side-effects, and dropouts were recorded. Of the 480 patients in the study, 238 patients received alprenolol and 242 placebo. During the year of follow-up 108 patients dropped out from the study. Mortality was not reduced in patients greater than 65 years of age. In those less than or equal to 65 years alprenolol significantly reduced mortality-rate (20% mortality in placebo group vs 9% in treated group). There was also a significant reduction in mortality-rate among those with definite infarction (28% in the placebo vs 15% in the treated group).

Acute Disease↗
PubMed1979

Q waves and coronary artery disease.

In a consecutive series of 234 patients admitted for selective coronary arteriography, 78 had pathological Q waves. In 32 of these 78 patients, ECG showed left ventricular hypertrophy, QRS duration of greater than or equal to 0.12 sec, incomplete left bundle branch block, or left axis deviation. Fourteen (44%) of these 32 patients had coronary artery disease (CAD), while 40 (87%) of the remaining 46 patients without these ECG changes had CAD (p less than 0.0005). Among the 46 patients, 34 of 35 with angina pectoris had CAD compared to 6 of 11 without angina pectoris (p less than 0.01). Our study thus shows that Q waves may be reliable predictors of CAD especially in patients with angina pectoris.

Angina Pectoris↗