Search PubMed⌕ Search

Biomedical subjects

J Kjekshus

Publications and source records attributed to J Kjekshus.

At least 19 recordsLinked to original sources
PubMed1992

[Sudden cardiac death. Significance of beta blockaders].

Sudden death accounts for about 15-20% of all natural fatalities in the industrially developed world. Most of the victims have a substrate of extensive myocardial injury caused by coronary heart disease, cardiomyopathy and hypertensive heart disease. In most cases, the immediate cause of death is triggered by ventricular tachycardia which degenerates into ventricular fibrillation. Changes in myocardial electrical properties may be critically modified by ischemia, imbalance in the autonomic nervous system, electrolytic disorders, and haemodynamic factors. We review the causes of sudden cardiac death, giving special attention to the effect of beta-adrenoceptor blockade as a preventive measure.

Adrenergic beta-Antagonists↗
PubMed1992

Effects of the early administration of enalapril on mortality in patients with acute myocardial infarction. Results of the Cooperative New Scandinavian Enalapril Survival Study II (CONSENSUS II)

BACKGROUND: Long-term administration of angiotensin-converting--enzyme (ACE) inhibitors has been shown to improve survival in patients with symptomatic left ventricular failure and to attenuate left ventricular dilatation in patients with myocardial infarction. We studied whether mortality could be reduced during the 6 months after an acute myocardial infarction with use of the ACE inhibitor enalapril. METHODS: At 103 Scandinavian centers patients with acute myocardial infarctions and blood pressure above 100/60 mm Hg were randomly assigned to treatment with either enalapril or placebo, in addition to conventional therapy. Therapy was initiated with an intravenous infusion of enalapril (enalaprilat) within 24 hours after the onset of chest pain, followed by administration of oral enalapril. RESULTS: Of the 6090 patients enrolled, 3046 were assigned to placebo and 3044 to enalapril. The life-table mortality rates in the two groups at one and six months were not significantly different (6.3 and 10.2 percent in the placebo group vs. 7.2 and 11.0 percent in the enalapril group, P = 0.26). The relative risk of death in the enalapril group was 1.10 (95 percent confidence interval, 0.93 to 1.29). Death due to progressive heart failure occurred in 104 patients (3.4 percent) in the placebo group and 132 (4.3 percent) in the enalapril group (P = 0.06). Therapy had to be changed because of worsening heart failure in 30 percent of the placebo group and 27 percent of the enalapril group (P less than 0.006). Early hypotension (systolic pressure less than 90 mm Hg or diastolic pressure less than 50 mm Hg) occurred in 12 percent of the enalapril group and 3 percent of the placebo group (P less than 0.001). CONCLUSIONS: Enalapril therapy started within 24 hours of the onset of acute myocardial infarction does not improve survival during the 180 days after infarction.

Administration, Oral↗
PubMed1992

Renal function in severe congestive heart failure during treatment with enalapril (the Cooperative North Scandinavian Enalapril Survival Study [CONSENSUS] Trial).

The effect on renal function of long-term treatment with either enalapril (n = 123) or placebo (n = 120) in addition to conventional therapy was studied in a randomized trial in patients with severe congestive heart failure (New York Heart Association functional class IV; the Cooperative North Scandinavian Enalapril Survival Study). Enalapril was administered in a dose of 2.5 to 40 mg/day. The analysis was restricted to the first 6 months of treatment. There was an average initial increase of 10 to 15% (10 to 20 mumol/liter) irrespective of baseline serum creatinine within the first 3 weeks of enalapril treatment, whereafter mean serum creatinine remained on a similar level during the first 6 months. Enalapril was well-tolerated by most patients, and serum creatinine was reduced in 24%. Serum creatinine increased by greater than 100% in 13 patients (11%) in the enalapril group (mainly as a consequence of intercurrent disease or severe hypotension, and usually transiently) and in 4 (3%) in the placebo group. The maximal increase in serum creatinine in the enalapril group was inversely correlated to the diastolic blood pressure (p = 0.008) at baseline and to the mean diastolic and systolic blood pressures measured at the time of the maximal increase in serum creatinine (p = 0.0001). According to multivariate regression analysis, the maximal increase in serum creatinine was also slightly influenced by the dose of furosemide taken. The development of hypotension emerged as the strongest factor explaining an abnormal increase in serum creatinine.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1992

[Myocardial disease in diabetes mellitus].

Diabetes mellitus is associated with excessive cardiovascular morbidity and mortality. Patients with diabetes mellitus suffer premature and severe atherosclerosis, and the relative impact is greater in women than in men. Clinical, experimental and pathological studies support the existence of a specific cardiomyopathy associated with diabetes mellitus. The cardiomyopathy plays an essential role in the pathogenesis of primary myocardial involvement, resulting in ventricular dysfunction, diminished cardiac pump performance and eventually overt heart failure. The authors discuss coronary heart disease and diabetic cardiomyopathy and indicate relevant treatment regimens.

Cardiomyopathies↗
PubMed1992

Effects of enalapril on long-term mortality in severe congestive heart failure. CONSENSUS Trial Group.

All surviving patients in a double-blind study comparing the effects of enalapril and placebo on survival in severe congestive heart failure were recommended to be treated with active drug after stopping the trial. Two-year follow-up from the end of the blinded trial demonstrated that among 77 survivors of 127 patients originally allocated to the group with enalapril, 38 were still alive. Of 126 patients allocated to the group with placebo 58 survived the blinded study, and after 2-year follow-up 26 were still alive. Thus, the difference between the original treatment groups remained, despite that treatment with enalapril was made available to all surviving patients and that those in the group with enalapril were sicker at baseline than those in the group with placebo. If enalapril was prescribed, the mortality was 47% compared with 75% if it was not. Life-table analysis suggests a marked carry-over effect of treatment in the group with enalapril that lasted for up to 15 months before mortality rates became comparable in the 2 treatment groups. This strongly suggests that enalapril confers structural protection to the failing myocardium.

Adult↗
PubMed1992

Oral magnesium supplementation improves metabolic variables and muscle strength in alcoholics.

Magnesium deficiency is common among chronic alcoholics, but the knowledge of oral magnesium supplementation to this group is limited. We, therefore, randomized 49 chronic alcoholics, moderate to heavy drinkers for at least 10 years to receive oral magnesium or placebo treatment for 6 weeks according to a double-blind protocol. Effects on metabolic variables and muscle strength were analyzed. Significant reduction of aspartate-aminotransferase (ASAT), alanine-aminotransferase (ALAT) and gamma-glutamyl-transpeptidase (GGT) were seen after magnesium, whereas no change was observed with placebo. Bilirubin decreased in both groups. Serum Na, Ca, and P increased significantly during magnesium therapy compared with no statistically significant change in the placebo group. Serum K and Mg increased slightly after magnesium supplementation and decreased in the placebo group, resulting in a significant difference between the two groups at the end of the study. Muscle strength increased significantly during magnesium treatment, contrasting to no change with placebo. Blood pressure, heart rate, hematological variables, serum lipids (cholesterol, HDL, TG), glucose tolerance, and creatinine were unchanged in the two groups after treatment. Alcohol consumption was similar before and during the trial and does not explain the differences between the two groups The results shows that short-term oral magnesium therapy may improve liver cell function, electrolyte status, and muscle strength in chronic alcoholics.

Administration, Oral↗
PubMed1992

Magnesium deficiency diagnosed by an intravenous loading test.

Magnesium deficiency is common but difficult to diagnose and to assess in clinical practice. The use of a magnesium loading test was therefore evaluated to diagnose magnesium deficiency in 661 hospitalized patients with medical conditions assumed to interfere with magnesium uptake and excretion. Thirty millimoles of magnesium sulphate were administered intravenously during 8 h as a loading test and related to the urinary excretion in the following 24 h. A group of 30 patients without any known predisposition for magnesium deficiency and a group of 27 healthy volunteers served as controls. The mean (with 95% confidence interval) magnesium retention was 4 (-2-10)% in the control group of patients and 3 (-2-8)% in healthy subjects. A significantly higher retention was observed in all the groups of the patients: atrial fibrillation 18 (11-25)%, other arrhythmias 18 (11-24)%, hypertension 27 (20-33)%, coronary artery disease 25 (20-30)%, congestive heart failure 31 (26-37)%, cerebrovascular events 38 (24-51)%, gastrointestinal disorders 22 (14-29)%, diabetes mellitus 16 (9-22)%, and alcoholics 33 (29-36)%. The percentage of patients with a retention greater than mean + 2 SD of the two control groups varied between 22% and 54% among the different patient groups. The mean serum magnesium among the patient groups was similar to the control group of patients, except for the alcoholics, hypertensives and young healthy controls, who had significantly reduced levels. Magnesium retention was significantly correlated to age and renal function, and among the alcoholics negatively correlated to serum magnesium.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Effects of selective beta 2-adrenoceptor blockade on serum potassium and exercise performance in normal men.

1. The differential effects of beta-adrenoceptor subtypes on potassium fluxes and exercise capacity were compared in eight healthy young men using single oral doses of the selective beta 2-adrenoceptor antagonist ICI-118551, the selective beta 1-adrenoceptor antagonist atenolol or the non-selective beta-adrenoceptor antagonist propranolol. The study was randomized, double-blind and placebo controlled. 2. Potassium in the venous effluent from the exercising muscles increased progressively with increasing exercise intensity. This response was augmented by propranolol, whereas neither atenolol nor ICI-118551 modified the response. After exercise potassium concentration fell exponentially with no difference between the treatment regimens. 3. Cumulative work was significantly reduced by ICI-118551 (6.4%, P = 0.04) and by propranolol (12.4%, P less than 0.01), whereas the reduction with atenolol (5.6%) did not reach statistical significance. 4. Atenolol and propranolol reduced peak heart rate by 23% and 29%, and peak systolic blood pressure by 9% and 11% respectively during maximal exercise. ICI-118551 caused a non-significant reduction in heart rate during submaximal exercise, with a significant reduction at maximum exercise (6% reduction), whereas systolic blood pressure was not different from placebo. Diastolic blood pressures were similar across all treatment regimens. 5. Similar glucose concentrations were obtained at baseline and at exhaustion during all treatment regimens. Lactate concentrations were comparable for any given exercise intensity irrespective of treatment regimens. Propranolol reduced lactate concentrations from the exercising muscles at maximum exercise in proportion to the reduction of maximal exercise capacity. 6. The subjective perception of fatigue was not affected by either beta 1- or beta 2-adrenoceptor blockade.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Agonists↗
PubMed1990

Effects of enalapril and neuroendocrine activation on prognosis in severe congestive heart failure (follow-up of the CONSENSUS trial). CONSENSUS Trial Study Group.

This study enrolled 253 patients with severe heart failure (New York Heart Association functional class IV) from 35 centers in Scandinavia, randomly assigned to treatment with placebo or enalapril, in addition to their usual treatment for heart failure. After an initial titration period, the daily doses of enalapril ranged from 2.5 to 40 mg. At the end of the trial, 46% of the placebo-treated patients and 61% of the enalapril-treated patients were alive (p = 0.003); the survival figures at 8 months after completion of the trial were 32 and 48%, respectively (p = 0.001); and 21 and 30%, respectively (p = 0.006) at the 2-year follow-up. In the placebo group, there was a significant positive association between mortality and baseline levels of norepinephrine, epinephrine, angiotensin II, aldosterone and atrial natriuretic peptide; no such association was found in the enalapril-treated patients. The results suggest that the effects of enalapril on mortality are related to a counteraction of the neuroendocrine activation in general and to the renin-angiotensin system in particular.

Enalapril↗
PubMed1990

Arrhythmias and mortality in congestive heart failure.

The extent and severity of myocardial dysfunction and risk of dying are associated with the occurrence of ventricular arrhythmias. However, there is a dissociation between the frequency of ventricular arrhythmias and the prevalence of sudden death among patients with congestive heart failure. Sudden death occurs in 8 to 10% of New York Heart Association functional class I patients and in 20% of class II, III and IV patients, despite increased frequency of malignant arrhythmias and functional deterioration. Yearly mortality rates increase from 12 to 15% in class I and II and is 60% in class IV. Sudden death in class I and II is 50 to 60% of all deaths, whereas in class IV it amounts to only 20 to 30%. The most important cause of death in class IV is progressive congestive heart failure. Ventricular arrhythmia is a trigger event in the development of fatal arrhythmia which depends on a substrate of myocardial scar tissue, hypertrophy and aberrant conducting pathways. However, regional myocardial ischemia, transmembrane electrolyte differences and myocardial stores of catecholamines are important modulators. Depletion of myocardial catecholamines and down-regulation of myocardial beta-adrenergic receptors in the myocardium may explain tolerance to ventricular tachyarrhythmias observed in patients with severe congestive heart failure and intolerance to conventional antiarrhythmic drugs. Although angiotensin-converting enzyme (ACE) inhibitors may reduce ventricular arrhythmias, the important role of ACE inhibitors in severe congestive heart failure is to prevent progression of myocardial dysfunction and congestive heart failure. To date, however, ACE inhibitors have not been demonstrated to have a significant effect on the incidence of sudden death. This does not preclude an effect on fatal arrhythmias among patients with milder heart failure and intact stores of myocardial catecholamines.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1990

Influence of heart rate on mortality after acute myocardial infarction.

Elevated heart rate (HR) during hospitalization and after discharge has been predictive of death in patients with acute myocardial infarction (AMI), but whether this association is primarily due to associated cardiac failure is unknown. The major purpose of this study was to characterize in 1,807 patients with AMI admitted into a multicenter study the relation of HR to in-hospital, after discharge and total mortality from day 2 to 1 year in patients with and without heart failure. HR was examined on admission at maximum level in the coronary care unit, and at hospital discharge. Both in-hospital and postdischarge mortality increased with increasing admission HR, and total mortality (day 2 to 1 year) was 15% for patients with an admission HR between 50 and 60 beats/min, 41% for HR greater than 90 beats/min and 48% for HR greater than or equal to 110 beats/min. Mortality from hospital discharge to 1 year was similarly related to maximal HR in the coronary care unit and to HR at discharge. In patients with severe heart failure (grade 3 or 4 pulmonary congestion on chest x-ray, or shock), cumulative mortality was high regardless of the level of admission HR (range 61 to 68%). However, in patients with pulmonary venous congestion of grade 2, cumulative mortality for patients with admission HR greater than or equal to 90 beats/min was over twice as high as that in patients with admission HR less than 90 beats/min (39 vs 18%, respectively); the same trend was evident in patients with absent to mild heart failure (mortality 18 vs 10%, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗
PubMed1990

Predicting 1-year outcome following acute myocardial infarction: physicians versus computers.

Whether decision rules derived statistically from patient data can produce better decisions than an expert clinician or a model of the expert clinician (expert system) is controversial. We examined this issue in the context of predicting cardiac death by 1 year for patients discharged from the hospital following acute myocardial infarction. Decision rules were derived from a base sample of 781 patients. These decision rules and three experienced cardiologists then estimated probability of death by 1 year for each patient in a separate test sample (n = 400). In our evaluation of the performance of the decision rules and physicians, we detected no differences, although the decision rules and physicians tended to classify the patients somewhat differently. Further multivariate analyses on the physicians' predictions showed that two of the physicians paid attention to somewhat different variables than the third physician. Lack of agreement among expert cardiologists would complicate modeling of a consensual decision-making process within the framework of an expert system.

Aged↗
PubMed1990

Diabetic patients and beta-blockers after acute myocardial infarction.

Whether diabetic patients may benefit, compared with non-diabetic patients, from beta-blocker therapy following acute myocardial infarction was examined in a large multicentre cohort of 2024 patients, including 340 diabetics, 281 of whom survived hospitalization. One-year mortality following discharge was 17% for diabetics compared with 10% for non-diabetics (P less than 0.001). However, diabetics discharged on beta-blockers had a 1-year mortality of only 10%, compared with 23% for diabetics not on beta-blockers. In non-diabetics, mortality rates were 7% and 13% for those taking and not taking beta-blockers, respectively. Bias in patient selection for beta-blocker therapy might be responsible for the trends exhibited in our population since patients were not randomized to treatment. In diabetics, evidence of pulmonary congestion on X-ray was more prevalent than in non-diabetics; this appeared to be true both for patients taking beta-blockers and for those not taking beta-blockers. However, even in diabetics without evidence of pulmonary congestion on X-ray, 1-year mortality was 7% vs 17% for those with and without beta-blocker therapy, respectively (P less than 0.04). In multivariate analysis, beta-blocker use was an independent predictor of 1-year cardiac survival following hospital discharge for all diabetics, even those without evidence for pulmonary congestion on X-ray, but not for non-diabetics. These data suggest a beneficial effect, but a definitive answer regarding the benefit of beta-blockade in diabetic patients after acute myocardial infarction would require a prospective, randomized study.

Adrenergic beta-Antagonists↗
PubMed1990

Hormones regulating cardiovascular function in patients with severe congestive heart failure and their relation to mortality. CONSENSUS Trial Study Group.

There is a varying hormonal activation in heart failure. To be able to evaluate this activation and relate it to prognosis, we took blood samples at baseline and after 6 weeks from 239 patients with severe heart failure (all in New York Heart Association class IV) randomized to additional treatment with enalapril or placebo. In this study (CONSENSUS), which has previously been reported, there was a significant reduction in mortality among patients treated with enalapril. The present data show in the placebo group a significant positive relation between mortality and levels of angiotensin II (p less than 0.05), aldosterone (p = 0.003), noradrenaline (p less than 0.001), adrenaline (p = 0.001), and atrial natriuretic factor (p = 0.003). A similar relation was not observed among the patients treated with enalapril. Significant reductions in mortality in the groups of patients treated with enalapril were consistently found among patients with baseline hormone levels above median values. There were significant reductions in hormone levels from baseline to 6 weeks in the group of patients treated with enalapril for all hormones except adrenaline. There were no correlations between these changes in hormone levels. Summarily, there is a pronounced but variable neurohormonal activation in heart failure even in patients with similar clinical findings. This activation is reduced by enalapril therapy. The results suggest that the effect of enalapril on mortality is related to hormonal activation in general and the renin-angiotensin system in particular.

Aged↗
PubMed1990

M-mode echocardiography in patients with severe congestive heart failure. A subgroup analysis in the Cooperative North Scandinavian Enalapril Survival Study (CONSENSUS).

In the CONSENSUS study, M-mode echocardiography was used as an optional examination. All patients were in severe congestive heart failure [New York Heart Association (NYHA) functional class IV], and all patients had radiologically marked increased heart size. Of 253 patients, M-mode echocardiography was done at baseline in 105 patients. M-mode echocardiographic recordings from 70 patients were received, and of these, only 54 patients (77%) had recordings of acceptable quality for evaluation. At follow-up, M-mode echocardiography was done after 6 weeks, 6 months and 12 months. However, because of the high mortality and the premature cessation of the study, only a limited number of patients had M-mode echocardiographic registrations after greater than 6 weeks. All M-mode echocardiographic registrations were analysed by 2 investigators independently. Systolic time interval (STI) decreased from 0.58 to 0.48 (p less than 0.05) in the enalapril group after 6 weeks. In the placebo group, a small increase in STI from 0.54 to 0.56 (not significant) was seen after 6 weeks. The decrease in STI in the enalapril group was secondary to an increase in left ventricular ejection time. No significant change was seen in left ventricular and left atrial diameters at follow-up: this finding can be explained by a type 2 error. These findings indicate an increased STI in the enalapril-treated group, which could explain why enalapril treatment reduced mortality in the CONSENSUS study.

Aged↗
PubMed1990

Effect of enalapril on mortality in congestive heart failure. Follow-up survival data from the CONSENSUS trial.

The CONSENSUS trial, which compared the effects of enalapril and placebo on survival in severe heart failure, had a limited blinded treatment period. Follow-up for 8.5 months from the end of blinded therapy was performed. Enalapril therapy was encouraged in all patients during follow-up. Of the 135 surviving patients, 58 had previously been allocated placebo and 77 had been allocated enalapril. The follow-up mortality rates in those receiving enalapril were 18 (31%) and 16 (21%), respectively. Mortality was markedly lower in patients treated with enalapril than in those not started on the drug (16% vs 61%). The follow-up data strongly support the original CONSENSUS data regarding reduction of mortality in severe heart failure after the addition of enalapril.

Enalapril↗