Search PubMed⌕ Search

Biomedical subjects

J Kjekshus

Publications and source records attributed to J Kjekshus.

At least 91 records · Page 5Linked to original sources
PubMed1995

Beta-blockers and sudden cardiac death.

OBJECTIVES: To 1) consider the problem of sudden death from heart disease and the role of beta-blockers and other agents in preventing sudden death and 2) review perceived problems with beta-blocker therapy, such as effects on blood lipids, complications in diabetes, and adverse effects on heart failure and quality of life. DATA SOURCES: MEDLINE and EMBASE searches done from July 1994 on, and recognized texts. STUDY SELECTION: More than 400 original and review articles were evaluated, of which the most relevant were selected. DATA EXTRACTION: Data were extracted and reviewed by two authors. Accuracy was confirmed, when necessary, by the other authors. DATA SYNTHESIS: Of all of the therapies currently available for the prevention of sudden cardiac death, none is more established or more effective than beta-blockers. Indeed, the evidence that beta-blockers have a cardioprotective effect is compelling. They probably reduce the rate of atheroma formation; they reduce the risk for ventricular fibrillation in animal models of myocardial ischemia; they appear to reduce cardiac mortality in primary prevention trials; and they reduce mortality, particularly from sudden death, in patients who have had infarction. Moreover, withholding beta-blockers because of problems perceived to be associated with them is usually not warranted and may frequently prevent their use in those who will benefit most from them. CONCLUSION: Clinicians should reappraise the evidence for the significant effect of beta-blockers on morbidity and mortality, and they should recognize the importance of initiating and maintaining beta-blocker therapy when the less well-informed might suggest otherwise.

Adrenergic beta-Antagonists↗
PubMed1995

[Intermittent claudication and beta-blockaders. An unfortunate combination?].

beta-adrenergic blockers have been considered relatively contraindicated in patients with peripheral arterial disease because of reports claiming that these drugs may worsen intermittent claudication. The authors review the published randomized controlled trials and discuss the results of comparisons of this treatment with treatment with alternative drugs. None of the studies of beta-blockade in patients with intermittent claudication showed a reduction of walking distance or impairment of peripheral flow compared with patients given placebo, except one study using a beta-blocker with intrinsic sympathomimetic activity. Alternative drugs are included in only few trials and do not seem to be beneficial. There is a lack of evidence to suggest that beta-blockers adversely effect walking capacity or worsen symptoms in mild to moderate intermittent claudication. beta-blockers should not be avoided if considered in other respects to be the optimal therapy for associated atherosclerotic disease.

Adrenergic beta-Antagonists↗
PubMed1995

[Chronic left heart ventricle failure and inotropic stimulation].

Congestive left heart failure can be treated using three main strategies: change preload to optimize the Frank-Starling relationship, decrease after-load to reduce external work and increase cardiac contractility by inotropic stimulation. The third option is reviewed in this article, which discusses the pharmacological and clinical effects of different inotropic drugs as known in 1994. It is concluded that digitalis should be considered apart from other inotropic drugs. Even when in sinus rhythm, digitalis seems reasonable as an adjuvans to after-load reduction and diuretics. Chronic use of other inotropic drugs for congestive left heart failure is not recommended.

Adrenergic beta-Agonists↗
PubMed1995

[Reduced physical tolerance in patients with heart failure. Mechanisms and therapeutic effects].

Physical performance is markedly reduced in patients with congestive heart failure, but the reason has not been precisely defined. It has been generally assumed that reduced exercise performance is related to ventricular systolic performance, or as more recently suggested, to impaired left ventricular diastolic function. However, there is no clear relationship between the indices of left ventricular performance and exercise capacity, and there is a dissociation between improvement in haemodynamic parameters and exercise performance. Recent studies suggest that peripheral changes may be major determinants of exercise performance. This may involve reduced blood flow to the exercising limbs because of impaired vasodilatory capacity or intrinsic changes in the skeletal muscle itself. In this review, these factors are considered, and the impact of different therapeutic strategies is discussed.

Exercise↗
PubMed1995

Comparison of the effects of losartan and enalapril on clinical status and exercise performance in patients with moderate or severe chronic heart failure.

OBJECTIVES: This study assessed the feasibility of an efficacy trial comparing angiotensin-converting enzyme inhibition and angiotensin II receptor antagonism in heart failure. Patients with moderate or severe heart failure whose condition had previously been stabilized by treatment with a converting enzyme inhibitor were randomly assigned to receive enalapril or losartan. The study was designed to detect any signs of clinical deterioration during double-blind treatment. BACKGROUND: Losartan is a specific, nonpeptide angiotensin II receptor-1 antagonist with a vasodilator hemodynamic profile similar to that of converting enzyme inhibitors. Although therapy with specific receptor blockade has certain theoretic advantages over nonspecific converting enzyme inhibition, demonstration of a comparable therapeutic effect in patients with congestive heart failure will require a major effort comparing two active agents. METHODS: One hundred sixty-six patients with stable heart failure in New York Heart Association functional class III or IV and an ejection fraction < or = 35% were included in a multicenter, double-blind, parallel, enalapril-controlled trial. After a 3-week stabilization period with optimal therapy, including digitalis, diuretic drugs and a converting enzyme inhibitor, patients were randomly assigned to 8 weeks of therapy with losartan, 25 mg/day (n = 52); losartan, 50 mg/day (n = 56); or enalapril, 20 mg/day (n = 58). Patients were assessed with frequent clinical and laboratory evaluation and exercise testing. RESULTS: No significant differences between groups in terms of changes in exercise capacity (6-min walk test), clinical status (dyspnea-fatigue index), neurohumoral activation (norepinephrine, N-terminal atrial natriuretic factor), laboratory evaluation or incidence of adverse experience were observed. CONCLUSIONS: The results suggest that losartan and enalapril are of comparable efficacy and tolerability in the short-term treatment of moderate or severe congestive heart failure. A trial designed to compare the efficacy, tolerability and effect on mortality of long-term angiotensin II receptor blockade with converting enzyme inhibition is both feasible and ethically responsible.

Adult↗
PubMed1995

Atrial natriuretic peptide ANP(1-98) and ANP(99-126) in patients with severe chronic congestive heart failure: relation to echocardiographic measurements. A subgroup analysis from the Cooperative North Scandinavian Enalapril Survival Study (CONSENSUS).

Studies in patients with moderate heart failure have shown a positive relation between atrial size and plasma atrial natriuretic peptide (ANP)(99-126) concentrations; however, the relation of the hormone level and left atrial size and left ventricular function in patients with severe chronic heart failure has not been determined. Fifty-three patients from the Cooperative North Scandinavian Enalapril Survival Study with severe chronic heart failure were evaluated with M-mode echocardiography and determination of plasma concentrations of ANP(99-126). In 35 patients, the plasma level of N-terminal ANP(1-98) was also measured. A significant negative relation was found between ANP(1-98), ANP(99-126), and left atrial diameter (r = -.28, P = .05 and r = -.41, P < .005, respectively). Plasma concentrations of both ANP(1-98) and ANP(99-126) were related to left ventricular systolic function as determined by the systolic time interval index (r = .4, P < .05 and r = .29, P < .05, respectively). A significant improvement of left ventricular systolic function was found in the enalapril group but not in the placebo group. After 6 weeks of therapy, no correlation was found between changes in left atrial size or systolic function or changes in either the ANP(1-98) or ANP(99-126) concentration. The results indicate that high ANP(1-98) or ANP(99-126) plasma concentration is determined by the depressed left ventricular function rather than increased left atrial size in patients with chronic severe heart failure. The findings suggest that the ANP release relation to atrial pressure/atrial size is distorted in severe heart failure.

Aged↗
PubMed1994

[Chronic heart failure. A management program. Proposal for diagnosis and treatment].

An expert meeting on the treatment of heart failure was organized by the Swedish Medical Products Agency in 1992. There were four participants from Norway. Two of these (AW, JK), in cooperation with a group of cardiologists with a special interest in heart failure, present in this article a modified Norwegian programme for treatment of chronic heart failure. When evaluating risk for patients with chronic heart failure, it is necessary to take into account both symptoms and left ventricular systolic function determined by ejection fraction. Specific recommendations are made for treatment of asymptomatic patients with left ventricular dysfunction and for symptomatic patients with mild, moderate and severe heart failure.

Chronic Disease↗
PubMed1994

The plasma concentration of N-terminal proatrial natriuretic factor ANF(1-98) is related to prognosis in severe heart failure.

Due to its longer halflife, the N-terminal of ANF prohormone, ANF(1-98), has plasma concentrations that exceed those of ANF itself by a factor of 10 or more. It is also less prone to rapid changes secondary to hemodynamic alterations. To evaluate the prognostic significance of ANF(1-98) plasma levels in severe heart failure (NYHA IV), the peptide was measured by radioimmunoassay in plasma samples from patients randomized to additional treatment with enalapril (n = 78) or placebo (n = 61) (CONSENSUS study). In the placebo group there was a positive relation between mortality after 6 months and baseline ANF(1-98) level. Because of a reduced mortality, especially among patients with high ANF(1-98) levels, there was no such relation in the patients treated with enalapril. For both groups there was a positive relationship between increase in ANF(1-98) after 6 weeks of treatment and mortality, while a decrease signaled a favorable prognosis. It is concluded that the magnitude and changes of plasma ANF(1-98) provide information on prognosis and therapeutic effects with respect to mortality in patients with severe heart failure. Plasma ANF(1-98) may serve as a useful clinical biochemical parameter in the treatment of heart failure.

Aged↗
PubMed1994

Neuroendocrine activation in relation to left ventricular function in chronic severe congestive heart failure: a subgroup analysis from the Cooperative North Scandinavian Enalapril Survival Study (CONSENSUS).

Left ventricular (LV) function and plasma levels of cardiovascular hormones were examined in patients with severe chronic congestive heart failure (CHF), randomized to placebo or enalapril, in addition to conventional therapy. M-mode echocardiography and plasma hormone concentrations were available at baseline and after 6 weeks of treatment. There was a significant relationship between LV systolic function and levels of angiotensin-II and norepinephrine. Enalapril increased LV fractional shortening (FS%) (13.3 +/- 5.6 to 15.4 +/- 5.8, p < 0.05) and decreased the systolic time interval index (0.58 +/- 0.14 to 0.48 +/- 0.15, p < 0.05) concurrent with a significant decrease in angiotensin-converting enzyme activity and in aldosterone, angiotensin-II, and norepinephrine concentrations after 6 weeks. No changes were found in the placebo group. However, there was no direct relationship between the amount of change in neurohormones and improvement in LV function after 6 weeks. These findings indicate that in patients with severe chronic CHF, severe LV systolic dysfunction is associated with high plasma levels of angiotensin-II and norepinephrine, which can be favorably modified by enalapril. This may be of importance for prolonging life in severe heart failure. The lack of relationship between changes in individual hormones and systolic function suggests complex dynamic interaction. It is, therefore, not sufficient to predict changes in LV function by measuring changes in only one hormone.

Aldosterone↗
PubMed1994

Magnesium status in healthy free-living elderly Norwegians.

OBJECTIVE: Magnesium (Mg) status has previously not been properly assessed among healthy elderly subjects. METHODS: Thirty-six healthy elderly subjects participated. Their Mg status was assessed by serum Mg, basal urinary Mg output, and with a Mg loading test (30 mmol infused during 8 hours; urine sampled 24 hours), and compared with 53 healthy younger subjects. Their dietary intake was assessed by a quantified food frequency questionnaire. Fourteen of the subjects received 300 mmol Mg to study the effect on Mg status. RESULTS: With the exception of vitamin D in women, average energy and nutrient intakes were adequate. All subjects had serum Mg levels within the reference value of the laboratory. Basal urinary Mg excretion was 3.3 +/- 1.1 mmol/day and 24-hour Mg retention after a Mg load was 28 +/- 16% compared to 6 +/- 11% in younger controls, suggesting Mg deficiency in the elderly. In the 14 subjects who received oral Mg supplementation there was a statistically significant increase in basal urinary Mg excretion and creatinine clearance, and decreases in Mg retention, serum Mg and serum creatinine. CONCLUSIONS: This study suggests that a significant subclinical Mg deficit, not detected by serum Mg, was present in many of these healthy elderly subjects. Mg supplementation improved Mg status and renal function.

Aged↗
PubMed1994

Patient characteristics in cases of chronic severe heart failure with different degrees of left ventricular systolic dysfunction.

It has not been determined previously whether patients with severe chronic congestive heart failure differ in demographic characteristics with respect to left ventricular systolic dysfunction (LVD). In patients with severe chronic congestive heart failure in NYHA IV, an optional protocol in the CONSENSUS-I trial was designed to ascertain whether there were any differences in patient characteristics regarding the degree of LVD defined as left ventricular fractional shortening (FS). A subgroup of 54 patients from the CONSENSUS-I trial were evaluated with M-mode echocardiography. Patients with FS above median (14%) were older (74 +/- 7 vs. 68 +/- 7, p < 0.01), more often female (48 vs. 15%, p < 0.05) and had lower heart rates (77 +/- 15 vs. 95 +/- 17, p < 0.01). Analysis of the 2-year follow-up from the end of the trial was also performed. In the placebo group, patients with FS > 14% had significantly better prognosis than patients with FS < 14%. In the enalapril-treated group no such difference in survival was seen. The difference between the original treatment groups remained, despite the fact that treatment with enalapril was then made available to all surviving patients. In conclusion, patients with advanced chronic congestive heart failure and less severe LVD have different demographic characteristics than patients with more severe LVD. In the placebo group, but not in the enalapril group, prognosis was better in patients with less severe LVD.

Aged↗
PubMed1994

The magnesium loading test: reference values in healthy subjects.

The magnesium loading test is a useful tool in the diagnosis of magnesium deficiency. In order to establish a reference range in normal subjects, 88 healthy men and women aged between 18 and 66 years were given 30 mmol magnesium intravenously during eight hours as a loading test, urine was collected from start of infusion for 24 h for measurement of magnesium excretion. The magnesium mean retention was 6.3 +/- 10.3% of the loading dose, and the 0.025 and 0.975 fractiles were -19.5% and 27.5%, respectively. There was no significant difference between the sexes or in the different age groups studied. There was no correlation between the magnesium retention and serum magnesium or with basal urinary magnesium excretion. An excess excretion of magnesium was observed the postload day compared to baseline, but the excretion 24 and 48 h after the magnesium loading were closely correlated, suggesting that 24 h urinary sampling is sufficient. In order to examine the reproducibility of the test 23 of the subjects underwent two magnesium loading tests 4 weeks apart. The mean difference between two repeat magnesium loading tests was 2.0% with a SD of 8.1% and a 95% confidence interval of -1.6-5.5%. Normal saline did not affect baseline magnesium excretion. Concomitant administration of ethanol or physical exercise caused greater variation in magnesium excretion, whereas furosemide was without effect. The 8 h magnesium loading test with 24 h urine sampling seems to be fairly reproducible, is adequate for clinical use, but the normal range is wide.

Adolescent↗
PubMed1993

The effect of magnesium versus verapamil on supraventricular arrhythmias.

Magnesium has previously been used in the treatment of various arrhythmias, but few randomized and prospective studies are available. In a single-blind study, the efficacy and safety of intravenous magnesium sulfate (bolus doses of 5 + 5 mmol followed by infusion of 0.04 mmol/min) versus verapamil (5 + 5 mg followed by 0.1 mg/min) was evaluated in 57 patients with supraventricular arrhythmias (supraventricular tachycardia, atrial fibrillation, and atrial flutter) of recent onset (less than 1 week). Fifteen (58%) of the patients receiving magnesium (n = 26) converted to sinus rhythm within 4 h, and 16 (62%) within 24 h. Verapamil caused a lower ventricular rate, but only six (19%) of the patients (n = 31) converted to sinus rhythm within 4 h (p < 0.01) and 16 (52%) within 24 h (NS). No side effects were observed during magnesium infusion, whereas six patients receiving verapamil had to be withdrawn from further study medication due to symptomatic side effects (hypotension in three, cardiac failure in three). Magnesium appears to be an effective and safe drug for the treatment of supraventricular arrhythmias. The overall efficacy for conversion to sinus rhythm is at least as effective as with verapamil, and its action is more rapid.

Arrhythmias, Cardiac↗
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↗