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Biomedical subjects

K Swedberg

Publications and source records attributed to K Swedberg.

At least 73 records · Page 4Linked to original sources
PubMed1998

Angiotensin-converting enzyme gene expression in skeletal muscle in patients with chronic heart failure.

BACKGROUND: Skeletal muscle factors may influence functional limitation in patients with heart failure. The renin-angiotensin system is activated in chronic heart failure. Treatment with angiotensin-converting enzyme (ACE) inhibitors improve symptoms and prognosis. The goal of this study was to quantify and localize skeletal muscle ACE-mRNA in patients with chronic heart failure and in control subjects, and to elucidate skeletal muscle fiber area and capillary density. METHODS AND RESULTS: Biopsies from the lateral vastus muscle were taken from 9 patients before and after treatment with enalapril and in 10 control subjects. ACE-mRNA was quantified with reverse transcription polymerase chain reaction. Immunohistochemistry was used to localize ACE within skeletal muscle. No difference in ACE-mRNA transcripts between patients and control subjects was detected, nor did ACE gene expression change after treatment with enalapril. The number of ACE-mRNA transcripts was related to muscle fiber area, whereas an inverse relationship between the number of ACE transcripts and capillary density was found. ACE was detected in the endothelial cells of capillaries in skeletal muscle. CONCLUSION: ACE is expressed in skeletal muscle and is confined to endothelial cells. The close relationship between capillary density and number of ACE transcripts indicate that activation of the renin-angiotensin system has an impact on capillary growth.

3-Hydroxyacyl CoA Dehydrogenases↗
PubMed1998

Electrocardiographic and clinical predictors of torsades de pointes induced by almokalant infusion in patients with chronic atrial fibrillation or flutter: a prospective study.

The aim of this study was to identify predictors of torsades de pointes (TdP) in patients with atrial fibrillation (AF) or flutter exposed to the Class III antiarrhythmic drug almokalant. TdP can be caused by drugs that prolong myocardial repolarization. One hundred patients received almokalant infusion during AF (infusion 1) and 62 of the patients during sinus rhythm (SR) on the following day (infusion 2). Thirty-two patients converted to SR. Six patients developed TdP. During AF, T wave alternans was more common prior to infusion (baseline) in patients developing TdP (50% vs 4%, P < 0.01). After 30 minutes of infusion 1, the TdP patients exhibited a longer QT interval (493 +/- 114 vs 443 +/- 54 ms [mean +/- SD], P < 0.01), a larger precordial QT dispersion (50 +/- 74 vs 27 +/- 26 ms, P < 0.05), and a lower T wave amplitude (0.12 +/- 0.21 vs 0.24 +/- 0.16 mV, P < 0.01). After 30 minutes of infusion 2, they exhibited a longer QT interval (672 +/- 26 vs 489 +/- 74 ms, P < 0.001), a larger QT dispersion in precordial (82 +/- 7 vs 54 +/- 52 ms, P < 0.01) and extremity leads (163 +/- 0 vs 40 +/- 34 ms, P < 0.001), and T wave alternans was more common (100% vs 0%, P < 0.001). Risk factors for development of TdP were at baseline: female gender, ventricular extrasystoles, and treatment with diuretics; and, after 30 minutes of infusion: sequential bilateral bundle branch block, ventricular extrasystoles in bigeminy, and a biphasic T wave. Patients developing TdP exhibited early during almokalant infusion a pronounced QT prolongation, increased QT dispersion, and marked morphological T wave changes.

Aged↗
PubMed1997

Effect of metoprolol on the prognosis for patients with suspected acute myocardial infarction and indirect signs of congestive heart failure (a subgroup analysis of the Göteborg Metoprolol Trial).

The aim of this study is to describe the impact of early treatment with metoprolol on prognosis during 1 year of follow-up in patients with suspected acute myocardial infarction (AMI) and indirect signs of congestive heart failure (CHF). Patients aged 40-74 years who presented within 48 hours of onset of symptoms raising suspicion of AMI were assessed for inclusion. All patients participated in the Göteborg Metoprolol Trial and had indirect indices of CHF according to various clinical criteria. As soon as possible after hospital admission, patients received either placebo or metoprolol (15 mg) divided into 3 intravenous injections, then oral treatment, 200 mg daily for 3 months. Thereafter, most patients in both treatment groups received metoprolol in an open manner. Among the 1,395 randomized patients, 262 (19%) had signs of mild-to-moderate CHF before randomization. Of these, 131 were randomized to metoprolol and 131 to placebo. During the first 3 months, mortality was 10% among patients randomized to metoprolol versus 19% among patients randomized to placebo (p = 0.036). The corresponding figures for the first year were 14% and 27%, respectively (p = 0.0099). Patients randomized to placebo who showed signs of CHF had a 1-year mortality rate of 28% compared with 10% among patients without such signs (p <0.001). The results suggest that early treatment with metoprolol markedly reduces mortality in patients having suspected AMI and signs of CHF.

Adrenergic beta-Antagonists↗
PubMed1997

A randomized controlled trial of epoprostenol therapy for severe congestive heart failure: The Flolan International Randomized Survival Trial (FIRST).

This trial evaluated the effects of epoprostenol on patients with severe left ventricular failure. Patients with class IIIB/IV congestive heart failure and decreased left ventricular ejection fraction were eligible for enrollment if angiography documented severely compromised hemodynamics while the patient was receiving a regimen of digoxin, diuretics, and an angiotensin-converting enzyme inhibitor. We randomly assigned 471 patients to epoprostenol infusion or standard care. The primary end point was survival; secondary end points were clinical events, congestive heart failure symptoms, distance walked in 6 minutes, and quality-of-life measures. The median dose of epoprostenol was 4.0 ng/kg/min, resulting in a significant increase in cardiac index (1.81 to 2.61 L/min/m2), a decrease in pulmonary capillary wedge pressure (24.5 to 20.0 mm Hg), and a decrease in systemic vascular resistance (20.76 to 12.33 units). The trial was terminated early because of a strong trend toward decreased survival in the patients treated with epoprostenol. Chronic intravenous epoprostenol therapy is not associated with improvement in distance walked, quality of life, or morbid events and is associated with an increased risk of death.

Aged↗
PubMed1997

Skeletal muscle alterations in patients with chronic heart failure.

AIMS: To investigate skeletal muscle in patients with chronic heart failure and controls, and relate skeletal muscle variables to functional class, exercise capacity, central haemodynamics, muscle strength and medical treatment. METHODS: Biopsy from the lateral vastus muscle was obtained in 43 patients and 20 controls. Right sided heart catheterization was performed in 19 patients and maximal exercise testing in 26 patients. In nine patients muscle strength was measured. Patients had higher lactate levels, higher lactate dehydrogenase activity, and lower oxidative enzymes activity than controls. In patients, the percentage of type I fibres and capillarization were decreased while the percentage of type II B fibres were increased. Lactate dehydrogenase activity correlated with exercise capacity, muscle strength and right atrial pressure. Digoxin-treated patients had significantly lower oxidative enzyme activity than patients without digoxin treatment. CONCLUSION: Patients with chronic heart failure have several skeletal muscle abnormalities. Central haemodynamics and medical treatment may, in addition to inactivity, be important in skeletal muscle changes.

Adenosine Triphosphate↗
PubMed1997

Vectorcardiographic monitoring of patients with acute myocardial infarction and chronic bundle branch block.

AIMS: This study was set up to describe vectorcardiographic patterns in patients with bundle-branch block and acute myocardial infarction. METHODS AND RESULTS: Sixty-five patients admitted to the coronary care unit with bundle-branch block and suspected acute myocardial infarction were monitored by dynamic vectorcardiography with trend analysis. In 28 patients, a clinical diagnosis of acute myocardial infarction was made. In patients with left bundle-branch block and acute myocardial infarction, the pattern of QRS vector-difference evolution was similar to that in patients with the narrow QRS complex, while ST vector-magnitude changes increased over time. Using a cut-off value for QRS vector-difference at 12 h of more than 20 microVs and a specific trend curve pattern, acute myocardial infarction in the presence of left bundle-branch block could be diagnosed with an accuracy of 71%. For patients with right bundle branch block, using a maximum ST vector-magnitude of > 200 microV during the first 4 h, acute myocardial infarction could be diagnosed with a 78% accuracy. CONCLUSION: Our results indicate that dynamic vectorcardiography is a valuable tool in diagnosing and monitoring acute myocardial infarction in patients with bundle branch block.

Aged↗
PubMed1996

Meta-analysis of morbidity and mortality in five exercise capacity trials evaluating ramipril in chronic congestive cardiac failure.

In 5 separate exercise capacity trials in similar patients with chronic congestive heart failure performed in Europe, the United States, and South Africa, 627 patients were randomized to ramipril and 428 to placebo. The dose of ramipril ranged from 1.25 to 20 mg/day. Follow-up was at 12 or 24 weeks. None of the trials were designed to assess efficacy with regard to clinical outcome. To assess in the combined experience whether there was an effect of ramipril on mortality, hospitalization, functional classification (New York Heart Association class), and exercise capacity, we pooled data from each trial and performed a mata-analysis. Of the patients randomized to ramipril and placebo, respectively, and based on intention to treat, 14 (2.2%) and 18 (3.8%) patients died (odds ratio 0.60, 95% confidence interval 0.28 to 1.29), and 59 (9.4%) and 67 (14.3%) patients died or were hospitalized (odds ratio 0.68, 95% confidence interval 0.46 to 1.00). The New York Heart Association class improved in 29% and 25% respectively, whereas 8% and 15% deteriorated (p=0.04, based on intention to treat; death and hospitalization considered as deterioration). In ranked comparisons based on intention to treat and with imputation of exercise time as 0 for patients who were unable to exercise because of death or who were hospitalized, exercise capacity was significantly improved by rampril. We concluded that rampiril is likely to have an effect on mortality, morbidity, and functional capacity in patients with chronic congestive heart failure similar to that of other angiotensin-converting enzyme inhibitors.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1996

Quality of life on treatment with metoprolol in dilated cardiomyopathy: results from the MDC trial. Metoprolol in Dilated Cardiomyopathy trial.

Quality of life in heart failure patients is receiving increased attention as a reflection of a treatment's potential secondary benefit of general well-being and daily functioning. The Metoprolol in Dilated Cardiomyopathy (MDC) trial was conducted as a large, multicenter trial to establish the effects of metoprolol on mortality and need for heart transplantation in patients with symptomatic idiopathic cardiomyopathy. It was found that metoprolol was well tolerated, improved symptoms and cardiac function, and prevented clinical deterioration in patients with symptomatic idiopathic dilated cardiomyopathy. Quality of life was evaluated as a secondary endpoint in 345 out of 383 randomized patients using a disease-specific questionnaire, the Quality of Life in Heart Failure Questionnaire, depicting physical activity, somatic symptoms, emotions, and life satisfaction. In a comparison of patients treated with metoprolol or placebo, patients treated with metoprolol noted a significantly more favorable response than those treated with placebo in terms of the overall treatment evaluation (p < 0.05). Additionally, an analysis of the changes from baseline to 18 months, using 95% confidence intervals, revealed that patients treated with metoprolol showed a significant improvement from baseline to 18 months in life satisfaction, physical activity, and the total score, while patients treated with placebo did not change at all. The improvement in quality of life was supported by the correlations with improvement in traditional clinical parameters.

Adrenergic beta-Antagonists↗
PubMed1996

Nucleoside transport inhibition by draflazine in unstable coronary disease.

OBJECTIVES: In a randomised, double-blind, placebo controlled study, we evaluated the tolerability and safety of draflazine, a nucleoside transport inhibitor, in the treatment of patients with unstable angina and non-Q-wave infarction. METHODS: Twenty-one patients were randomised to treatment with draflazine 3.5 mg or matching placebo given as an i.v. infusion and haemodynamic and symptomatic tolerability were investigated. Myocardial ischaemia was evaluated by means of vectorcardiography and blood analysis of the MB fraction of creatine kinase. RESULTS: The study drug was well tolerated by all patients and it did not cause any adverse haemodynamic effects, nor other serious adverse events. Three patients in the placebo group reported five adverse events, as compared to a single adverse event in the draflazine group. Cardiovascular events were detected in 7 patients in the placebo group and in 5 patients receiving draflazine. The mean duration of chest pain during the 24 hour observation period was 91.4 min in the placebo group compared to 75.5 min in draflazine treated patients. Neither the vectorcardiographic nor biochemical measures of ischaemia differed between treatment groups. CONCLUSION: Nucleoside transport inhibition by draflazine was well tolerated by patients with unstable coronary disease. It seems to be a promising method of adenosine enhancement in acute myocardial ischaemia. The potential cardioprotective effect of the drug needs further evaluation in larger trials.

Aged↗
PubMed1996

Treatment of heart failure.

Effective treatment of heart failure depends on a correct functional and aetiological diagnosis. In asymptomatic patients with cardiac dysfunction following myocardial infarction, treatment is directed to prevent recurrent infarction by aggressive lipid lowering with statins and antiplatelet drugs. Beta blockers are important to reduce sudden death. In symptomatic heart failure, clinical improvement is obtained by inhibition of the renin-angiotensin and sympathetic system. Angiotensin-converting-enzyme inhibitors in combination with diuretics reduce morbidity and mortality caused by progression of the myocardial dysfunction and recurrent myocardial infarction. Drugs that activate the neurohormonal systems are clearly counteractive. Digitalis has a definite favourable effect on systems, and in patients with atrial fibrillation, but its effect on mortality is still unsettled. Beta blockers in routine treatment of symptomatic heart failure still remains controversial, but may benefit selected patients.

Adrenergic beta-Antagonists↗