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T Gundersen

Publications and source records attributed to T Gundersen.

At least 19 recordsLinked to original sources
PubMed2000

[Oxygen therapy of patients with chronic obstructive pulmonary disease reduces the development of pulmonary hypertension].

The development of secondary pulmonary hypertension in patients with chronic obstructive pulmonary disease worsens their prognosis; oxygen therapy seems to improve prognosis in these patients. We measured the effect of oxygen therapy on mean pulmonary artery pressure in four women and four men aged 64 to 82 years (average 73 years) with chronic obstructive pulmonary disease. A right cardiac catheterisation was performed before and on average 11 months (8-16 months) after start of oxygen therapy. The mean pulmonary artery pressure decreased on average 5 mm Hg, from 24 to 19 mm Hg. As prognosis seems to be associated with pulmonary artery pressure, more patients with chronic obstructive pulmonary disease should be evaluated for oxygen therapy.

Aged↗
PubMed1999

[Chronic heart failure--suggestion to a management program].

In 1994, a Norwegian programme for diagnosis and treatment of chronic heart failure was published. Recently the American College of Cardiology, the American Heart Association and the Task Force on Heart Failure of the European Society of Cardiology have published similar guidelines. In this article, the Working Group on Heart Failure of the Norwegian Society of Cardiology presents an updated programme for evaluation and management of patients with chronic heart failure.

Adrenergic beta-Antagonists↗
PubMed1999

Felodipine-metoprolol combination tablet: a valuable option to initiate antihypertensive therapy?

The aim of the present study was to assess the efficacy and tolerability of a calcium antagonist/beta-blocker fixed combination tablet used as first-line antihypertesnive therapy in comparison with an angiotensin converting enzyme inhibitor and placebo. Patients with uncomplicated essential hypertension (diastolic blood pressure between 95 and 110 mm Hg at the end of a 4-week run-in period) were randomly allocated to a double-blind, 12-week treatment with either a combination tablet of felodipine and metoprolol (Logimax), 5/50 mg daily (n = 321), enalapril, 10 mg daily (n = 321), or placebo (n = 304), with the possibility of doubling the dose after 4 or 8 weeks of treatment if needed (diastolic blood pressure remaining >90 mm Hg). The combined felodipine-metoprolol treatment controlled blood pressure (diastolic < or =90 mm Hg 24 h after dose) in 72% of patients after 12 weeks, as compared with 49% for enalapril and 30% for placebo. A dose adjustment was required in 38% of patients receiving the combination, in 63% of patients allocated to placebo, and 61% of enalapril-treated patients. The overall incidence of adverse events was 54.5% during felodipine-metoprolol treatment; the corresponding values for enalapril and placebo were 51.7% and 47.4%, respectively. Withdrawal of treatment due to adverse events occurred in 18 patients treated with the combination, in 10 patients on enalapril, and 12 patients on placebo. No significant change in patients' well-being was observed in either of the three study groups. These results show that a fixed combination tablet of felodipine and metoprolol allows to normalize blood pressure in a substantially larger fraction of patients than enalapril given alone. This improved efficacy is obtained without impairing the tolerability. The fixed-dose combination of felodipine and metoprolol, therefore, may become a valuable option to initiate antihypertensive treatment.

Administration, Oral↗
PubMed1999

The impact of an end-point committee in a large multicentre, randomized, placebo-controlled clinical trial: results with and without the end-point committee's final decision on end-points.

BACKGROUND: A multicentre study permits rapid recruitment of a large number of patients. However, there is a risk of heterogeneities in end-point evaluations, as complex definitions of criteria are interpreted by several local investigators from different hospitals. Reports discussing end-point evaluation are sparse. The TRIM trial was a multicentre trial of a thrombin inhibitor in patients with unstable angina or non-Q myocardial infarction. In this study, an independent end-point committee evaluated all the reported events of death, acute myocardial infarction and refractory angina pectoris in order to obtain uniform judgements of major end-points. STUDY AIMS: To describe the work of the end-point committee, to analyse its possible effect on the final study results and to discuss the impact on the design of future trials. METHOD: The end-point committee consisted of four members, one from each participating country. After the data were processed by the study monitors, completed case record forms and patient files for patients with reported end-points were mailed to the national member of the end-point committee for judgement. The end-point committee met regularly and made final decisions about the end-points. The work of the end-point committee was documented on a separate case record form. RESULTS: The end-point committee assessed 246 events of death, acute myocardial infarction and refractory angina pectoris in 187 of the 1209 patients (15.5%) in the TRIM trial. Misinterpretation of the index event, an inclusion myocardial infarction, as an early cardiac event was found in 12 patients. After end-point committee judgements, the number of patients with acute myocardial infarction or refractory angina pectoris during 30 days of follow-up was reduced from 177 to 153 (13. 6% reduction). The classification of events was changed in 53 of 187 patients (28.3%) with death, acute myocardial infarction or refractory angina pectoris. The data assessed by the safety committee was significantly different from the final database after end-point committee judgements. CONCLUSION: The end-point committee corrected misinterpretations in such a high proportion of cases that the final results differed significantly from the preliminary results delivered to the safety committee. End-point judgements by an end-point committee should be performed in multicentre clinical trials to improve the quality and reliability of study results.

Anticoagulants↗
PubMed1998

[Implantation of atrial pacemaker in patients with sinoatrial failure].

From 1990 to 1997 a total of 42 atrial pacemakers (41 of them rate responsive) were implanted in patients with sick sinus syndrome at Aust-Agder Central Hospital, Arendal, Norway. 22 women and 20 men aged 42-86 years (average 69 years) were treated. Follow-up time was from 1-80 months (average 26 months). Sinusbradycardia and sinoatrial block were diagnosed in 17 patients, whereas 25 patients suffered from tachybrady syndrome. It was not necessary to change the pacemaker in any of the patients. One patient developed a second degree atrioventricular, Wenckebach type block, two patients developed permanent atrial fibrillation after seven and 43 months, respectively, and five patients were treated for paroxysmal atrial fibrillation. Thus, 34 patients had no need of antiarrhythmic treatment in the follow-up period. Although over 30% of patients who need a pacemaker in Norway suffer from sick sinus syndrome, only 8-12% of them are treated with atrial pacemakers. Recent studies have demonstrated that in patients with sick sinus syndrome there is greater improvement in prognosis and quality of life with physiological pacing than with ventricular pacing. Therefore, more patients should be considered for implantation of atrial pacemakers.

Adult↗
PubMed1998

[Cardiopulmonary complications in acute subarachnoid hemorrhage].

Pathologic electrocardiogram (ECG) may be present in more than 90% of patients with subarachnoid haemorrhage. The ECG findings are often transient and may mimic acute myocardial ischaemia or infarction. These ECG findings may cause diagnostic problems in patients with subarachnoid haemorrhage who are unconscious or who have atypical symptoms. Life-threatening arrhythmias are also seen and may be responsible for sudden deaths in patients with subarachnoid haemorrhage. Other signs of myocardial injury, such as ventricular wall motion dysfunction, elevated enzymes, and histological evidence of contraction band necrosis are described. The myocardial dysfunction known as neurogenic stunned myocardium is reversible if the patient survives the acute phase, but it may lead to haemodynamic instability and contribute to the origin of neurogenic pulmonary oedema. The myocardial injury in subarachnoid haemorrhage may be due to a massive sympathetic stimulation of the myocardium in response to rapidly increasing intracranial pressure. We illustrate myocardial injury and dysfunction in a case report where a patient had subarachnoid haemorrhage with ventricular fibrillation, pulmonary oedema, left ventricular dysfunction and ST-segment elevation, initially thought to be acute myocardial infarction.

Adult↗
PubMed1997

[Calcium channel blockers in heart failure].

Patients with heart failure are particularly susceptible to the negative effects of calcium channel blockers because the failing heart demonstrates a defect in the delivery of calcium to the contractile proteins, and an attenuation of the normal sympathetic reflexes. Currently these drugs have no place in the treatment of heart failure caused by systolic dysfunction of the left ventricle. Calcium channel blockers should probably not be described for patients with coronary artery disease and left ventricular dysfunction. When the patient needs additional treatment for angina and beta-blockers or nitrates have not given satisfactory results, it may be appropriate to prescribe amlodipine or felodipine.

Calcium Channel Blockers↗
PubMed1997

[Patients with diabetes mellitus--secodary prophylaxis after myocardial infarction].

The mortality rate after myocardial infarction is more than twice as large in diabetic patients than in patients without diabetes. Optimal blood sugar control in the acute phase and during follow-up might improve prognosis. The relative reduction in mortality and cardiac events after myocardial infarction by means of betablockers, ACE inhibitors and statins is the same for diabetics as for non-diabetes. However, because of the poorer prognosis, the absolute reduction in mortality is more than twice as high in diabetic as in non-diabetic patients. For this reason, diabetic patients comprise a target group for secondary prevention by means of betablockers, ACE inhibitors and statins after myocardial infarction.

Adrenergic beta-Antagonists↗
PubMed1997

[Nature medicine as intoxicant].

Documentation is often scarce about adverse effects of herbal products used in alternative medicine. Five patients were admitted to hospital with altered consciousness after taking the herbal product Relaxir, a remedy for insomnia and restlessness, produced mainly from the fruit from the passion flower (Passiflora incarnata). Relaxir is thought to have an intoxicating and sedative effect and may also potentiate the effect of other drugs. It is questionable that herbal products liable to cause intoxication are sold without restriction.

Adult↗
PubMed1997

[Treatment of heart failure with beta-blockaders].

Since 1975 several studies have indicated that treatment with beta-adrenergic blocking drugs has a positive effect on prognosis in patients with left ventricular dysfunction. After myocardial infarction, treatment with timolol and propranolol improves prognosis in patients with symptoms of cardiomegaly and heart failure. In patients with idiopathic dilated cardiomyopathy, treatment with metoprolol improves the left ventricular ejection fraction and symptoms of heart failure, and may have a positive effect on prognosis. Recent studies of patients with chronic congestive heart failure also indicate that carvedilol has a positive effect on mortality and morbidity. The authors review some relevant studies, to stimulate the use of beta-adrenergic blocking drugs to treat certain types of heart failure.

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

Effects of 12 weeks of ramipril treatment on the quality of life in patients with moderate congestive heart failure: results of a placebo-controlled trial. Ramipril Study Group.

The assessment of quality of life (QoL) has become recognized as an important tool for evaluating heart failure therapy. The angiotensin-converting enzyme inhibitor ramipril (mean dose 8 mg) was evaluated in 223 patients with moderate chronic congestive heart failure at 24 centers in 4 Nordic countries following a randomized, double-blind, placebo-controlled, parallel group design. The follow-up period was 12 weeks. QoL was evaluated using a questionnaire with 47 items, including the disease-specific Severe Heart Failure Questionnaire, the Sleep Dysfunction Scale, and the Psychological General Well-Being Index. In both treatment groups the total score increased from baseline to 12 weeks for both the Severe Heart Failure Questionnaire and for the Psychological Well-Being Index, reflecting relief of symptoms and improved well-being. However, no significant differences between the placebo and ramipril groups could be detected. Only a trend toward improvement in sleep on ramipril compared with placebo therapy was observed. In conclusion, in this placebo-controlled trial no significant effects of 12-week ramipril treatment of QoL could be demonstrated in patients with moderate congestive heart failure.

Adult↗
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

Absence of effect on exercise capacity of 12-weeks treatment with ramipril in patients with moderate congestive heart failure. Ramipril Study Group.

Pharmacological therapy in cases of chronic congestive heart failure (CHF) is usually evaluated by maximal exercise time. To assess the effect of an angiotensin converting enzyme inhibitor, ramipril, 223 patients with moderate CHF were studied in 24 centres in four Nordic countries in a randomized, double-blind, placebo-controlled, parallel group design. The study drug was titrated from 1.25 mg to a maximum of 10 mg once daily (o.d) over a period of 4 weeks (mean dose 8 mg). A symptom-limited bicycle exercise test, starting at 30 watts and increasing by 10 watts.min-1, was used to evaluate exercise capacity. Reproducible tests were required at baseline, and the test was repeated after 4, 8 and 12 weeks of treatment. Seven deaths were recorded in the placebo group and one death in the ramipril group. A total of 195 patients completed 12 weeks of treatment (placebo group n = 91, ramipril group n = 104). The groups had similar baseline characteristics. Maximal exercise time was increased by mean (SD) 35 s (9) and 41 s (8) in the placebo and ramipril groups, respectively. The adjusted difference between the groups at 12 weeks was 9 s (12) (ns). A significant decrease in blood pressure and rate-pressure product at rest and at end of exercise was obtained by ramipril as compared with placebo. Significantly fewer patients deteriorated in NYHA class from baseline to 12 weeks of ramipril treatment compared to placebo (P = 0.012). Concomitant medication for CHF increased significantly in the placebo group as compared with ramipril-treated patients (P = 0.003).(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac Output, Low↗
PubMed1994

Neurohormonal activation in patients with mild or moderately severe congestive heart failure and effects of ramipril. The Ramipril Trial Study Group.

OBJECTIVES: To describe neurohormonal activation in patients with mild or moderate heart failure and how it may be modified by treatment with ramipril. SETTING: Cardiology departments at 24 hospitals in Denmark, Finland, Norway, and Sweden. PATIENTS: 223 patients with mild or moderately severe congestive heart failure who were taking diuretics with or without digitalis. DESIGN: Randomised, double bind, multicentre, placebo controlled comparison of ramipril and placebo. Venous blood samples were drawn at rest, before blind treatment, and after 12 weeks of treatment with the study drug. A probability prediction score for mortality derived by stepwise linear discriminant from neurohormone data in the first cooperative north Scandinavian enalapril survival study (CONSENSUS I) was used to assess combined activity of the different neurohormonal systems. RESULTS: Plasma concentrations of atrial natriuretic peptide were raised at baseline but angiotensin II, aldosterone, and noradrenaline concentrations were within normal limits. There was, however, a wide interindividual variation. Plasma noradrenaline concentration and prediction score were higher among patients with class III congestive heart failure according to the New York Heart Association's classification than among patients with class II congestive heart failure (P < 0.05). There was a modest but significant inverse correlation between exercise duration at baseline and plasma noradrenaline concentration (r = -0.21, P = 0.0023), aldosterone concentration (r = -0.14, P = 0.04), and prediction score (r = -0.24, P = 0.0004). Prediction score at baseline was significantly higher among those who died (n = 10) than among survivors (P = 0.03). Angiotensin converting enzyme activity was suppressed and plasma concentrations of aldosterone and atrial natriuretic peptide were reduced after 12 weeks of treatment with ramipril compared with placebo. In patients with the most pronounced neurohormonal activation at baseline (highest third of noradrenaline concentration or prediction score), noradrenaline concentration and prediction score were significantly lower after 12 weeks of taking ramipril compared with placebo. Patients with a prediction score in the highest third at baseline had a higher heart rate than to those in the lowest third (P = 0.003). CONCLUSIONS: Neurohormonal activation is associated with the degree of symptoms and the severity of disease in mild or moderately severe congestive heart failure. Treatment with ramipril attenuates neurohormonal activation. This effect is most pronounced among patients with the highest circulating concentrations of neurohormones before the start of treatment.

Adult↗
PubMed1993

[Protein S deficiency, acute phase reaction and thrombosis].

Protein S deficiency increases risk of thrombosis. At present, we have information on 63 Norwegian individuals with hereditary protein S deficiency belonging to 25 different families. 42 of the individuals have experienced at least one thromboembolic episode, and seven a cerebral infarction before the age of 70 years. The amount of free protein S in plasma is dependent on variation of the acute phase protein C4b-binding protein (C4bBP). Acute phase response with increased C4bBP induces free protein S deficiency, and increases risk of thrombosis. In patients with protein S deficiency, warfarin may reduce free protein S to critically low levels, and thus explain why, in some patients, recurrent thrombosis occurs during warfarin treatment. In this situation, warfarin should be replaced by heparin.

Acute-Phase Proteins↗
PubMed1993

[Familial protein S deficiency].

Protein S deficiency is an autosomal dominant inherited disease. The authors describe a family in which 27 of the 52 members had a deficiency of S protein. Eight family members have suffered from thromboembolic disease.

Adult↗